OBESITY A M EDICAL D ICTIONARY , B IBLIOGRAPHY , AND A NNOTATED R ESEARCH G UIDE TO I NTERNET R E FERENCES
J AMES N. P ARKER , M.D. AND P HILIP M. P ARKER , P H .D., E DITORS
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ICON Health Publications ICON Group International, Inc. 4370 La Jolla Village Drive, 4th Floor San Diego, CA 92122 USA Copyright 2003 by ICON Group International, Inc. Copyright 2003 by ICON Group International, Inc. All rights reserved. This book is protected by copyright. No part of it may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without written permission from the publisher. Printed in the United States of America. Last digit indicates print number: 10 9 8 7 6 4 5 3 2 1
Publisher, Health Care: Philip Parker, Ph.D. Editor(s): James Parker, M.D., Philip Parker, Ph.D. Publisher's note: The ideas, procedures, and suggestions contained in this book are not intended for the diagnosis or treatment of a health problem. As new medical or scientific information becomes available from academic and clinical research, recommended treatments and drug therapies may undergo changes. The authors, editors, and publisher have attempted to make the information in this book up to date and accurate in accord with accepted standards at the time of publication. The authors, editors, and publisher are not responsible for errors or omissions or for consequences from application of the book, and make no warranty, expressed or implied, in regard to the contents of this book. Any practice described in this book should be applied by the reader in accordance with professional standards of care used in regard to the unique circumstances that may apply in each situation. The reader is advised to always check product information (package inserts) for changes and new information regarding dosage and contraindications before prescribing any drug or pharmacological product. Caution is especially urged when using new or infrequently ordered drugs, herbal remedies, vitamins and supplements, alternative therapies, complementary therapies and medicines, and integrative medical treatments. Cataloging-in-Publication Data Parker, James N., 1961Parker, Philip M., 1960Obesity: A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References / James N. Parker and Philip M. Parker, editors p. cm. Includes bibliographical references, glossary, and index. ISBN: 0-597-83663-9 1. Obesity-Popular works. I. Title.
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Disclaimer This publication is not intended to be used for the diagnosis or treatment of a health problem. It is sold with the understanding that the publisher, editors, and authors are not engaging in the rendering of medical, psychological, financial, legal, or other professional services. References to any entity, product, service, or source of information that may be contained in this publication should not be considered an endorsement, either direct or implied, by the publisher, editors, or authors. ICON Group International, Inc., the editors, and the authors are not responsible for the content of any Web pages or publications referenced in this publication.
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Acknowledgements The collective knowledge generated from academic and applied research summarized in various references has been critical in the creation of this book which is best viewed as a comprehensive compilation and collection of information prepared by various official agencies which produce publications on obesity. Books in this series draw from various agencies and institutions associated with the United States Department of Health and Human Services, and in particular, the Office of the Secretary of Health and Human Services (OS), the Administration for Children and Families (ACF), the Administration on Aging (AOA), the Agency for Healthcare Research and Quality (AHRQ), the Agency for Toxic Substances and Disease Registry (ATSDR), the Centers for Disease Control and Prevention (CDC), the Food and Drug Administration (FDA), the Healthcare Financing Administration (HCFA), the Health Resources and Services Administration (HRSA), the Indian Health Service (IHS), the institutions of the National Institutes of Health (NIH), the Program Support Center (PSC), and the Substance Abuse and Mental Health Services Administration (SAMHSA). In addition to these sources, information gathered from the National Library of Medicine, the United States Patent Office, the European Union, and their related organizations has been invaluable in the creation of this book. Some of the work represented was financially supported by the Research and Development Committee at INSEAD. This support is gratefully acknowledged. Finally, special thanks are owed to Tiffany Freeman for her excellent editorial support.
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About the Editors James N. Parker, M.D. Dr. James N. Parker received his Bachelor of Science degree in Psychobiology from the University of California, Riverside and his M.D. from the University of California, San Diego. In addition to authoring numerous research publications, he has lectured at various academic institutions. Dr. Parker is the medical editor for health books by ICON Health Publications. Philip M. Parker, Ph.D. Philip M. Parker is the Eli Lilly Chair Professor of Innovation, Business and Society at INSEAD (Fontainebleau, France and Singapore). Dr. Parker has also been Professor at the University of California, San Diego and has taught courses at Harvard University, the Hong Kong University of Science and Technology, the Massachusetts Institute of Technology, Stanford University, and UCLA. Dr. Parker is the associate editor for ICON Health Publications.
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About ICON Health Publications To discover more about ICON Health Publications, simply check with your preferred online booksellers, including Barnes & Noble.com and Amazon.com which currently carry all of our titles. Or, feel free to contact us directly for bulk purchases or institutional discounts: ICON Group International, Inc. 4370 La Jolla Village Drive, Fourth Floor San Diego, CA 92122 USA Fax: 858-546-4341 Web site: www.icongrouponline.com/health
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Table of Contents FORWARD .......................................................................................................................................... 1 CHAPTER 1. STUDIES ON OBESITY ..................................................................................................... 3 Overview........................................................................................................................................ 3 The Combined Health Information Database................................................................................. 3 Federally Funded Research on Obesity ........................................................................................ 15 E-Journals: PubMed Central ....................................................................................................... 71 The National Library of Medicine: PubMed ................................................................................ 79 CHAPTER 2. NUTRITION AND OBESITY ......................................................................................... 167 Overview.................................................................................................................................... 167 Finding Nutrition Studies on Obesity....................................................................................... 167 Federal Resources on Nutrition ................................................................................................. 175 Additional Web Resources ......................................................................................................... 176 CHAPTER 3. ALTERNATIVE MEDICINE AND OBESITY ................................................................... 179 Overview.................................................................................................................................... 179 The Combined Health Information Database............................................................................. 179 National Center for Complementary and Alternative Medicine................................................ 180 Additional Web Resources ......................................................................................................... 192 General References ..................................................................................................................... 202 CHAPTER 4. DISSERTATIONS ON OBESITY..................................................................................... 203 Overview.................................................................................................................................... 203 Dissertations on Obesity............................................................................................................ 203 Keeping Current ........................................................................................................................ 216 CHAPTER 5. CLINICAL TRIALS AND OBESITY ............................................................................... 217 Overview.................................................................................................................................... 217 Recent Trials on Obesity............................................................................................................ 217 Keeping Current on Clinical Trials ........................................................................................... 238 CHAPTER 6. PATENTS ON OBESITY ............................................................................................... 241 Overview.................................................................................................................................... 241 Patents on Obesity ..................................................................................................................... 241 Patent Applications on Obesity ................................................................................................. 335 Keeping Current ........................................................................................................................ 393 CHAPTER 7. BOOKS ON OBESITY ................................................................................................... 395 Overview.................................................................................................................................... 395 Book Summaries: Federal Agencies............................................................................................ 395 Book Summaries: Online Booksellers......................................................................................... 400 The National Library of Medicine Book Index ........................................................................... 415 Chapters on Obesity................................................................................................................... 416 Directories.................................................................................................................................. 425 CHAPTER 8. MULTIMEDIA ON OBESITY ........................................................................................ 427 Overview.................................................................................................................................... 427 Video Recordings ....................................................................................................................... 427 Audio Recordings....................................................................................................................... 432 Bibliography: Multimedia on Obesity........................................................................................ 433 CHAPTER 9. PERIODICALS AND NEWS ON OBESITY ..................................................................... 435 Overview.................................................................................................................................... 435 News Services and Press Releases.............................................................................................. 435 Newsletters on Obesity .............................................................................................................. 441 Newsletter Articles .................................................................................................................... 442 Academic Periodicals covering Obesity ..................................................................................... 454 APPENDIX A. PHYSICIAN RESOURCES .......................................................................................... 457 Overview.................................................................................................................................... 457
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Contents NIH Guidelines.......................................................................................................................... 457 NIH Databases........................................................................................................................... 459 Other Commercial Databases..................................................................................................... 467 The Genome Project and Obesity............................................................................................... 467 APPENDIX B. PATIENT RESOURCES ............................................................................................... 473 Overview.................................................................................................................................... 473 Patient Guideline Sources.......................................................................................................... 473 Associations and Obesity ........................................................................................................... 494 Finding Associations.................................................................................................................. 497 APPENDIX C. FINDING MEDICAL LIBRARIES ................................................................................ 499 Overview.................................................................................................................................... 499 Preparation................................................................................................................................. 499 Finding a Local Medical Library................................................................................................ 499 Medical Libraries in the U.S. and Canada ................................................................................. 499
ONLINE GLOSSARIES................................................................................................................ 505 Online Dictionary Directories ................................................................................................... 508 OBESITY DICTIONARY.............................................................................................................. 509 INDEX .............................................................................................................................................. 605
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FORWARD In March 2001, the National Institutes of Health issued the following warning: "The number of Web sites offering health-related resources grows every day. Many sites provide valuable information, while others may have information that is unreliable or misleading."1 Furthermore, because of the rapid increase in Internet-based information, many hours can be wasted searching, selecting, and printing. Since only the smallest fraction of information dealing with obesity is indexed in search engines, such as www.google.com or others, a non-systematic approach to Internet research can be not only time consuming, but also incomplete. This book was created for medical professionals, students, and members of the general public who want to know as much as possible about obesity, using the most advanced research tools available and spending the least amount of time doing so. In addition to offering a structured and comprehensive bibliography, the pages that follow will tell you where and how to find reliable information covering virtually all topics related to obesity, from the essentials to the most advanced areas of research. Public, academic, government, and peer-reviewed research studies are emphasized. Various abstracts are reproduced to give you some of the latest official information available to date on obesity. Abundant guidance is given on how to obtain free-of-charge primary research results via the Internet. While this book focuses on the field of medicine, when some sources provide access to non-medical information relating to obesity, these are noted in the text. E-book and electronic versions of this book are fully interactive with each of the Internet sites mentioned (clicking on a hyperlink automatically opens your browser to the site indicated). If you are using the hard copy version of this book, you can access a cited Web site by typing the provided Web address directly into your Internet browser. You may find it useful to refer to synonyms or related terms when accessing these Internet databases. NOTE: At the time of publication, the Web addresses were functional. However, some links may fail due to URL address changes, which is a common occurrence on the Internet. For readers unfamiliar with the Internet, detailed instructions are offered on how to access electronic resources. For readers unfamiliar with medical terminology, a comprehensive glossary is provided. For readers without access to Internet resources, a directory of medical libraries, that have or can locate references cited here, is given. We hope these resources will prove useful to the widest possible audience seeking information on obesity. The Editors
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From the NIH, National Cancer Institute (NCI): http://www.cancer.gov/cancerinfo/ten-things-to-know.
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CHAPTER 1. STUDIES ON OBESITY Overview In this chapter, we will show you how to locate peer-reviewed references and studies on obesity.
The Combined Health Information Database The Combined Health Information Database summarizes studies across numerous federal agencies. To limit your investigation to research studies and obesity, you will need to use the advanced search options. First, go to http://chid.nih.gov/index.html. From there, select the “Detailed Search” option (or go directly to that page with the following hyperlink: http://chid.nih.gov/detail/detail.html). The trick in extracting studies is found in the drop boxes at the bottom of the search page where “You may refine your search by.” Select the dates and language you prefer, and the format option “Journal Article.” At the top of the search form, select the number of records you would like to see (we recommend 100) and check the box to display “whole records.” We recommend that you type “obesity” (or synonyms) into the “For these words:” box. Consider using the option “anywhere in record” to make your search as broad as possible. If you want to limit the search to only a particular field, such as the title of the journal, then select this option in the “Search in these fields” drop box. The following is what you can expect from this type of search: •
The Association of Obesity with Osteoarthritis of the Hand and Knee in Women: A Twin Study Source: Journal of Rheumatology. 23(7):1221-26; 1996. Summary: This study examines the association of obesity and osteoarthritis (OA) at various sites in middle aged women and estimates the magnitude of the weight difference associated with OA. Researchers performed a co-twin control study within a population of women aged 48 to 70 years. OA was defined radiologically using site specific features and a standard atlas. Twin pairs discordant for OA disease traits were analyzed. Findings reveal the mean weight differences within twin pairs discordant for different OA traits were: tibiofemoral osteophytes 3.75 kg; patellofemoral osteophytes 3.05 kg; and carpometacarpal (CMC) osteophytes 3.06 kg. There was no significant difference in weight within twin pairs discordant for osteophytes at the distal
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interphalangeal or proximal interphalangeal joints or for joint space narrowing at all sites examined except the patellofemoral joint, 4.73 kg. For each kg increase in weight the increased likelihood of developing different OA traits was: tibiofemoral osteophytes 1.14, patellofemoral osteophytes 1.32, patellofemoral narrowing 1.15, and CMC 1.09. The authors suggest obesity is an important risk factor for development of OA at the tibiofemoral and patellofemoral joints of the knee and CMC joints of the hands, with significant increases of 9 to 13 percent in risk of OA per kg increase in body weight. This emphasizes the potential importance of even minor weight reduction as a preventive health measure for OA. 26 references, 6 tables. (AA-M). •
Self-reported Functional Status in Osteoarthritis of the Knee in a Rural Southern Community: The Role of Sociodemographic Factors, Obesity, and Knee Pain Source: Arthritis Care and Research. 9(4):273-278; August 1996. Summary: This journal article for health professionals describes a study that examined the role of Sociodemographic factors, such as age, race, gender, education, and marital status; obesity; severity of radiographic knee osteoarthritis (OA); and severity of knee pain in self-reported disability from OA. The sample included 1,272 African- Americans and Caucasians, aged 45 years or older, from the Johnston County Osteoarthritis Project. Analysis of variance was used to assess variation in mean Health Assessment Questionnaire (HAQ) scores by the above variables. Results indicate that mean HAQ scores differed by severity of radiographic knee OA and knee pain, obesity, and all demographic factors, except race. Only age, female sex, obesity, and knee pain severity were independent effects. Disability associated with knee pain varied by both radiographic knee OA severity and obesity. Findings suggest that knee pain severity was more important than radiographic knee OA severity in determining disability and that obesity compounded disability from knee pain. The article recommendations that future studies of disability in knee OA should include assessment of obesity, severity of radiographic knee OA, and severity of knee pain, as well as their interactions. 30 references and 4 tables. (AA-M).
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Can Obesity Explain the Racial Difference in Stage of Breast Cancer at Diagnosis Between Black and White Women? Source: Journal of Women's Health and Gender-based Medicine. 11(6):527-536, JulyAugust 2002. Summary: Researchers identified 966 incident cases of breast cancer between 1991 and 1997 from Baltimore, Maryland, hospitals to assess to what extent the racial difference in stage at diagnosis can be explained by racial differences in obesity. They reviewed hospital medical records to gather data on (1) age, (2) race, (3) weight, (4) height, (5) cancer detection methods, (6) treatment procedures, and (7) pathology reports. Of the participants, (1) 585 (60 percent) were white; (2) 381 (40 percent) were black; and (3) black women were less educated, resided in an area with a lower median income, were more likely to be uninsured or on Medicaid, and were more likely to be unmarried. Results showed that (1) black women had significantly higher body mass index (BMI) than white women; (2) about 48 percent of black women were obese compared with 26 percent of white women; (3) after adjusting for age, black women had 3.85 times the odds of being obese compared with white women; (4) black women had more advanced breast cancer than white women at diagnosis; (5) high BMI was associated with an advanced stage of breast cancer at diagnosis; and (6) adjustment for the higher prevalence of obesity in black women reduced the risk estimate of more advanced stage of breast cancer at diagnosis in black women compared with white women by about 30
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percent. The researchers conclude that the higher prevalence of obesity among black women explains part but not all of their relative disadvantage in stage at diagnosis of breast cancer. 4 tables, 87 references. •
Screening for Cervical and Breast Cancer: Is Obesity an Unrecognized Barrier to Preventive Care? Source: Annals of Internal Medicine. 132(9):697-704, May 2, 2000. Summary: Researchers examined the relationship between obesity and screening for cervical and breast cancer with Papanicolaou (Pap) smears and mammography. Investigators extracted data from the Year 2000 Supplement of the 1994 National Health Interview Survey. The responses on Pap smears and mammography screening were related to the body mass index (BMI). Obesity was divided into three classes: (1) Class I, BMI 30 to less than 35 kg/m2; (2) class II, BMI 35 to less than 40 kg/m2; and (3) class III, BMI 40 kg/m2 or greater. Women who were underweight made up approximately 3 percent of the sample and were included in all analyses, but their results are not reported. The following sociodemographic factors were included in the analysis as potential confounders: (1) Age, (2) ethnicity/race, (3) marital status, (4) education, (5) annual income, (6) type of health insurance coverage, and (7) region of the United States. Adjustments were made for illness burden using surrogate markers such as (1) selfreported health status, (2) number of days hospitalized in the past year, (3) number of days spent in bed, and (4) number of visits to a physician in the past year. Factors related to the provider, such as specialty of the usual provider and usual place where medical care was received, were also incorporated in the analysis. Of 8,394 women in the survey who were eligible for Pap smear analysis (age 18 to 75 who had not undergone a hysterectomy), 7,857 had complete data on height, weight, and performance of Pap smears. More than 50 percent of these women had normal BMI's. Overweight and obese women reported significantly lower Pap smear screening rates in the past 3 years than did normal weight women, 78 and 78 percent versus 84 percent, respectively. Heavier women were usually older, were less likely to be white or to have private health insurance, and had lower socioeconomic status. They reported a greater illness burden and were more likely to receive their usual health care from general internists and family practitioners than from gynecologists. After adjustment for sociodemographic factors, insurance, and access to health care, Pap smear screening rate differences were still seen between overweight and obese women compared to normalweight women. Of 3,397 women eligible for mammography analysis (age 50 to 75) who had complete information on weight and height, more than half of these were considered overweight or obese. Overall, the unadjusted rate of mammography use during the past 2 years was 65 percent. Overweight and obese women were significantly less likely to report previous mammography in the past 2 years compared to normalweight women. After adjustment for sociodemographics, insurance, and access to health care, mammography screening rate differences between overweight and obese women were also statistically significant compared to normal-weight women. The researchers concluded that overweight and obese women were found less likely to be screened for cervical and breast cancer with Pap smears and mammography than normal-weight women, even after adjusting for other known barriers. Because overweight and obese women have higher mortality rates for cervical and breast cancer, they should be targeted for increased screening. 4 tables, 35 references.
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Effect of Obesity on Screening Mammography: Outcomes Analysis of 88,346 Consecutive Examinations Source: American Journal of Roentgenology. 174(5):1251-1255, May 2000. Summary: Researchers examined the effects of obesity on screening mammography outcome. They performed a retrospective review of 88,346 consecutive screening examinations performed at the Department of Radiology, University of California San Francisco Medical Center (SFMC) between April 1985 and August 1997. They correlated self-reported weights of the patients with their self-reported heights and normalized these to their ideal weight using standard height/weight tables. Based on this, researchers divided patients into adiposity cohorts: (1) Underweight by at least 11 percent, (2) within 10 percent of ideal weight, (3) overweight by 11 to 24 percent, (4) overweight by 25 to 39 percent, and (5) overweight by more than 40 percent. The rates of recall, biopsy, and breast cancer detection of the patients were determined by contacting each woman's personal physician and searching the SFMC's radiology and pathology databases. Mammography screening of the 88,346 women resulted in 4,484 recalls, 1,228 biopsies performed, and 425 cases of screening-detected breast cancer. Differences between the adiposity cohorts for rates of recall, biopsy, and cancer detection were statistically reliable and meaningful. The recall rate increased with progressively increasing adiposity, from 3.88 percent of women who were underweight to 5.55 percent for those who overweight by more than 40 percent. Similar progressive increases in the rate of biopsy and cancer detection per 1,000 women screened with increasing adiposity were also seen, from 0.98 to 1.65 percent and from 3.74 to 6.04 percent. Increasing adiposity also could be correlated with increasing median tumor size and with a more advanced disease stage at diagnosis. Researchers conclude that increasing adiposity correlates with progressive increases in the rates of recall, biopsy, and cancer detection in women undergoing screening mammography. Increasing adiposity also correlates with increased cancer size and stage. These findings provide additional support for the view that obesity is a risk factor for breast cancer. 8 tables, 34 references.
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Is Obesity a Barrier to Physician Screening for Cervical Cancer? Source: American Journal of Medicine. 98(5):491-496, May 1995. Summary: Researchers examined whether obesity affects adherence to recommended guidelines for the performance of Papanicolaou (Pap) smears. Researchers collected data prospectively from May through October of 1989 at the Regenstrief Health Center's General Medicine Practice in Indianapolis, Indiana. This practice provides primary care to a low-income, inner-city population. Researchers gathered data during a clinical trial from 92 randomly-selected physicians who received reminders that required a response as to whether they had performed the Pap smear, and the reason for the action or inaction. Researchers also collected data from questionnaires completed during the first study visit by 970 patients. Patient-specific data came from the health center's medical record system. Researchers defined a body weight greater than 130 percent of ideal as obesity, and a body weight greater than 200 percent of ideal as morbid obesity. To examine the relationship of obesity to the reasons physicians noted for not performing a Pap smear, researchers grouped physician responses into five categories: (1) Patient's psychological concerns; (2) lack of patient time; (3) physician's belief that the patient was terminally ill or too old; (4) patient's physiological reason (acute illness, vaginitis, or menstruation); and (5) lack of physician time. Results showed no significant demographic differences between nonobese and all other women, except for age; obese and morbidly-obese women were younger than nonobese women. According to physician responses, 200 (21 percent) of the women received Pap smears, 136 (14
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percent) were not truly eligible, 143 (15 percent) refused Pap smears, and 491 (51 percent) had their Pap smears rescheduled. All three weight categories had low Pap smear performance, but differences between groups were neither clinically- nor statistically-significant. Comparisons of the odds ratios for obese and morbidly-obese women demonstrated a significant dose-response effect of weight on the proportion of women whose physicians reported not performing a Pap smear due to acute illness, vaginitis, or menstruation. Overall, results did not demonstrate an association between obesity and a reduction in Pap smear performance. 1 figure, 4 tables, 26 references. •
Smell and Taste in Children with Simple Obesity Source: International Journal of Pediatric Otorhinolaryngology. 55(3): 191-196. October 16, 2000. Contact: Available from Elsevier Science. P.O. Box 945, New York, NY 10159-0945. (888) 437-4636. Fax (212) 633-3680. E-mail:
[email protected]. Summary: This article reports on a study of 30 children, aged 10 to 16 years and suffering from simple obesity, in whom significantly lowered odor detection thresholds were noted. The thresholds were lower than the average for a given age group in around 20 percent of obese children in cases of odors that stimulated the olfactory nerve and in approximately 57 percent in cases of substances that stimulated both olfactory and trigeminal nerves. Odor identification thresholds were similarly affected, with identification of olfactory nerve plus trigeminal nerve stimulating odors affected more than twice as frequently. In 77 percent of cases, the electrogustometric thresholds were found below the normal range values when anode was used as the stimulating electrode. The authors hypothesize that the detected alterations may be linked to metabolic disturbances, which accompany simple obesity. 3 figures. 1 table. 18 references.
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Obesity: Effects on the Liver and Gastrointestinal System Source: Current Opinion in Gastroenterology. 15(2): 154-158. March 1999. Contact: Available from Lippincott Williams and Wilkins Publishers. 12107 Insurance Way, Hagerstown, MD 21740. (800) 637-3030. Fax (301) 824-7390. Summary: Obesity, determined by a body mass index (BMI) greater than 30, has assumed epidemic proportions in the U.S. More than a cosmetic issue, obesity is associated with many comorbidities that contribute to multiple organ dysfunction, illness, and shortened life span. This review article covers new and emerging information on the relationship between obesity and common and debilitating hepatic and gastrointestinal disorders, including nonalcoholic steatohepatitis, gastroesophageal reflux, gallstones, and colon and esophageal cancer. Because these complications can be prevented or treated by optimizing body weight, it is important that the practicing gastroenterologist include the evaluation and treatment of obesity as part of the general approach to the patient. Calculation of BMI is the most reliable and predictive tool for assessing obesity and effective weight reduction. Multiple, often unsatisfactory, medical strategies exist for weight reduction, each optimally requiring the ancillary services of a professional dietitian. Compelling evidence points to the surgical approach to the severely obese. The author concludes that understanding the role of obesity in these disorders should lead to new insights into the pathogenesis of common liver and gastrointestinal diseases and to new treatment strategies for the practicing gastroenterologist. 41 references (21 annotated).
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Leptin, Obesity, and Liver Disease Source: Gastroenterology. 115(4): 997-1001. October 1998. Contact: Available from W.B. Saunders Company. 6277 Sea Harbor Drive, Orlando, FL 19106-3399. (800) 654-2452 or (407) 345-4000. Summary: This review article summarizes emerging information about relationships among obesity, liver disease, and leptin, a cytokine intimately involved in regulating weight and energy metabolism. Obesity is a multisystem disease that results from a failure of normal homeostatic mechanisms regulating food intake, fat storage, and energy utilization. Common gastrointestinal sequelae of obesity are gastroesophageal reflux disease, gallstones, hepatic steatosis, and nonalcoholic steatohepatitis. The regulation of body weight and fat stores is a complex process involving multiple neural, endocrine, and paracrine regulatory pathways; tight regulation of energy metabolism is one of the critical homeostatic functions of the hypothalamus. Leptin is a circulating cytokine discovered through its role in regulating body weight and energy metabolism. Accumulating evidence suggests that, like other cytokines, leptin has diverse and complex metabolic effects. In the liver, these effects may include a role in regulating fat deposition, fibrogenesis, and inflammation. Obesity in humans, like diet-induced obesity in rodents, is associated with elevated levels of circulating leptin and hypothalamic insensitivity to this protein. Because leptin is an important regulator of both insulin secretion and hepatic responsiveness to insulin action, altered leptin signaling in obese people may contribute to hepatic steatosis. Additional study on the nature and magnitude of leptin's activities in the liver and digestive tract is needed. 1 figure. 34 references.
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Obesity and Gastro-Oesophageal Reflux: Is There a Relationship? Source: European Journal of Gastroenterology and Hepatology. 8(7): 625-626. July 1996. Summary: In this article, the author considers the relationship between obesity and gastroesophageal reflux disease (GERD). The author reviews some of the information that might support or refute even the hypothetical possibility that obesity is a cause of excessive acid reflux. The author concludes that obesity per se should not be considered an etiologic factor in GERD. However, the relationship of GERD symptoms to weight gain and loss cannot go unnoticed. The author hypothesizes that common clinical observations linking GERD symptoms to acute changes in weight are related to changes in the quantity of fat ingested and the volume of the meals. 9 references.
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Obesity and Its Health Risks Source: Current Opinion in Gastroenterology. 12(2): 204-209. March 1996. Contact: Available from Rapid Science Publishers. 400 Market Street, Suite 700, Philadelphia, PA 19106. (215) 574-2266. Fax (215) 574-2292. Summary: This article reviews obesity and its health risks, focusing on the following gastrointestinal complications: increased risk of gallstones (especially during weight reduction); pancreatitis related to gallstones or hyperlipidemia with worse clinical outcome; nonalcoholic steatohepatitis; and increased risks of adenocarcinoma of the esophagus, colorectal adenoma, and cancer. The authors also discuss new studies that define abnormalities in the genetic regulation of appetite and energy metabolism. Treatment options continue to evolve, with improved pharmacologic approaches to appetite and strong support for gastric bypass surgery as the most effective treatment of severely obese patients. 39 references (20 annotated). (AA-M).
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Risk of Symptomatic Gallstones in Women with Severe Obesity Source: American Journal of Clinical Nutrition. 55(3): 652-658. March 1992. Summary: This article reports on a study that investigated the risk of symptomatic gallstones in women with severe obesity. Among 90,302 women aged 34-59 at baseline followed from 1980 to 1988, 2,122 cases of newly diagnosed symptomatic gallstones occurred. From 1980 to 1986, 488 cases of newly diagnosed unremoved gallstones were documented. The authors note a striking increase in gallstone disease risk with obesity. Recent weight loss was associated with a modestly increased risk after adjustment for body mass index (BMI) before weight loss. Current smoking was an independent risk factor for gallstones. 5 tables. 33 references. (AA-M).
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Obesity Surgery Regaining Favor Source: Medical World News. 32(5): 37. May 1991. Summary: This article discusses the recent interest and partial approval by the medical community of gastrointestinal sugery for severe obesity. After a definition of the situations in which such surgery may be appropriate, the author details the complications that might be encountered. Investigators reported sustained weight loss in 50 to 60 percent of patients after five to ten years of follow-up, results clearly surpassing the generally dismal track record of a multitude of special diets and behavior modification programs in treating severely obese patients. The author also considers costs of the surgery, insurance coverage, and the issue of primary care physicians not being interested in managing severely obese patients through nonsurgical strategies.
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Hormone Replacement Therapy, Insulin Sensitivity, and Abdominal Obesity in Postmenopausal Women Source: Diabetes Care. 25(1): 127-133. January 2002. Contact: Available from American Diabetes Association. 1701 North Beauregard Street, Alexandria, VA 22311. (800) 232-3472. Website: www.diabetes.org. Summary: This article reports on a study undertaken to determine whether insulin sensitivity differs between postmenopausal women taking estradiol, women on estrogen plus progesterone hormone replacement therapy (HRT), and women not on HRT and whether differences are explained by the differences in total or abdominal adiposity and fat deposition in the muscle. The authors studied 28 obese, sedentary postmenopausal Caucasian women. Women taking oral estrogen (n = 6) were matched for age, weight, and body mass index (BMI) with women not on HRT (n = 6). Eight women taking oral estrogen plus progesterone were matched with eight different women not on HRT for age, weight, and BMI. Maximal aerobic capacity, percentage of fat, total body fat mass, and fat-free mass (FFM) were similar between groups. Visceral fat, subcutaneous abdominal fat, sagittal diameter, and mid thigh low density lean tissue (intramuscular fat) did not differ by hormone status. Basal carbohydrate and fat utilization was not different among groups. Fasting plasma glucose and insulin did not differ by hormone use. Glucose utilization (M) was measured; postmenopausal women taking oral estrogen had a 31 percent lower M than women not on HRT. M was 26 percent lower in women taking estrogen plus progesterone than women not on HRT. M per I, the amount of glucose metabolized per unit of plasma insulin (I), an index of insulin sensitivity, was 36 percent lower in women taking estrogen compared with matched women not on HRT and 28 percent lower in women taking estrogen plus progesterone compared with matched women not on HRT. The authors conclude that
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postmenopausal women taking oral estrogen or those taking a combination of estrogen and HRT are more insulin-resistant than women not on HRT, even when women are of comparable total and abdominal adiposity. 1 figure. 3 tables. 49 references. •
New Insights in Obesity Source: Diabetes Care. 25(4): 789-795. April 2002. Contact: Available from American Diabetes Association. 1701 North Beauregard Street, Alexandria, VA 22311. (800) 232-3472. Website: www.diabetes.org. Summary: Next to tobacco use, low levels of physical activity and poor dietary habits are the major factors in the United States leading to increases in mortality. This article is the sixth in a series of reports on the American Diabetes Association (ADA) 61st Scientific Sessions held in Philadelphia, Pennsylvania in June 2001; this article covers topics related to the treatment of type 2 diabetes, primarily obesity. Topics include childhood obesity, clinical studies of obesity, obesity treatment, adipocyte secretory products, and obesity and the brain. In each area, the author summarizes research presented during the conference. 5 references.
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Surgery for Obesity Source: Diabetes Forecast. 55(4): 81-86. April 2002. Contact: Available from American Diabetes Association. 1701 North Beauregard Street, Alexandria, VA 22311. (800) 232-3472. Website: www.diabetes.org. Summary: This article, one in a series of six articles on healthy weight loss, describes the use of surgery for obesity. Written for people with diabetes, the article first defines morbid obesity, which includes being at least 100 pounds over ideal body weight, having a body mass index (BMI) of 35 or more, and having 25 percent or more body fat. The authors then note that indications for surgery for morbid obesity include BMI greater than 40 or BMI greater than 35 in patients with medical problems that would improve with weight loss. The authors discuss the different procedures that can be used (restrictive, malabsorptive, or combination procedures), patient selection, common complications, weight loss potential, reversal of type 2 diabetes, and the long term results for patients who have undergone this type of surgery. The authors conclude with a brief section reviewing the decision making process that accompanies any consideration of surgery for obesity. 3 figures. 2 tables.
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Prevention of Overweight and Obesity in Children: Influences on the Food Environment Source: Diabetes Educator. 28(3): 415-423. May-June 2002. Contact: Available from American Association of Diabetes Educators. 100 West Monroe Street, 4th Floor, Chicago, IL 60603-1901. (312) 424-2426. Summary: There is an epidemic of pediatric overweight and obesity leading to type 2 diabetes in youth. This review article describes the multiple paths of influence on the food environment of youth and identifies diabetes education strategies that are focused on the early prevention of overweight and obesity. The authors conducted a review of relevant professional literature. Their results show that models of obesity prevention in youth need to address genetic factors that influence the development of food preferences in the young child, parenting influences on eating pattern development, and access to and availability of foods in the physical environment of the child. Early
Studies 11
intervention with parents of young children is required to prevent the development of eating patterns that lead to pediatric obesity and type 2 diabetes in youth. Diabetes educators need to be able to inform parents of the multiple paths of influence on the food environment of the child and to suggest strategies to encourage the development of positive food preferences and intake. 1 figure. 1 table. 52 references. •
Diabetes Contributes to Cholesterol Metabolism Regardless of Obesity Source: Diabetes Care. 25(9): 1511-1513. September 2002. Contact: Available from American Diabetes Association. 1701 North Beauregard Street, Alexandria, VA 22311. (800) 232-3472. Website: www.diabetes.org. Summary: This article reports on a study undertaken to investigate cholesterol metabolism in obesity with and without diabetes. The authors performed cross-sectional metabolic studies in individuals with and without type 2 diabetes. The study included 16 obese subjects with diabetes (mean age 52 years, plus or minus 2 years) and 16 nondiabetic control subjects of similar age and weight. Serum total cholesterol did not differ between the groups, but LDL and HDL cholesterol were significantly lower and VLDL cholesterol and serum total and CLDL triglycerides were higher in the diabetes group compared to the control group. Cholesterol synthesis was higher and neutral sterol and bile acid excretion and cholesterol turnover tended to be higher in the diabetes group than in the control group. In addition, blood glucose was significantly positively related to fecal neutral sterol excretion in both groups. Cholesterol absorption efficiency was lower and cholesterol synthesis was higher in obese subjects with diabetes than in those without diabetes, suggesting that diabetes modulates cholesterol metabolism more than obesity alone. 1 figure. 3 tables. 32 references.
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Prospective Study of Obesity and Risk of Coronary Heart Disease Among Diabetic Women Source: Diabetes Care. 25(7): 1142-1148. July 2002. Contact: Available from American Diabetes Association. 1701 North Beauregard Street, Alexandria, VA 22311. (800) 232-3472. Website: www.diabetes.org. Summary: This article reports on a study undertaken to examine the relationship of obesity, measured as BMI, and weight change to incidence of coronary heart disease (CHD) among women with diabetes. The authors followed 5,897 women with type 2 diabetes in the Nurses' Health Study for up to 20 years. Women were aged 40 to 74 years and had no history of cardiovascular disease or cancer at the beginning of the follow up period. During follow up, the authors document 418 incident cases of CHD (236 of nonfatal myocardial infarction and 182 of fatal CHD). After adjustment for age, smoking, and other coronary risk factors, current BMI (body mass index) was strongly associated with increased risk of CHD among women with diabetes. Increasing BMI values from age 18 years to 1976, before diagnosis of diabetes, were also positively associated with risk of CHD. Weight gain before the diagnosis of diabetes was related to increased risk of CHD. In contrast, weight change after diagnosis of diabetes was not associated with risk of CHD. The authors conclude that these findings provide strong evidence that obesity and weight gain before diagnosis of diabetes are associated with future risk of CHD among women with type 2 diabetes. 1 figure. 2 tables. 34 references.
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Behavioral Science Research in Diabetes: Lifestyle Changes Related to Obesity, Eating Behavior, and Physical Activity Source: Diabetes Care. 24(1): 117-123. January 2001. Contact: Available from American Diabetes Association. 1701 North Beauregard Street, Alexandria, VA 22311. (800) 232-3472. Website: www.diabetes.org. Summary: This review article, which grew out of a National Institute of Diabetes and Digestive and Kidney Diseases conference on behavioral science research in diabetes, focuses on lifestyle changes related to obesity, eating behavior, and physical activity. Lifestyle factors related to obesity, eating behavior, and physical activity play a major role in the prevention and treatment of type 2 diabetes. In recent years, there has been progress in the development of behavioral strategies to modify these lifestyle behaviors. Further research, however, is clearly needed because the rates of obesity in the United States are escalating and changing behavior for the long term has proven to be very difficult. The article identifies four key topics related to obesity and physical activity that should be given high priority in future research efforts. These topics are environmental factors related to obesity, eating, and physical activity; adoption and maintenance of healthful eating, physical activity, and weight; the etiology of eating and physical activity; and multiple behavior changes. The article discusses the significance of each of these four topics, reviews prior research in each area, identifies barriers to progress, and makes specific research recommendations. The article concludes that, given the strong association between lifestyle behaviors and the prevention and treatment of type 2 diabetes, it is important that greater research attention be directed at issues related to the development of healthful eating and physical activity habits and strategies for modifying unhealthy behaviors. 81 references. (AA-M).
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Obesity, Type 2 Diabetes and Physical Activity: What's the Connection? Source: Diabetes Self-Management. 18(3): 39-51. May-June 2001. Contact: Available from R.A. Rapaport Publishing, Inc. 150 West 22nd Street, New York, NY 10011. (800) 234-0923. Website: www.diabetes-self-mgmt.com. Summary: This article discusses the connection between obesity, type 2 diabetes, and physical activity. Obesity and type 2 diabetes are strongly related. Both obesity and type 2 diabetes are on the rise at a time when physical inactivity is common. People who are physically inactive tend to be heavier than people who are active, and they tend to develop diabetes more often. The risk of developing diabetes increases as body mass index (BMI) increases. Overweight people tend to get type 2 diabetes at a higher rate than lean people probably because their body is resistant to insulin. Overweight refers to an excess of body weight from muscle, body, fat, or body fluid compared with standards set by the National Institutes of Health and the National Heart, Lung, and Blood Institute, whereas obesity refers specifically to having an abnormally high proportion of body fat. Calculating BMI is the most up to date method of assessing whether a person is overweight or obese. BMI is determined by dividing body weight in kilograms by height in meters squared. Although BMI is simple to calculate, it may misclassify people who are muscular. The health risks of being overweight or obese include type 2 diabetes, cardiovascular and gastrointestinal diseases, various cancers, and other problems. Deep abdominal fat that surrounds the organs is the fat most likely to cause the health risks of obesity. Obesity is caused by an interaction of genetics, physiology, metabolism, and lifestyle. Although there is no cure for obesity, ways of treating and managing it include dietary changes, increased physical activity, behavior therapy, and medication. Research indicates that regular physical activity can improve
Studies 13
insulin sensitivity by 20 percent to 30 percent by building muscle and reducing body fat. The article suggests ways people can be more active during the day and lists additional resources on healthy weight loss. 1 table. •
Acarbose Improves Glycemic Control in Overweight Type 2 Diabetic Patients Insufficiently Treated with Metformin Source: Diabetes Care. 26(2): 269-273. February 2003. Contact: Available from American Diabetes Association. 1701 North Beauregard Street, Alexandria, VA 22311. (800) 232-3472. Website: www.diabetes.org. Summary: This article reports on a study undertaken to investigate the efficacy and safety of acarbose as add-on therapy in overweight patients with type 2 diabetes inadequately controlled by metformin. After a 4 week placebo run-in period, subjects were randomized to either acarbose or placebo. The primary efficacy variable was the change in HbA1c (glycosylated hemoglobin, a measure of blood glucose over time) from baseline to the end of the 24 week treatment period. The intention to treat analysis from baseline to week 24 (81 patients for HbA1c and 82 for fasting blood glucose) showed statistically significant differences between acarbose and placebo treatment in HbA1c and fasting blood glucose. In all, 18 patients (47 percent) in the acarbose group were classified as responders with a greater than 5 percent reduction in HbA1c (relative to baseline) at the end point compared to 6 (14 percent) in the placebo group. The safety profiles were similar for both treatment groups except for the higher incidence of gastrointestinal side effects during acarbose therapy. The authors conclude that the addition of acarbose to metformin monotherapy provides an efficacious and safe alternative for glycemic improvement in overweight type 2 patients inadequately controlled by metformin alone. 1 figure. 2 tables. 27 references.
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Effect of Orlistat in Overweight and Obese Patients with Type 2 Diabetes Treated with Metformin Source: Diabetes Care. 25(7): 1123-1128. July 2002. Contact: Available from American Diabetes Association. 1701 North Beauregard Street, Alexandria, VA 22311. (800) 232-3472. Website: www.diabetes.org. Summary: This article reports on a study of the effect of orlistat, a gastrointestinal lipase inhibitor, on body weight, glycemic control, and cardiovascular risk factors in metformin-treated patients with type 2 diabetes. The 1 year, multicenter, randomized, double blind, placebo controlled trial of 120 milligrams orlistat (n = 249) or placebo (n = 254) combined with a reduced calorie diet was conducted in overweight and obese patients with suboptimal control of type 2 diabetes. After 1 year of treatment, mean weight loss was greater in the orlistat than in the placebo group (minus 4.6 percent of baseline weight versus minus 1.7 percent of baseline weight, respectively). Orlistat treatment caused a greater improvement in glycemic control than placebo, as evidenced by a greater reduction in serum HbA1c (glycosylated hemoglobin, a measure of blood glucose over time), adjusted for changes in metformin and sulfonylurea therapy. Compared with the placebo group, patients treated with orlistat also had greater decreases in total cholesterol, LDL cholesterol, and systolic blood pressure. Although more subjects treated with orlistat experienced gastrointestinal side effects than placebo, more subjects in the placebo group withdrew prematurely from the study than in the orlistat group (44 percent versus 35 percent). The authors conclude that orlistat is a useful adjunctive treatment for producing weight loss and improving glycemic control,
14 Obesity
serum lipid levels, and blood pressure in obese patients with type 2 diabetes who are being treated with metformin. 1 figure. 2 tables. 31 references. •
Evaluation of the Insulin Resistance Syndrome in 5-to 10-Year-Old OverweightObese African-American Children Source: Diabetes Care. 24(8): 1359-1364. August 2001. Contact: Available from American Diabetes Association. 1701 North Beauregard Street, Alexandria, VA 22311. (800) 232-3472. Website: www.diabetes.org. Summary: This review article describes a study that characterized the insulin sensitivity of overweight and obese 5 to 10 year old African American children screened for participation in a diabetes prevention study and identified the association of insulin sensitivity with obesity, hyperlipidemia, and hypertension. Measures of insulin resistance and insulin sensitivity were calculated from a 2 hour oral glucose tolerance test in 137 African American children. Measures of low density lipoprotein (LDL), high density lipoprotein (HDL), total cholesterol, triglycerides, blood pressure, and body composition were obtained for a subset of the children. The study found that, in response to a glucose challenge, girls and older and heavier children produced significantly more insulin. As body mass index increased, there was a statistically significant decrease in insulin sensitivity, particularly in girls. Insulin sensitivity was inversely correlated with increases in blood pressure, triglycerides, subcutaneous fat, the percentage of total body fat, and Tanner stage, but it was not correlated with LDL and HDL. Total cholesterol was inversely related to whole body insulin sensitivity. These associations suggest that a clustering of risk factors is present in these children. Results provide evidence that overweight African American children should be monitored for insulin resistance and cardiovascular risk factors early in life and that this monitoring should occur as part of their ongoing medical care. 2 figures. 1 table. 32 references. (AA-M).
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Type 2 Diabetes and Metabolic Syndrome in Filipina-American Women: A High-Risk Nonobese Population Source: Diabetes Care. 25(3): 494-499. March 2002. Contact: Available from American Diabetes Association. 1701 North Beauregard Street, Alexandria, VA 22311. (800) 232-3472. Website: www.diabetes.org. Summary: This article reports on a study undertaken to compare the prevalence of type 2 diabetes and features of the metabolic syndrome among Filipina and Caucasian women in San Diego County, California. Data on several chronic diseases were collected between 1992 and 1999 from community dwelling Filipina (n = 294) and Caucasian (n = 379) women aged 50 to 69 years. Filipina and Caucasian women did not differ in mean age, body mass index (BMI), percentage of body fat, or waist to hip ratio, although Filipinas had larger waist circumferences and higher percentages of truncal fat. Compared with Caucasians, Filipinas were less likely to be obese, and less likely to smoke, consume alcohol, or take postmenopausal estrogen; Filipinas also had lower levels of HDL cholesterol. Compared with Caucasians, Filipinas had higher prevalence of type 2 diabetes by oral glucose tolerance test criteria and the metabolic syndrome. These differences persisted after adjusting for age, body size, fat distribution, percentage of body fat, smoking, alcohol consumption, exercise, and estrogen therapy. A total of 10 percent of Filipinas with diabetes were obese, compared with one-third of Caucasians with diabetes. The finding of a high prevalence of diabetes in an unstudied nonobese ethnic group reinforces the importance of expanding the study of diabetes to diverse
Studies 15
populations. The authors caution that the high prevalence of diabetes in populations who are not of Northern European ancestry may be missed when they are not obese by Western standards. 1 figure. 3 tables. 32 references. •
Effects of an Energy-Restrictive Diet with or Without Exercise on Abdominal Fat, Intermuscular Fat, and Metabolic Risk Factors in Obese Women Source: Diabetes Care. 25(3): 431-438. March 2002. Contact: Available from American Diabetes Association. 1701 North Beauregard Street, Alexandria, VA 22311. (800) 232-3472. Website: www.diabetes.org. Summary: This article reports on a study undertaken to examine whether the combination of diet and aerobic exercise (DA) or diet and resistance exercise (DR) is associated with greater improvements in metabolic risk factors by comparison to diet only (DO) in obese women. A second objective considered whether reductions in metabolic risk factors are related to concurrent changes in abdominal or intermuscular fat distribution. The study included a total of 38 premenopausal obese women who were randomly assigned to one of three 16 week treatments: DO (n = 13), DR (n = 11), or DR (n = 14). Plasma glucose (sugar), insulin, and lipid (fats) levels were measured in a fasting state and after a 75 gram oral glucose challenge. Total, abdominal subcutaneous, visceral, and intermuscular fat were measured by magnetic resonance imaging (MRI). Significant reductions in body weight and in total, abdominal subcutaneous, visceral, and intermuscular fat were observed within each group. Fasting and OGTT insulin, total cholesterol, LDL cholesterol, and apoliprotein B also decreased within each group. The changes in the body fat and metabolic variables were not different across treatment. Visceral fat alone was related to the metabolic risk factors both before and after the treatment. Weight loss was associated with reductions in metabolic risk factors in obese women. The improvement in the metabolic profile was not enhanced by the addition of aerobic or resistance exercise. The findings reinforce the importance of diminished visceral fat in the treatment of insulin resistance. 2 tables. 66 references.
Federally Funded Research on Obesity The U.S. Government supports a variety of research studies relating to obesity. These studies are tracked by the Office of Extramural Research at the National Institutes of Health.2 CRISP (Computerized Retrieval of Information on Scientific Projects) is a searchable database of federally funded biomedical research projects conducted at universities, hospitals, and other institutions. Search the CRISP Web site at http://crisp.cit.nih.gov/crisp/crisp_query.generate_screen. You will have the option to perform targeted searches by various criteria, including geography, date, and topics related to obesity. For most of the studies, the agencies reporting into CRISP provide summaries or abstracts. As opposed to clinical trial research using patients, many federally funded studies use animals or simulated models to explore obesity. The following is typical of the type of information found when searching the CRISP database for obesity: 2 Healthcare projects are funded by the National Institutes of Health (NIH), Substance Abuse and Mental Health Services (SAMHSA), Health Resources and Services Administration (HRSA), Food and Drug Administration (FDA), Centers for Disease Control and Prevention (CDCP), Agency for Healthcare Research and Quality (AHRQ), and Office of Assistant Secretary of Health (OASH).
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Project Title: ALTERED GLUCOSE AND LIPID METABOLISM IN OBESITY AND CVD Principal Investigator & Institution: Charron, Maureen J.; Professor of Biochemistry; Biochemistry; Yeshiva University 500 W 185Th St New York, NY 10033 Timing: Fiscal Year 2003; Project Start 01-AUG-2003; Project End 31-JUL-2008 Summary: (provided by applicant): Obesity is associated with metabolic abnormalities that increase the risk of type 2 diabetes and cardiovascular disease (CVD). Obese patients with a substantial accumulation of visceral adipose tissue are characterized by higher insulinemic and glycemic responses during an oral glucose challenge and a deteriorated plasma lipoprotein-lipid profile compared to normal body weight or obese individuals with low level visceral adiposity. We will use a mouse model with a primary impairment in insulin-mediated glucose flux into adipocytes to define the molecular mechanisms underlying the pathogenesis of obesity associated CVD. Male mice carrying only one functional copy of the insulin-stimulatable GLUT4 transporter (GLUT4) first display reduced GLUT4 expression specifically in white adipose tissue (WAT). Reduced GLUT4 in WAT leads to visceral obesity, progressive impairment in insulin sensitivity, altered lipid metabolism, and eventually to type 2 diabetes with associated CVD. As such, male GLUT4 mice represent an excellent model to study pathophysiological changes associated with visceral obesity in humans. Interestingly, changes in adipose cell secretory proteins, such as the adipocyte-specific Acrp30, precede the onset of measurable changes in other metabolic parameters in GLUT4 mice. We and others have demonstrated profound effects of Acrp30 on insulin resistance in liver and muscle through specific effects on carbohydrate and lipid metabolism. The objectives of this proposal are I) to understand the molecular mechanisms underlying the metabolic changes that specifically affect male, but not female GLUT4 mice or GLUT4 mice that overexpress GLUT4 in muscle; lI) to test genetically whether correction of Acrp30 downregulation in male GLUT4 will prevent or delay the onset of insulin resistance, visceral obesity and/or CVD. Additionally, we will test whether complete lack of circulating Acrp30 in Acrp30-/-mice will provoke metabolic disturbance in female GLUT4 and exacerbate disease in male GLUT4 mice; III) to assess the effects of high fat diet-induced changes in disease progression in GLUT4 compared to C57BL/6J mice; and IV) to determine transcripitional and translational changes in WAT associated with visceral obesity and alterations following treatment with thiazolidinedione insulin sensitizers in hope of identifying novel therapeutic targets. Combined, this approach will provide a comprehensive systematic characterization of a mouse model of obesity associated CVD derived from early impairment of insulinmediated glucose flux into WAT, and directly address for the first time whether alterations in Acrp30 influence disease progression. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: AN OBESITY LOCUS ON MOUSE CHROMOSOME 7 Principal Investigator & Institution: West, David B.; Visiting Scientist; Division of Life Sciences; University of Calif-Lawrenc Berkeley Lab Lawrence Berkeley National Laboratory Berkeley, CA 94720 Timing: Fiscal Year 2001; Project Start 20-FEB-1998; Project End 31-JAN-2004 Summary: Obesity results in significant morbidity and mortality in the North American population and effective long-term treatments are not available. The etiology of obesity is complex with both genetic predisposition and environmental factors playing a role. One approach to further our understanding of the causal factors responsible for obesity
Studies 17
is to identify the genes and characterize the genetic mechanisms contributing to the disease. An understanding of the genetic mechanisms contributing to obesity may lead to new therapeutic developments and will help us to understand the relevant environmental factors causing obesity. Although finding genes contributing to a complex disease in human populations is possible, appropriate mouse models offer many advantages including the availability of inbred strains and rich genetic resources. It is likely that the same pathways involved in energy metabolism in mouse models will be involved in human disease. There is now significant evidence from a number of different studies in independent laboratories that a genetic locus on proximal mouse chromosome 7 is contributing to variation of body fat in the mouse. We have preliminary data using radiation deletion mutants in the mouse indicating that this gene is having a significant effect on body fat content, is paternally imprinted, and we have localized it to a narrow region just distal to the pink eyed dilution locus on mouse chromosome 7. In this application we propose to further narrow the critical region containing the gene using a panel of additional deletion mutants. We will physically map the critical region, develop a gene expression map for this area and evaluate the role of candidate genes which are located in this physical map. At the end of this project we will have identified a gene contributing to the regulation of body fat in the mouse. Follow-up studies in subsequent funding periods will be dir ected at characterizing the mechanism of action of this gene and determining if it is involved in human obesity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ANGIOTENSIN: A LINK BETWEEN OBESITY AND HYPERTENSION Principal Investigator & Institution: Cassis, Lisa A.; Professor; Pharmaceutical Sciences; University of Kentucky 109 Kinkead Hall Lexington, KY 40506 Timing: Fiscal Year 2003; Project Start 03-JUN-2003; Project End 31-MAY-2008 Summary: (provided by applicant): The proposed studies are in response to RFA-HL-02016 and will address the working hypothesis that a moderately high fat diet (MHF) stimulates the adipose renin-angiotensin system, contributing to obesity-related elevations in blood pressure. Preliminary data demonstrates that rats fed a MHF diet segregate into obesity prone (OP) versus obesity-resistant (OR) populations. In OP rats, blood pressure was increased coincident with activation of the systemic and adipose renin-angiotensin system. The first hypothesis is that a MHF diet activates the adipose renin-angiotensin system, resulting in an increase in circulating angiotensin peptides and blood pressure. Time-dependent regulation of adipose versus non-adipose components of the renin-angiotensin system will be examined in control, OR and OP rats and compared to the time course for elevations in blood pressure. The contribution of various circulating angiotensin peptides to blood pressure elevations in control, OR and OP rats will be determined. The second hypothesis is that adipocytes from OP rats exhibit a redistribution of free cholesterol from the plasma membrane to intracellular triglyceride pools, thereby increasing the activity of sterol regulatory binding protein-2 and stimulating angiotensinogen (Ao) mRNA expression. This would provide an adipocyte-specific mechanism for regulation of Ao gene expression in response to the MHF diet. The intracellular localization of free cholesterol in adipocytes prepared from control, OR and OP rats will be determined and compared to the level of Ao mRNA expression. The effect of depletion of intracellular free cholesterol pools on adipocyte Ao mRNA expression will be determined. The third hypothesis is that elevations in circulating angiotensin peptides increase blood pressure in OP rats by stimulating sympathetic drive. The responsiveness of the baroreceptor reflex and the blood pressure response to ganglionic blockade will be determined in control, OR and OP rats. A
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second approach will determine the effect of neonatal sympathectomy on blood pressure elevations in diet-induced obesity. In hypothesis 4 a novel animal model will be developed to determine the effect of targeted deficiency of Ao in adipose tissue on blood pressure regulation in diet-induced obesity. The goals of this research are to definitively determine the role of adipose-derived angiotensins and the systemic reninangiotensin system in blood pressure elevations in diet-induced obesity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: BEHAVIORAL PHYSIOLOGY OF BODY WEIGHT REGULATION Principal Investigator & Institution: Lattemann, Dianne F.; Research Professor; Psychology; University of Washington Seattle, WA 98195 Timing: Fiscal Year 2001; Project Start 01-SEP-1988; Project End 31-MAR-2004 Summary: Diet composition plays a significant role in the development of human obesity. A genetic propensity towards dietary obesity has been identified in rodents, and obese individuals demonstrate differences in food preferences from lean individuals. In rodent models, dietary-induced obesity is associated with decreased sensitivity to exogenous administration of the candidate adiposity signal insulin. This suggests that some difference-metabolic, neurochemical, or both-as a consequence of eating a highly palatable, high energy diet is present, resulting in a change in the physiological regulation of body adiposity. Activation of the CNS mesolimbic dopamine (DA) neurons is implicated in the reinforcing or rewarding aspects of several classes of stimuli, including food. We have obtained preliminary evidence that insulin can downregulate the activity of these DA neurons, both at the level of the synapse and at the level of behavior. In this proposal, we pursue the hypothesis that activity of these neurons is altered in association with dietary obesity, and that there is a loss of insulininduced downregulation of DA neuronal activity. To test this hypothesis, we will evaluate performance in two behavioral tasks in which DA has been implicated: lick rates of sweet and fat solutions, and the conditioned place preference (CPP) paradigm; release of DA from the mesolimbic DA neurons by in vivo microdialysis; and the cellular mechanisms underlying altered DA release, using our established methodologies. All studies will utilize normal weight and dietary obese rats (both outbred rats, and the inbred dietary-induced obese (DIO)/dietary obese-resistant (DR) rats, which are genotypically distinct in their propensity to develop dietary obesity), infused with intraventricular (IVT) vehicle or insulin. Together, these studies will evaluate the ability of a candidate adiposity signal to interact with brain pathways associated with reward; and the influence of palatable high energy diets on the function and regulation of the mesolimbic DA neurons. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: OBESITY
BETA-ADRENOCEPTOR
GENETIC
POLYMORPHISMS
AND
Principal Investigator & Institution: Johnson, Julie A.; Professor of Pharmacy Practice & Medicin; Pharmacy Practice; University of Florida Gainesville, FL 32611 Timing: Fiscal Year 2001; Project Start 01-APR-2001; Project End 31-MAR-2003 Summary: (Provided by Applicant) Obesity is increasing in prevalence in Western societies, and it represents a major health concern because it increases the risk of cardiovascular disease, metabolic disorders and some forms of cancer. It is estimated that 40% to 70% of the variability in body weight is genetically mediated. A number of genes have been studied as candidate genes for obesity. In the proposed analysis of the
Studies 19
Women's Ischemic Syndrome Evaluation Study (WISE) database, we will test the hypothesis that the beta- adrenergic receptor (betaAR) genes and certain G protein genes are associated obesity. Specifically, we will be studying the association between obesity and genes of the beta1AR (ADRB1), the beta2AR (ADRB2), the beta3AR (ADRB3), the Gs protein alpha subunit (GNAS1) (all three betaARs couple with Gs) and the G protein beta3 subunit (GNB3) (a component of Gi, to which beta3ARs couple). We will also examine the multivariate contributions to obesity of genotype, demographic (e.g., age, region) and environmental (e.g., exercise, childbirth history) factors and their possible interactions. Data for the proposed analysis will derive from the database of the WISE study, a four center NHLBI-funded study of ischemic heart disease in women. Genotypes will be assessed by a high through-put genetic bit analysis method. Analyses on approximately 590 white women and 130 black women will be performed separately, and will include multiple regression analysis to test for impact of the various genes, and various demographic and behavioral factors on body mass index. The proposed analyses are important and novel because they will: a) provide the first information on the relationship between ADRB1 and GNAS1 and obesity, b) provide the first information on the ADRB2 and obesity when assessed by haplotype, c) provide information on potential additive or synergistic effects of the genes under study with respect to obesity, d) for some of the genes, provide the first data on the gene-obesity associations in blacks, e) assess the gene-obesity association with respect to certain environmental/behavioral factors such as physical activity and previous childbirth, and f) utilize a state-of-the-art high throughput method for genetic analysis. The information generated from this study should help identify candidate genes that are worthy of further, extensive investigation. Knowledge about genes that are associated with obesity is important as this information may aid in the drug discovery process for anti-obesity drugs. Additionally, genotyping individuals early in age may help to identify those at increased risk of obesity prior to them becoming obese so that they may take appropriate preventive measures. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: BODY FAT AND HORMONES IN ADOLESCENT OBESITY TREATMENT Principal Investigator & Institution: Saelens, Brian; Children's Hospital Med Ctr (Cincinnati) 3333 Burnet Ave Cincinnati, OH 45229 Timing: Fiscal Year 2002; Project Start 01-APR-2002; Project End 31-MAR-2007 Summary: (provided by applicant) This K23 application will establish the candidate's independent research career in patient-oriented research in adolescent obesity treatment. The candidate, Brian E. Saelens, Ph.D., is a recently appointed Assistant Professor of Pediatrics at Children's Hospital Medical Center (CHMC) in Cincinnati. This K23 proposal combines mentoring in biological and behavioral factors that influence adolescent obesity. The proposed career development plan will provide the candidate necessary training in body fat distribution measurement, weight-affecting hormones, weight-related behaviors, and pubertal maturation. This training will lead to the development of more efficacious intervention for adolescent weight control, specifically to target the reduction of intra-abdominal fat mass accumulation, as this type of fat accretion is most highly related to the negative health consequences of obesity. The candidate's career plan capitalizes on the biologic obesity-related resources and expertise at CHMC and the University of Cincinnati to augment prior and planned training in the behavioral aspects of pediatric obesity. The proposed research plan consists of a targeted prospective (Study 1) and pilot intervention study (Study 2). Study
20 Obesity
1 aims include examining the time course of total body fat and intra-abdominal fat accretion through early puberty among already overweight youth. Study 1 will identify specific periods of relatively high and low intra-abdominal fat accretion. This prospective study also examines potential hormonal and behavioral precursors of changing body fat distribution. Based on Study 1 findings, Study 2 will investigate the differential impact of providing similar behavioral weight control intervention to overweight youth at different time periods of intra-abdominal fat mass accumulation. Intervention efficacy will be examined among overweight youth either 1) timingmatched by intervention during high intra-abdominal fat accumulation or 2) timingmismatched by intervention during low intra-abdominal fat accumulation. Study 2 will also examine baseline hormonal, body composition, and behavioral correlates of weight control treatment success. These studies will provide exceptional training in the biological aspects of obesity, while also having the potential to begin identifying the timing of behavioral intervention that will optimize health benefit of behavioral weight control programs for the increasing population of overweight youth. The combined skill set and experience garnered from the candidate's career development and research plan will provide the necessary early career support for the candidate to establish a successful independent research career in the important area of pediatric obesity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: BOSTON OBESITY NUTRITION RESEARCH CENTER Principal Investigator & Institution: Corkey, Barbara E.; Professor; Boston Medical Center Gambro Bldg, 2Nd Fl, 660 Harrison Ave, Ste a Boston, MA 02118 Timing: Fiscal Year 2001; Project Start 30-SEP-1992; Project End 31-MAR-2003 Summary: This application represents the competing renewal of the Boston Obesity/Nutrition Research Center. The Boston Obesity/Nutrition Research Center represents a collaboration of four major institutions representing three major universities in Boston, all located within a 1.5 mile radius of each other. The Boston Obesity Center includes the New England Medical Center, the Beth Israel Deaconess Medical Center, the Harvard School of Public Health, and Boston Medical Center. The institutions represent respectively Tufts University, Harvard University, and Boston University. The Boston Obesity/Nutrition Research Center consists of five Core Laboratories. These includes an Epidemiology Core, directed by Dr. Graham Colditz at the Harvard School of Public Health, a Clinical/Metabolic Core, directed by Dr. George Blackburn at the Beth Israel Deaconess Medical Center, a Body Composition/Energy Expenditure Core, directed b Dr. William Dietz at the New England Medical Center, an Adipocyte Core, initially designed as a Cellular Biochemistry Signal Transduction Core, at Boston Medical Center, now directed by Dr. James Kirkland, and a Transgenic Core at the Beth Israel Deaconess Medical Center directed by Dr. Jeffrey Flier. The Obesity Center offers multiple opportunities for education and training in obesity research to fellows on training grants held by Obesity Center investigators in each of the collaborating universities. The investigators represented in this application hold 65 funded R0-1 grants, approximately 45 which are directed at the study of obesity, energy metabolism or other nutritional disease. In the past four years, Boston Obesity Center investigators have published 135 papers with Center support. Twenty percent of the Obesity Center budget provide support for pilot and feasibility studies. Pilot and feasibility award recipients have published almost 50 papers and received a total of 7 grants from NIH or other funding agencies based on the data obtained from their Center funded investigations. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: CENTRAL OOBESITY SYNDROME IN A SUBSET OF TYPE 1 DIABETES Principal Investigator & Institution: Brunzell, John D.; Prpfessor of Medicine; University of Washington Seattle, WA 98195 Timing: Fiscal Year 2002; Project Start 01-SEP-1976; Project End 31-MAR-2007 Summary: (provided by applicant): Project 2 started as an ancillary study of lipoprotein metabolism to the NIH sponsored clinical trial of intensive diabetes therapy in type 1 diabetics to prevent microvascular disease called the Diabetes Control and Complication Trial (DCCT). The Epidemiology of Diabetes Intervention and Complications (EDIC) is a ten year non-interventional follow-up of DCCT to evaluate the natural history of macrovascular and nephropathy complications in type 1 diabetes. In DCCT, we found that atherogenic small dense LDL were increased with hyperglycemia, microalbuminuria and were increased in that subset of subjects who gained excess weight as a complication of intensive diabetes therapy during DCCT. Those who gained weight with intensive diabetes therapy were centrally obese, insulin resistant, hypertensive, dyslipidemic and had type 2 diabetic parents. This suggests they had inherited the metabolic-central obesity syndrome in addition to type 1 diabetes. This new proposal will use the phenotypes of 1) excessive weight gain with intensive diabetes therapy and 2) the presence of small dense LDL particles as markers of the central obesity-insulin resistance metabolic syndrome that occurred in this subset of type 1 subjects during intensive diabetes therapy. These markers of the central obesity syndrome will be used to predict the occurrence of cardiovascular events and the development or progression of microalbuminuria during the course of EDIC. Candidate genes for development of the central obesity syndrome and for the interaction of excess weight gain with the development of hypertension will be examined. Intraabdominal fat by CT scan and postheparin plasma hepatic lipase will be measured to further develop the phenotype associated with the excessive weight gain with intensive therapy and with development of nephropathy in the Seattle cohort and three Minnesota cohorts of EDIC. The development of the central obesity syndrome with intensive diabetes therapy in type 1 diabetic patients may predispose them to increased risk of cardiovascular disease and nephropathy. If so, modifications of clinical therapy will need to be made in this subset of individuals. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: CLINICAL AND EXPERIMENTAL STUDY OF HUMAN OBESITY Principal Investigator & Institution: Stunkard, Albert J.; Professor Emeritus of Psychiatry; Psychiatry; University of Pennsylvania 3451 Walnut Street Philadelphia, PA 19104 Timing: Fiscal Year 2001; Project Start 01-APR-1997; Project End 31-MAR-2003 Summary: (Applicant's Abstract): We propose to continue the most complete, prospective, longitudinal study of growth and development yet undertaken of children at high risk of obesity. The study of 78 children, now 32 to 53 months of age, selected on the basis of maternal obesity or leanness, has already achieved its initial goal: it has disconfirmed, the results of an influential study and the associated, widely held belief that a low total energy expenditure (TEE) and maternal obesity predict body size and composition at 1 year of age. Instead, it has found, unexpectedly, that the two independent measures of energy intake at 3 months of age predict body size and composition at 1 year of age. We now propose to search further for the risk factors for obesity in this large, carefully studied cohort as it enters the early childhood years. After
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24 months in which there was minimal evidence of genetic influence, our high risk strategy has begun to bear fruit: at 30 months 14% of our sample now exceeds the 95th percentile of weight for height. As at 3 and 24 months, and now at 48 months, we will assess, at 6 and at 8 years, the influence of maternal and paternal body mass index (BMI = kg/m2), subject's body weight, TEE and resting metabolic rate. In addition, to identify behaviors that might be modified in programs of obesity prevention, we will continue to measure food intake (both 3-day records and test meals), taste (especially fat) preferences and psychosocial factors that have been implicated in the development of obesity. These efforts will be greatly enhanced by the ability (for the first time) to assess the environmental factors in a cohort that has been defined genetically as being at high risk for obesity and where metabolic status is known. Our ultimate objective is to identify behaviors that contribute to adiposity and that might be modified in programs of prevention and treatment. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CNS ACTION OF APPETITE SUPPRESSANT AMINOSTEROL Principal Investigator & Institution: Ahima, Rexford S.; Assistant Professor; Medicine; University of Pennsylvania 3451 Walnut Street Philadelphia, PA 19104 Timing: Fiscal Year 2002; Project Start 15-JUL-2002; Project End 31-MAY-2005 Summary: (provided by applicant): The prevalence of obesity in the United States has reached epidemic proportions and poses enormous public health challenges, as obesity is a major risk factor for type 2 diabetes, hypertension, cardiovascular disease and cancer, as well as an independent risk factor for mortality. Although diet and exercise are essential to weight management, it has become increasingly clear that a large proportion of patients would require drug treatment to decrease and maintain body weight. The goal of this grant is to understand the action of a novel cholesterol derivative with potent anti-obesity and anti-diabetic properties. MSI- 1436 is an aminosterol which we have found to cause reversible suppression of food intake, increased energy expenditure and normalization of glucose levels when administered by peripheral and more potently intracerebroventricular injection to rodents. Unlike other anorectics, a single injection of MSI-1436 produces a prolonged effect lasting several days. MSI- 1436 is effective in ob/ob and db/db mice, fa/fa rats, and dietinduced obese mice, suggesting that leptin signaling is not critical to its action. By contrast, MSI-1436 effect is blunted in agouti (Ay/a) mice, suggesting that its central action may involve the melanocortin pathway. Although acute MSI1436 administration strongly induces Fos-immunoreactivity in the paraventricular nucleus and to a lesser extent in the arcuate, ventromedial and pre-mammillary nuclei, the neuronal circuitry mediating the anti-obesity vs anti-diabetic effects of MSI-1436 is not known. We hypothesize that MSI-1436 enters the braii via a specific transport mechanism and engages hypothalamic neuronal targets to regulate energy balance and glucose homeostasis. Specific Aim 1 involves the injection of MSI-1436 into specific hypothalamic nuclei to determine which sites mediate the effects on feeding, body weight and glucose levels. Specific Aim 2 will analyze the distribution of MSI-1436 binding sites and determine the chemical phenotypes 01 MSI-1436 responsive neurons. Specific Aim 3 will determine the contribution of the central melanocortin system by analyzing MSI-1436 response in melanocortin receptor (MCR)-3 and 4 knockout mice. Finally, Specific Aim 4 will utilize GeneChip microarray to determine whether MSI-1436 regulates novel hypothalamic genes. Putative MS-1436 targets will be validated in multiple mouse models. Together these studies will provide insights into the mechanisms underlying MSI-1436 action in the brain. Understanding the basis for the
Studies 23
novel effects of MSI-1436 on feeding behavior, body weight and glucose will greatly enhance the field of obesity and metabolism. New pathways affected by MSI-1436 may elucidate novel cellular targets for the treatment of obesity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: CORE--EPIDEMIOLOGY Principal Investigator & Institution: Colditz, Graham A.; Professor of Medicine and Epidemiology; Boston Medical Center Gambro Bldg, 2Nd Fl, 660 Harrison Ave, Ste a Boston, MA 02118 Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-MAR-2008 Summary: (provided by applicant): Objectives of the Epidemiology Core 1. To provide statistical and epidemiologic support to ongoing or planned obesity studies in the Boston area, which will, in turn, expand the nucleus of expertise and familiarity with design and analysis issues unique to obesity research. 2. To continue to support the development and maintenance of data sets amenable to secondary epidemiologic analyses regarding obesity and nutrition issues, as well as to develop and refine measures of obesity. 3. To interface epidemiology, basic sciences, and clinical medicine so that hypotheses generated by these areas can be tested in ongoing epidemiologic studies. 4. To train young investigators in epidemiologic and statistical techniques used for the study of obesity in populations. 5. To disseminate methods/approaches to data analysis to a broad audience, as Core members gain experience in applying and refining quantitative methods. Obesity research presents unique analytic challenges, solutions to which are of great interest. 6. To help identify groups at high and low risk of the development of obesity, and population characteristics for obesity clinical trials. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: CULTURAL ASPECTS OF LATINO EARLY CHILDHOOD OBESITY Principal Investigator & Institution: Clark, Lauren; Associate Professor; None; University of Colorado Hlth Sciences Ctr P.O. Box 6508, Grants and Contracts Aurora, CO 800450508 Timing: Fiscal Year 2003; Project Start 15-AUG-2003; Project End 31-JUL-2005 Summary: (provided by applicant): Childhood obesity in the U.S. has reached a 20-25% prevalence. Latinos have higher rates of obesity across the lifespan, contributing to an ethnic disparity in rates of obesity-related morbidity and mortality. Obesity in childhood tracks into adulthood, making early childhood a key developmental time period for prevention. This study will use qualitative focus group methodology and freelisting to: (1) describe the characteristics Latino mothers use to identify and categorize infants as "obese" and "overweight;" (2) assess the kinds of behaviors, foods, feeding patterns, and other risks believed by Latino family members to contribute to early childhood obesity; (3) ascertain what Latino mothers and father would consider appropriate interventions for young children considered "obese" or "overweight" by health care professionals; (4) identify whom Latinos would consider appropriate persons to intervene in nutrition and activity issues for children; and (5) explore various program characteristics preferred by Latino families for a future obesity prevention program; and (6) identify differences among less- and more-acculturated Latino families regarding early childhood obesity issues, food and feeding practices, and intervention preferences. The study is a qualitatively-driven exploration of cultural dimensions of childhood obesity, cultural knowledge about what constitutes "obesity" and "overweight," and the kinds of feeding and nutrition knowledge parents share about
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young children. Analysis of focus group data will identify cultural models of childhood obesity, cultural knowledge about feeding practices and other factors that contribute to childhood obesity, beliefs about healthful feeding practices, and avenues for intervention congruent with Latino families' preferences. Based on this pilot work, a culturally competent primary prevention program will be designed to prevent Latino early childhood obesity and overweight, and promote healthful nutrition and feeding. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: DIET AND PHYSICAL ACTIVITY INTERACTIONS IN OBESITY Principal Investigator & Institution: Hill, James O.; Professor; Pediatrics; University of Colorado Hlth Sciences Ctr P.O. Box 6508, Grants and Contracts Aurora, CO 800450508 Timing: Fiscal Year 2001; Project Start 01-MAY-1990; Project End 31-JUL-2003 Summary: The current epidemic of obesity has occurred despite the existence of a body weight regulatory system which, for most of mankind's history, has matched energy intake with energy expenditure sufficiently to avoid obesity. This suggests that the primary cause of the current obesity epidemic is not genetic, but may be due to an environment in which the energy balance regulatory system cannot function with sufficient precision to keep the population lean. In this application, we propose research aimed at understanding how factors in the environment, namely high fat/energy dense diets and physical inactivity, can promote obesity by affecting the precision of regulation of energy and fat balance. It is our intent to identify dietary and physical activity patterns that are associated with increased precision of energy balance regulation and which can prevent development of obesity. Laboratory data suggest that high fat diets promote obesity by increasing the probability of overconsumption of total energy. Our first aim is to systematically examine the relationship between dietary fat and energy intake across a range of diet compositions in sedentary subjects. While this has been done for diets with extreme variation in dietary fat (i.e., less than or equal to 20 percent vs greater than or equal to 40-60 percent) it has not been done for dietary fat content within the range of usual consumption of U.S. adults (i.e. 20-40 percent fat diets). We hypothesize that this relationship will not be linear and that there will be a threshold level or a range of dietary fat associated with a low probability of increased energy intake and positive energy balance. This information will be useful in developing dietary guidelines for obesity prevention. Our second aim is to determine how level of physical activity interacts with dietary fat content to affect the likelihood of developing positive energy balance. We hypothesize that the optimum level of dietary fat to minimize the probability of positive energy balance will depend on level of physical activity and the optimum level of physical activity to minimize the likelihood of positive energy balance will vary with dietary fat content. This work will be among the first to study the interaction of dietary and physical activity patterns in promotion and prevention of obesity. The results will help identify the changes required in current dietary and physical activity patterns if we are going to be successful in preventing the development of obesity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: DIETARY OBESITY Principal Investigator & Institution: Bray, George A.; Director; None; Lsu Pennington Biomedical Research Ctr 6400 Perkins Rd Baton Rouge, LA 70808 Timing: Fiscal Year 2001; Project Start 01-AUG-1982; Project End 31-JUL-2003
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Summary: The objective of this research grant is to characterize the mechanisms for the differences between two strains of rats which differ in their susceptibility to obesity when eating a high fat diet. The Osborne- Mendel rat (OM) rapidly becomes obese when maintained on a high fat diet while the S5B/PI (S5B) rat remains lean when eating the same diet. We have recently demonstrated that the OM rat increases its intake of a high fat diet after administration of the 5-HT1A agonist, 8-hydroxy-2- (di-nproplyamino)tetralin, which inhibits serotonin synthesis and release. S5B rats do not increase food intake after this treatment. In addition, fenfluramine treatment prevents high fat diet-induced obesity in the OM rat. This proposal focuses on the mechanisms underlying two aspects of this dietary-induced obesity. Our first aim will be to elucidate the central nervous system neurotransmitter signals that mediate fat preference by examining the serotonin system in these two rat strains. We will test the hypothesis that the serotonergic system is more active in the S5B rat than the OM rat. The first three experiments in this aim will investigate the effects on food intake in OM and S5B rats by altering serotonin levels in the paraventricular nucleus. The next five experiments will determine the contribution of the dorsal raphe nucleus to the serotonin systems in OM and S5B rats. The last two experiments will examine the hypothesis that opioids in the hindbrain may modulate the serotonergic signals from the paraventricular nucleus. We will utilize the novel technique of central antisense oligonucleotide application in two critical experiments to test these systems. The second aim will examine the difference in peripheral signaling systems that responds to nutrient infusion in these two rat strains. We will test the hypothesis that fatty acids in the GI tract activate vagal mechanisms more effectively int the S5B rat. We have already demonstrated that S5B rats are much more sensitive to the satiating effects of intraintestinal fat infusions. There are seven experiments proposed which will examine the involvement of the vagus nerve, cholecystokinin, glutamate, c-fos activated neurons and serotonin in the differential responsiveness to nutrient infusion in OM and S5B rats. Our laboratory has made significant advances toward understanding dietary-induced obesity. We now propose these well founded, important and exciting studies which will provide critical new insights into anatomical, physiological and molecular mechanisms by which high levels of dietary fat induce obesity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: DRUG TARGET DISCOVERY IN OBESITY NEURONS Principal Investigator & Institution: Rao, Donald D.; Nt Two 5000 Gullen Mall, Rm 407 Detroit, MI 48202 Timing: Fiscal Year 2002; Project Start 15-JUN-2002; Project End 31-MAR-2004 Summary: Key advances in obesity research over the last decade have established the prominence of the central nervous system (CNS) in body weight regulation. The goal of the proposed research is to develop a target discovery approach that will mine neurons in the CNS known to express important obesity genes. This goal will be accomplished using recently-developed state-of-the-art techniques to genetically tag and then isolate, from the intact brain, specific neuronal subtypes already known to be important for body weight regulation. We will then catalog the transcriptome of these "obesity neurons" and determine gene expression profiles of these neurons under conditions designed to reveal gene function. The identification of genes selectively expressed in specific neuronal subtypes will provide the molecular raw material for the next generation of anti-obesity drug targets. The proposed approach for CNS target discovery combines three core technologies: (1) genetic tagging of neuronal subpopulations with modified bacterial artificial chromosome (BAC) transgenes, (2)
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harvesting of tagged "obesity neurons" and (3) RNA expression profiling analysis of the captured "obesity neurons" under conditions designed to reveal gene function. The ultimate commercial aim is to sell or license validated CNS anti-obesity drug targets, target-specific high through-put assays, and chemical leads for these targets. PROPOSED COMMERCIAL APPLICATION: The optimized drug discovery platform derived from this research will serve as a standardized method for identifying various CNS drug targets, not only those involved in obesity. The commercial value of the platform will be realized through the quality of targets and by the potential chemical leads developed against these targets. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: EARLY SOCIOECONOMIC & PSYCHOSOCIAL RISK FOR OBESITY Principal Investigator & Institution: Gahagan, Sheila; Pediatrics & Communicable Dis; University of Michigan at Ann Arbor 3003 South State, Room 1040 Ann Arbor, MI 481091274 Timing: Fiscal Year 2001; Project Start 01-JUN-2001; Project End 31-MAY-2006 Summary: (Adapted from applicant's description): The goal of this K23 proposal is to provide research training related to childhood obesity. The applicant is an academic pediatrician who has worked in settings serving children in poverty since 1983. She has worked with African American, American Indian and Hispanic American populations. The epidemic of obesity is more severe in underrepresented minority groups in the US and increasingly in some developing countries. Children from disadvantaged backgrounds are put at increased risk for obesity by a variety of factors. This proposal relies on five ongoing longitudinal US and international samples with rich growth, demographic and psychological data on the subjects and their families. The samples include: 260 preschool children from southeast Michigan; two cohorts (100 each) from an American Indian population showing recent rapid increases in birthweight and obesity; 150 Costa Rican children studied from 1 year, who are now age 19; 1000 Chileans who are currently 5 years old and studied since 4 months; and 3,400 Finnish men and women with high rates of cardiovascular disease. The research training and research plans proposed in this project are closely linked to activities involving these 5 longitudinal projects. These ongoing research projects will be the framework for continued data collection, new data analysis, and comparative study. Dr. Betsy Lozoff, Director of the Center for Human Growth and Development and Professor of Pediatrics is the project mentor. An outstanding committee composed of leaders in child nutrition, behavior, development, obesity, biostatistics and health disparities will direct the training and advise the research. Dr. Gahagan proposes to explore the behavioral and psychological factors that cause additive risk for obesity in young children. While not ignoring the importance of genetics, nutrition, and physical activity, this work will promote understanding the role of poverty in childhood obesity. The hypothesis that children are put at risk for obesity and its consequent health problems by biologic and social factors including poverty, parental mental health, and parental-decision making about childhood nutrition and activity will be examined in depth in five different populations at risk. If obesity is to be prevented, it is critical to understand the precursors on multiple levels and target those factors that are modifiable for intervention. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ENERGY BALANCE IN THE OBESE CCK A RECEPTOR DEFICIENT RAT Principal Investigator & Institution: Moran, Timothy H.; Professor; Psychiatry and Behavioral Scis; Johns Hopkins University 3400 N Charles St Baltimore, MD 21218 Timing: Fiscal Year 2001; Project Start 01-FEB-2001; Project End 31-JAN-2006 Summary: Obesity has reached epidemic proportions in the United States, and both genetic and environmental contributions to the development and maintenance of obesity have been identified in human studies and animal models. Recent rodent models of genetic obesity have hypothalamic signaling pathways related to the overall control of metabolism and energy balance. Unlike these strains, the obese Otsuka LongEvans Tokushima Fatty (OLETF) rat is a unique genetic model of obesity with an identified deficit in a peripheral gut-brain peptide signaling pathway critical to the within meal control of food intake. OLETF rats spontaneously lack the promoter region for the gene that encodes for the cholecystokinin (CCK) A receptor, the subtype that mediates the satiety actions of this meal-elicited peptide. OLETF rats are obese and hyperphagic, and we have shown that their hyperphagia is characterized by increased meal size, consistent with the lack of a meal related signal important in the negative feedback control of food intake. In this proposal, we hypothesize that OLETF hyperphagia and obesity: 1) depends upon their genetically determined inability to detect meal-related CCK negative feedback signals critical in the control of meal size, and 2) is not dependent on altered central nervous system processing of other metabolic and hypothalamic signals important in the overall control of energy balance. Experiments in this proposal are designed to address multiple aspects of this hypothesis. Specifically, we will: 1) identify the roles of increased meal size and hyperphagia in the development of obesity in OLETF rats, 2) characterize metabolic profiles and patterns of hypothalamic gene expression in ad lib and pair fed OLETF rats, 3) identify potential interactions between exercise and disordered patterns of food intake in OLETF rats, 4) characterize OLETF feeding and metabolic responses to high fat and macronutrient selection diets and 5) compare the OLETF rat to a newly available CCK-A knockout mouse that does not develop obesity. Together, results from these studies will: 1) identify and characterize the ways in which a unique genetic deficit in a peripheral satiety signaling pathway interacts with a range of environmental factors (exercise, dietary restriction, diet composition) to modulate the development and maintenance of obesity, and 2) identify how such a satiety deficit interacts with central hypothalamic pathways mediating the control of energy balance. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ENERGY EXPENDITURE AND THE INCIDENCE OF OBESITY Principal Investigator & Institution: Bandini, Linda G.; New England Medical Center Hospitals 750 Washington St Boston, MA 021111533 Timing: Fiscal Year 2001; Project Start 01-MAY-1989; Project End 31-OCT-2003 Summary: Adolescence in girls is a critical period for the development of obesity. Reduced energy expenditure represents a strong risk factor. We are continuing to follow annually a cohort (originally 197 pre- menarcheal girls) who were enrolled (1990-1993) in a longitudinal study of energy expenditure and its relationship to the development of obesity. One hundred and fifty-nine girls (80.7%) remain active in the study. Of these 159 subjects, 59 have completed the study and the other 100 continue to seen annually. A baseline measures of body composition, resting metabolic rate, total daily energy expenditure, and VO2 max were completed. Measures of diet and activity were
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obtained from a 7-day food record, a 7-day activity record, and activity questionnaires. Since enrollment, girls are seen annually until 4 years after menarche when they exit the study. At their annual visit, measures of diet, activity, growth and body composition by anthropometric measures are obtained. Blood is drawn for the measurement of sex hormones and insulin. At the end of this proposed grant period, all but five girls will be 4 years post menarcheal and will exit the study. At that time we will have determined whether reductions in energy expenditure at baseline (total daily energy expenditures, resting energy expenditure, percent non- resting energy expenditure or VO2 max) are associated with increases in body fat as girls mature. We will also determine whether differences in ethnicity, or parental obesity contribute to the changes in body fat in a subcohort of girls, visceral fat was previously measured at menarche by MRI. At the time of the MRI, measures of body composition and anthropometry were repeated, blood was drawn for the measurement of sex hormones, and questionnaires were completed rating to diet, activity and behaviors such as smoking and alcohol abuse. We will repeat these measures in these girls at their exit visit. This study will allow us to determine what factors contribute to visceral fat deposition in girls during puberty. These studies will clarify the role of energy expenditure in the development of obesity and identify factors that contribute to the deposition of visceral fat. Identification of factors which contribute to the development of obesity and central fat distribution will aid in the development of programs designed to reduce the incidence and morbidity associated with adolescent obesity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ENHANCED INTERNET BEHAVIOR THERAPY FOR TREATING OBESITY Principal Investigator & Institution: Tate, Deborah F.; Assistant Professor; Miriam Hospital Providence, RI 02906 Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 31-JUL-2006 Summary: (provided by applicant): Given the increasing prevalence of obesity and fact that many adults have a strong preference to lose weight without attending weekly treatment meetings, there is need to develop effective alternatives to behavioral lifestyle interventions requiring less face-to-face contact. The Internet offers exciting opportunities to deliver behavior change interventions that minimize face-to-face interaction. We have recently developed and tested an Internet behavioral weight loss program compared with an Internet educational program in a randomized trial and found the behavioral program produced significantly better weight losses (4.1 kg) at 6 months. Our study clearly establishes the potential for using the Internet to deliver alternative treatment programs; however, treatment efficacy research is needed to further develop an Internet approach that will promote longer-term weight loss. The objectives of the proposed study are I) to enhance our Internet program to develop a state of the art Internet Cognitive-Behavior Therapy (I-CBT) program for obesity treatment; and 2) to conduct a randomized trial comparing the enhanced program with a Minimal CBT program also delivered via the Internet. We propose to recruit 100 overweight adults and randomly assign them to Enhanced Internet CBT or Minimal Internet CBT programs. The Minimal I-CBT condition will be given links to weight loss websites, weekly structured cognitive-behavioral lessons for weight loss, weekly prompting, and an on-line bulletin board. The Enhanced I-CBT program will have these same features plus weekly on-line group therapy sessions, computer-aided selfmonitoring diaries, and weekly individual e-mail feedback from a therapist. The primary outcome is weight loss from 0-12 months. Secondary outcomes will examine
Studies 29
patterns of weight change and changes in waist, diet, physical activity, and social support. The proposed research has significant implications for expanding the audience served by obesity treatment program by using the Internet. This study utilizes an innovative approach and extends our programmatic research on the development of a cognitive-behavioral Internet treatment for obesity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: ENVIRONMENTAL TEMPERATURE, SNS DEVELOPMENT AND OBESITY Principal Investigator & Institution: Young, James B.; Medicine; Northwestern University Office of Sponsored Programs Chicago, IL 60611 Timing: Fiscal Year 2001; Project Start 01-JUL-1977; Project End 31-MAR-2006 Summary: (Scanned from the Applicant's Description): The long-term goal of this project is to determine how environmental exposures during development contribute to the acquisition of obese or hypertensive traits in the adult. If successful, it may be possible to devise strategies for early intervention which might prevent or at least forestall the development of these disorders. The studies proposed in this application address the lasting influence of several environmental factors during fetal and neonatal life (environmental temperature, maternal diet and prenatal exposure to glucocorticoids) on an animal's susceptibility to become obese as an adult. It is the contention of the applicants that these three exposures induce different obesity-prone phenotypes by altering specific aspects of sympathoadrenal function, along with possible increases in food intake. The applicants propose that early exposure to cool environmental temperatures will predispose animals to develop obesity without features of the so-called 'metabolic syndrome', while maternal ingestion of a synthetic diet will predispose similar animals to develop obesity along with the 'metabolic syndrome'. The applicants also predict that prenatal exposure to glucocorticoids will exacerbate any other tendencies in the offspring to develop the 'metabolic syndrome' in conjunction with obesity. Furthermore, since these exposures are not mutually exclusive of one another, the applicants propose that maternal exposure both to glucocorticoids and to a synthetic diet will interact synergistically to exaggerate tendencies in the offspring toward obesity and the 'metabolic syndrome'. In addition, since the brainstem locus for sympathetic premotoneurons to brown fat in raphe pallidus (RPa) may also contribute to regulation of glucose metabolism, it is hypothesized that activation or inhibition of RPa will produce corresponding changes in glucose disposal. The applicants propose to use techniques of norepinephrine (NE) turnover and urine catecholamine levels to assess sympathetic and adrenal medullary function, respectively, in unanesthetized animals and to utilize neurophysiological studies of impulse traffic in sympathetic fibers of anesthetized rats to examine the importance of RPa in mediating SNS activation by specific stimuli, such as insulin and leptin. The potential impact of changes in sympathetic activity regulated by RPa for glucose and energy metabolism will also be examined. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: FAMILY-BASED TREATMENT OF SEVERE PEDIATRIC OBESITY Principal Investigator & Institution: Marcus, Marsha D.; Professor; Psychiatry; University of Pittsburgh at Pittsburgh 350 Thackeray Hall Pittsburgh, PA 15260 Timing: Fiscal Year 2001; Project Start 01-JUL-2001; Project End 31-MAY-2005
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Summary: (adapted from investigator's abstract) The prevalence of pediatric obesity has increased significantly and approximately 11 percent of American children and adolescents are obese. Of particular concern, the greatest increase in prevalence has occurred among the heaviest medical and psychosocial morbidity than milder obesity is. Moreover, severely obese children are likelier than less severely obese children are to be become obese adults and suffer the long term health consequences of obesity. Although the efficacy of family based behavioral weight control programs in the treatment of moderate pediatric obesity is well established, few studies have focused on the treatment of severe obesity. Thus in this application, we propose a randomized controlled trial to evaluate the efficacy of a family-based behavioral weight control program in the management of severe pediatric obesity. Two hundred children aged 812 will be randomized to a 6-month family-based program or usual care, and will complete assessments at pre- and post-treatment and 6 month and 12 month follow-ups. It is hypothesized that: Children who participate in the family based program, when compared to children who receive usual care, will report symptoms. A secondary aim of the proposed investigation is to examine the relationships among gender, race, compliance to diet and exercise, level of parent adherence and treatment outcome. The proposed investigation will gather data about a serious public health problem and establish a foundation for programmatic research to develop effective treatments for an underserved population. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: FINE LOCALIZATION OF GENES FOR HUMAN OBESITY Principal Investigator & Institution: Price, R Arlen.; Professor; Psychiatry; University of Pennsylvania 3451 Walnut Street Philadelphia, PA 19104 Timing: Fiscal Year 2001; Project Start 01-APR-2000; Project End 31-MAR-2005 Summary: (Adapted from Investigator's Abstract) The long-term goal of this study is to identify genes for common forms of obesity. To this end, the investigators previously have completed studies of the epidemiology, heritability and mode of inheritance of obesity. They have developed a cohort of families having both extreme obesity and thinness, and they have used this sample to examine candidate genes and regions, and, more recently, in a genome scan searching for linkage to obesity phenotypes. In a first stage scan they identified several genomic regions of interest, particularly a 15 cM interval of 20ql3 which may contain one or more obesity related genes. They have separate support to expand their linkage sample and conduct another genome scan, which should refine existing linkages and identify additional candidate regions for the fine mapping studies proposed in this application. However, it is doubtful that linkage methods alone will permit a resolution finer than two to five cM, an interval too large for positional cloning. The investigators note that there is a need for a cohort of triads which can be used to fine map genes for obesity, including those identified through their own linkage studies as well as through reported linkage and association studies conducted by others. In the current application, the investigators propose to develop another cohort of families consisting of extremely obese individuals and their parents for family based linkage disequilibrium studies. Specifically, the investigators propose to do the following: 1) develop a sample of 600 triads (160 from currently supported studies and 440 newly collected triads) having extremely obese female probands (BMI >= 40 kg/m2) and two parents assessed for obesity phenotypes (one or more parents will be of normal weight with maximum lifetime BMIG), which results in a substitution of Ser for Gly at position 49, and at nucleic acid 1165 (G- >C, which results in a substitution of Gly for Arg and position 389. Beta1 AR polymorphisms have functional significance; whether or not they associate with obesity is unknown. Mutations in the 5' leader and coding regions of the human beta2 AR gene give rise to several polymorphisms, which can after receptor density and function. The working hypotheses of this submission are that polymorphisms at position 389 and haplotypes of beta2 AR polymorphisms in the 5' leader and coding regions associate with obesity. Specific Aim #1: to compare the beta1 AR allele frequencies and genotypes in healthy obese and non- obese subjects. The hypothesis driving this specific aim is that obesity associates with the Gly 389 beta1 AR allele. Specific Aims #2: to compare the distribution of beta2 AR haplotypes in healthy obese (Body Mass Indexes > 30) and non-obese (BMI < 25) subjects. Beta2 AR haplotypes will be determined by PCR and direct sequencing. The thesis driving this specific aim is that obesity associates with the Arg19-Gly16- Glu27 beta2 AR haplotype. The distribution of beta2 AR haplotypes in 118 non-obese and 118 otherwise healthy obese subjects will be compared. The results of this study will determine whether polymorphisms in beta1 and beta2 AR allels associate with obesity. The information obtained from our studies are important in designing clinical trials of interventions designed to reduce body weight. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PREVENTION OF OBESITY BY ALTERATION OF DIETARY FAT Principal Investigator & Institution: Donnelly, Joseph E.; Professor and Director; Educ Psychology and Research; University of Kansas Lawrence Lawrence, KS 66045 Timing: Fiscal Year 2001; Project Start 15-FEB-2001; Project End 31-JAN-2006 Summary: Treatment for obesity has proven difficult as most reduced obese individuals regain the weight which had been lost. The lack of success in treating obesity argues for strategies to prevent obesity or weight re-gain. The PIs propose to use 3 clinically appropriate levels of fat intake in a population at-risk for weight gain in a long-term study where energy intake and macronutrient composition is verified by multi-method techniques. Primary Aim-Prevention of weight gain. The PI will determine the effects of 3 levels of verified dietary fat intake on body weight and body composition in college students at-risk for weight gain. We hypothesize that ad libitum diets which contain greater than 35 percent fat will promote weight gain compared to subjects who ingest ad libitum diets which contain 28 to 32 percent fat or 25 percent fat or less. Specifically, the PI expects a dose response for the level of fat in the diet for body weight and fat mass. Secondary aims will may contribute to our understanding of how various levels of fat intake may prevent or promote obesity and may provide explanation for the anticipated differences in individual responses with the groups. Association of fat intake to total energy intake. The PI expects that subjects consuming diets with higher amounts of fat to have greater total energy intakes and will therefore show weight gain in a dose response fashion. Specifically, the PI will hypothesize that subjects consuming ad libitum diets with 35 percent fat or greater will show an increase in total energy intake compared to subjects consuming a 28 to 32 percent fat diet or subjects consuming a diet of 25 percent fat or less. Individual response - the PI expects subjects with greater body fat to gain more weight and fat mass compared to leaner subjects and expect subjects who are restrained eaters to gain less weight than those who exhibit disinhibited eating.
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Although the PI expects increase energy intake for the groups that receive high fat intakes, they do not expect all subjects within each group to respond in similar fashion. The long-term results expect to show those subjects who gained the least amount of weight during the intervention will have the lowest weights 1,2 and 3 years post intervention. The results of this study should advance our understanding of the role of dietary fat in the prevention of obesity and weight re-gain. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: PSYCHOSOCIAL DETERMINANTS OF NUTRIENT INTAKE IN GIRLS Principal Investigator & Institution: Striegel-Moore, Ruth H.; Professor; Psychology; Wesleyan University Middletown, CT 06459 Timing: Fiscal Year 2002; Project Start 01-AUG-2002; Project End 31-JUL-2005 Summary: (provided by applicant): Studies have documented the importance of eating behavior as a modifiable risk factor for the development of obesity and cardiovascular disease (CVD). The burden of obesity and CVD is not equally distributed in the population; women from ethnic minority populations are particularly likely to be obese and to have higher rates of CVD and stroke than white women. Thus, the broad, longterm goal of this research is to better understand the determinants of nutrient intake in black and white adolescent girls and to examine the effects of nutrient intake and eating behaviors on obesity, a significant risk factor for CVD. Overall we wish to determine the extent to which psychological and familial factors contribute to nutrient intake in black and white girls, beyond the well-established effects of ethnicity and socioeconomic factors. Specifically, the aims of the project are the following: 1) to provide a detailed developmental description of eating behaviors and nutrient intake in black and white girls and to examine the "clustering" of certain eating behaviors (e.g., skipping meals and snacking) into eating patterns; 2) to determine the clinical significance of eating behaviors and eating patterns by examining their contribution to nutrient intake and the development of obesity; 3) to examine the role of psychological and familial factors as determinants of eating behaviors, eating patterns, nutrient intake, and obesity in black and white girls. Capitalizing upon the availability of extensive data collected prospectively among an exceptionally well-maintained cohort of 2,379 black and white females over a 12-year period (from ages 9-10 to ages 21-23), we propose to apply innovative analytic procedures to further the scientific understanding of the determinants of nutrient intake and eating behaviors in adolescent girls. Participants were assessed annually for ten years as part of the National Heart, Lung and Blood Institute Growth and Health Study (NGHS) with measurements of anthropometry, food intake, eating and weight related attitudes and behaviors and family cohesion. Parents also provided information about weight, eating, and family environment at two assessments. In a subsequent study with the same sample, structured clinical interviews were conducted to determine history of psychiatric disorders and risk factors for eating disorders. Adult weight was also measured. Results from our secondary analyses will be useful for interventions aimed at improving nutritional health. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: RACE, LIPOPROTEIN LIPASE AND OBESITY AFTER MENOPAUSE Principal Investigator & Institution: Goldberg, Andrew P.; Professor; Medicine; University of Maryland Balt Prof School Baltimore, MD 21201 Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-MAR-2008
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Summary: (provided by applicant): This study is designed to determine the cellular mechanisms underlying the paradoxical association of insulin resistance with decreased visceral adiposity and circulating triglyceride (TG) levels in African-American (AA) compared to Caucasian (CAU) postmenopausal women. This will provide insight into mechanisms underlying racial differences in obesity and its associated metabolic dysfunction (insulin resistance, type 2 diabetes, dyslipidemia, hypertension). The hypothesis is that postmenopausal AA women have a higher skeletal muscle lipoprotein lipase (SM-LPL) and a lower adipose tissue LPL (AT-LPL) activity that leads to the preferential accumulation of TG in muscle (SM-TG), while the converse exists in CAU women. We also postulate that a weight loss (WL) intervention, by preferentially decreasing SM-LPL activity in AA and AT-LPL activity in CAU, will promote reductions of SM-TG in AA and of visceral adiposity in CAU to improve lipoprotein lipid profiles and insulin sensitivity. Specific aims determine whether: 1) decreased visceral (omental and mesenteric) and subcutaneous abdominal (SAT) AT-LPL activity and increased skeletal muscle LPL activity in rectus abdominis and vastus lateralis are the cellular mechanisms underlying racial differences in visceral obesity and SM-TG accumulation in AA compared to CAU postmenopausal women using tissue obtained during elective abdominal surgery and by needle biopsy, and 2) WL, by reducing SM (vastus lateralis - and SAT-LPL activity, is associated with a decrease in SM and visceral fat accumulation to increase in vivo insulin action (hyperinsulinemic euglycemic clamp) and the in vitro antilipolytic response to insulin in a homogeneous population of healthy obese AA and CAU postmenopausal women. We will study healthy, obese (BMI = 30-40 kg/m2), sedentary 50-65 year old postmenopausal women not on hormone-replacement therapy. We will measure AT- and SM-LPL activity, SM-TG content, visceral fat and mid-thigh low density lean tissue area (CT scans) insulin sensitivity in abdominal adipocytes as insulin suppression of lipolysis and in whole body estimated by hyperinsulinemic euglycemic clamps and using the Homeostasis Model Assessment of Insulin Resistance (HOMA IR), total body fat (DXA), lipoprotein lipids, oral glucose tolerance and obesity-related hormones (leptin, insulin, SHBG, free testosterone). Collectively, these results will determine whether racial differences in the tissue-specific LPL activity, the key enzyme for hydrolysis and the ensuing storage of circulating TGs, establish a metabolic setting in obese AA of increased SM-TG (due to increased SM-LPL and decreased visceral fat) and in obese CAU of increased visceral fat (due to increased AT-LPL) that predisposes them to insulin resistance and risk for type 2 diabetes. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: REDUCING TELEVISION VIEWING TO PREVENT CHILDHOOD OBESITY Principal Investigator & Institution: Robinson, Thomas N.; Assistant Professor Of; Medicine; Stanford University Stanford, CA 94305 Timing: Fiscal Year 2001; Project Start 01-APR-1999; Project End 31-MAR-2003 Summary: We propose to test the efficacy of reducing television, videotape and videotape and video game use to prevent obesity among third grade children, in a randomized controlled school-based trial. The United States has experienced dramatic increases in obesity among both children and adults. There is a pressing need for innovative interventions to prevent obesity. There has been widespread speculation that television viewing might be one of the most easily modifiable causes of obesity among children. This hypothesis has broad appeal, but has been difficult to validate. We propose an innovative experimental model. In the current environment, in which
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television viewing is already so prevalent, the question of greatest clinical, practical and policy importance is: Will reducing television, videotape and video game use prevent childhood obesity? As a foundation for this proposal, we have completed two pilot studies that demonstrate the feasibility and potential promise of the proposed study. We propose a school-based randomized controlled trial involving 12 ethnically-diverse elementary schools and approximately 900 third graders. Six schools will be randomly assigned to receive an intervention to reduce television, videotape and video game use and the other six schools will receive an attention-placebo control intervention. The intervention model is derived from principles of Bandura's social cognitive theory and includes a classroom curriculum and parent newsletters. The primary intervention will be delivered throughout the third grade school year. Survey and physical assessments of all children will occur at baseline, at the end of 3rd grade (post- test) and at the beginning and end of 4th grade (4 month and one year follow-ups, respectively). A subsample of children will also complete 4 days of activity monitoring and three 24-hour dietary recalls. Parents will be interviewed by phone at baseline, post-test and one-year follow up. We hypothesize that, compared to controls, third grade children exposed to a school-based intervention to reduce time spent watching television and videotapes and playing video games, will significantly reduce their prevalence of obesity over a single school year. The primary outcome measure will be body mass index. We will also test maintenance of the primary outcome over the follow-up period and effects of the intervention on hypothesized mediating variables; amount of television, videotape and video game use, physical activity, cardiorespiratory fitness, dietary fat and calorie intake and eating while watching television. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: REGULATORY RESPONSES TO POSITIVE ENERGY BALANCE Principal Investigator & Institution: Seeley, Randy J.; Professor; Psychiatry; University of Cincinnati 2624 Clifton Ave Cincinnati, OH 45221 Timing: Fiscal Year 2002; Project Start 30-SEP-1997; Project End 31-JAN-2007 Summary: (provided by applicant): The incidence of obesity has reached epidemic proportions, is a major health burden, and costs the U.S. billions of dollars in health care and lost productivity. Failure to develop effective treatments for obesity is in large part due to a lack of clear understanding as to how food intake and energy balance are regulated by the CNS. Thus, research to determine the processes by which food intake and energy balance are controlled is likely to have a major impact on public health, but the research to date has been imbalanced. For whereas considerable effort has been devoted to understanding the neurochemical response to negative energy balance, relatively little attention has been devoted to the inverse situation of positive energy balance. This oversight is significant since obesity is necessarily associated with periods of positive energy balance and therefore can be considered as a failure of the body weight regulatory system to respond appropriately to positive energy balance. Thus studying the responses to positive energy balance may provide valuable clues concerning the etiology of obesity. Moreover, the regulatory responses to positive energy balance represent the recruitment of endogenous systems that produce reduced food intake, increased energy expenditure and significant weight loss. Finding potential ways to mimic or trigger these endogenous regulatory response systems could provide unique insights and therapeutic strategies for the treatment of obesity. The current proposal seeks to identify critical aspects of this response system. When animals are force-fed calories in excess of caloric need (involuntary overfeeding), their spontaneous food intake drops to near zero and they gain body weight. Additionally, for some time
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after the overfeeding regimen is terminated, spontaneous food intake remains low until body weight has returned to control levels. Our data indicate that this regulatory response to positive energy balance is mediated by the CNS melanocortin system. We propose assessing several hypotheses concerning how the CNS melanocortin system orchestrates the response to positive energy balance. First, we will determine the critical population of melanocortin receptors that mediate the reduced food intake and increased energy expenditure that follow a period of positive energy balance. Second, we will determine the critical inputs into the melanocortin system that signal positive energy balance. Finally, we will evaluate the unique effects of an endogenous melanocortin receptor antagonist that counteracts the normal response to positive energy balance. The information from this proposal will be critical to a complete picture of how energy balance is regulated and how disorders of energy balance such as obesity may be treated. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: RESEARCH IN PRADER-WILLI SYNDROME AND OBESITY Principal Investigator & Institution: Driscoll, Daniel J.; Hayward Professorship in Genetics Resear; Pediatrics; University of Florida Gainesville, FL 32611 Timing: Fiscal Year 2001; Project Start 07-JUN-2000; Project End 31-MAY-2005 Summary: (Adapted from the candidate's description) The goals of this translational research project are to genetically and clinically dissert the imprinted genes underlying each component of Prader-Willi syndrome (especially the gene causing obesity), and to explore the potential role of early childhood morbid obesity plays in mental retardation. This will be accomplished by screening for mutations in candidate genes for various phenotypic components of PWS; performing psychometric testing on children with early onset morbid obesity and their families; and correlating hormonal and neurotransmitter levels from blood and CSF with the psychometric and mutation analyses. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: RESISTANCE TRAINING FOR THE PREVENTION OF OBESITY Principal Investigator & Institution: Washburn, Richard A.; Associate Professor; Energy Balance Laboratory; University of Kansas Lawrence Lawrence, KS 66045 Timing: Fiscal Year 2003; Project Start 01-AUG-2003; Project End 31-MAY-2005 Summary: (provided by applicant): Obesity is associated with numerous co-morbidities, including cardiovascular disease, diabetes, hypertension and some cancers. Weight loss is difficult; therefore interventions to prevent the development of obesity are warranted. In this project we will evaluate the potential of resistance training (RT) to prevent the development of obesity in healthy, sedentary, overweight, young (18-25 yrs) college men and women, an accessible group at high risk for becoming obese. RT offers an innovative approach to obesity prevention that differs in concept from. Unlike aerobic exercise, RT results in a minimal increase in energy expenditure during exercise, but may result in significant increases in total daily energy expenditure resulting from increased resting metabolic rate (RMR) mainly as a result of increased fat-free mass (FFM). The efficacy of the RT protocols recommended as part of adult fitness programs to alter FFM and RMR is unknown. Therefore; this research project will determine the level of RT necessary to induce increases in muscle mass and RMR, which may, in turn be associated with weight maintenance or loss. All RT will be supervised and verified by the research team. We will compare changes in FFM and RMR elicited by 24 weeks of
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RT conducted as recommended by ACSM (1 set, 3 d/wk, resistance 8-12 repetitions maximum (RM), 9 exercises) with a higher intensity RT program (1 set, 3 d/wk, resistance 3-6 RM, 9 exercises) in a volunteer sample of 108 young adults (36 men, 72 women) matched on muscle mass and randomly assigned to the RT protocols or a nonexercise control condition within gender. Fat-free and muscle mass (DEXA), RMR (indirect calorimetry), and muscular strength (1-RM) will be assessed at baseline, and at 12 and 24 weeks. Dietary intake (24hr. recall) will be assessed monthly. If our pilot project proves successful, i.e., our RT program results in clinically significant increases in RMR, we will propose a larger and longer (18 m) randomized trial to assess the efficacy of RT for weight loss or prevention of weight gain. This trial will employ a complete energy balance model including detailed assessments of total energy intake and expenditure using state-of-the-science techniques (doublylabeled water, wholeroom calorimetry, visual plate waste), and will investigate potential mechanisms, such as changes in protein turnover and sympathetic nervous system activity, that may be associated with increased RMR resulting from RT. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: RESISTIN'S ROLE IN OBESITY RELATED INSULIN RESISTANCE Principal Investigator & Institution: Steppan, Claire M.; Medicine; University of Pennsylvania 3451 Walnut Street Philadelphia, PA 19104 Timing: Fiscal Year 2001; Project Start 01-AUG-2001; Project End 31-JUL-2004 Summary: (provided by applicant) This proposed research plan describes a 3 year training program for the development of an academic career. The candidate has completed four years of post-doctoral fellowship training and will expand her training during this time period to progress to an academic position. This proposal will define the role of resistin in obesity-related insulin resistance. Mitchell A. Lazar, M.D., Ph.D. will mentor the applicant's scientific development. Dr. Lazar is a recognized leader in the field of nuclear receptors and adipogenesis. Dr. Lazar is the Chief of Endocrinology, Metabolism and Diabetes and the Director of the Penn Diabetes Center. To enhance the training, the applicant will enlist the expertise of Morris Birnbaum, M.D., Ph.D., Howard Hughes Professor and Rexford Ahima, M.D., Ph.D., assistant professor and Director of the Physiology Core of the Penn Diabetes Center. In addition to performing research, the Principal Investigator will benefit from lectures, seminars, and advisory committee meetings. The proposed research will focus on a newly identified hormone that is secreted from adipocytes and which has been shown to antagonize the effects of insulin. The proposed experiments will entail analyzing components in the insulin signaling cascade downstream of insulin binding to determine the mechanism of antagonism of insulin action by resistin (Specific Aim 1). In order to address the role of resistin in insulin resistance associated with obesity (Specific Aim 2), we will study the in vivo regulation of resistin in several different animal models of obesity. We plan to study obesity models in which leptin signaling is impaired (ob/ob, db/db) and intact (Agouti, Cpe-fat). The proposed research plan will reveal detailed information about resistin's role in obesity and diabetes. The scientific environment of the University of Pennsylvania provides the ideal opportunity for the candidate to develop her career by executing the proposed research while utilizing the expertise and resources of Dr. Mitchell A. Lazar. Such an environment should allow the candidate to maximize her potential to establish herself as an independent investigator. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: ROLE OF THE LOWER GUT IN THE CONTROL OF ENERGY BALANCE Principal Investigator & Institution: Koopmans, Henry S.; University of Calgary 2500 University Dr Nw Calgary, Timing: Fiscal Year 2002; Project Start 01-APR-2002; Project End 31-MAR-2006 Summary: Surgery has been the most successful treatment for morbid obesity. The main objective of this grant proposal is to determine why lower gut signals generated in bypass surgery have been so successful in causing reduced food intake and body weight loss. We recently discovered that lower gut signals also cause a 10-25 percent increase in energy expenditure. One objective of this grant proposal is to determine how stimulation of different lengths of the ileum, caecum and colon affect energy balance and the plasma levels of the lower gut hormones: neurotensin; PYY and GLP1. Another objective is to determine the role of the extrinsic nerves to the ileum in altering food intake, energy expenditure and body weight by doing ileal transplantation surgery or denervation of the superior mesenteric nerves. A time course of the changes in energy expenditure, upper gut tissue growth and plasma lower gut hormone levels resulting from ileal transposition will be investigated in preparation for a later peptide infusion study. The role of the various macronutrients in changing energy balance and lowering body weight will be assessed by feeding various diets to rats with a 20 cm segment of ileum moved up to the mid-duodenum. The short-term objective of this research is to understand the internal control of daily intake and energy expenditure. The long-term objective is to find a medical treatment (drug or hormone analog) for obesity. In Western societies, obesity is a major medical problem that causes a great deal of human suffering. Obesity is associated with such chronic and debilitating conditions as diabetes, cancer (breast, endometrial, prostate and colon), hypertension, hyperlipidemia, stroke and heart disease. An effective medical treatment for obesity would improve the quality of life for millions of people and would reduce the cost of long-term health care. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: RURAL COMMUNITY PARTNERSHIP TO PROMOTE FITNESS BY AGE 5 Principal Investigator & Institution: Dennison, Brbara A.; Mary Imogene Bassett Hospital Cooperstown, NY 13326 Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 31-JUL-2005 Summary: (provided by applicant): This proposal, Rural Community Partnership to Promote Fitness by Age 5, focuses on preventing the development of obesity among young, preschool-age children, by targeting the environment where children are increasingly spending time prior to the start of kindergarten-childcare centers (daycare, preschools, and Head Start centers). The theoretical frameworks of "Diffusion of Innovation" and "Social Marketing" will guide the development of this intervention by researchers and childcare center directors and staff. Support from community, medical, and educational organizations and collaboration with the local McDonald's restaurant, Price Chopper grocery stores, and SUNY-Cobleskill Culinary Institute will facilitate consistency of message. We propose to assess food and physical activity policies and environments at childcare centers, and then collaboratively develop innovative policy and environmental changes to promote healthy eating (especially snacking), decrease behaviors that encourage overeating, increase physical activity, and decrease TV/video viewing at these centers. We propose to develop and provide training sessions for staff at childcare centers that promote these policy changes and environmental innovations.
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As the primary outcome, we will evaluate the difference in the prevalence of child obesity at age 5, i.e., at the time of kindergarten entrance, between the intervention and the control communities. At the conclusion of this research project, a childcare centerbased environmental approach to prevent the development of child obesity will have been developed, implemented, and evaluated. This obesity prevention program will be transferable to other childcare centers to improve the health of America's children. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: SELF-MONITORED MANAGEMENT
PHYSICAL
ACTIVITY
FOR
WEIGHT
Principal Investigator & Institution: Walker, Karen E.; Temple University 406 Usb, 08345 Philadelphia, PA 19122 Timing: Fiscal Year 2003; Project Start 01-JUN-2003; Project End 31-MAY-2006 Summary: (provided by applicant): This application for a Mentored Research Scientist Development Award (K01) is a re-submission by a new investigator. The goal of the award is to provide the investigator further training in the fields of obesity and community health nursing. As part of this training, the investigator will receive mentoring and pursue academic study in the following areas: 1) etiology and complications of obesity; 2) behavioral treatment of obesity; 3) community health nursing; 4) conduct of clinical trials; 5) exercise physiology; 6) biostatistics; and 7) nutrition. The proposal builds on a background in cardiovascular research, clinical study of weight loss maintenance, and community-based activities. Recent data show that 61% of US adults are overweight or obese. As a result, there is an epidemic of obesity-related health problems such as diabetes, coronary artery disease, and high blood pressure. Losses of only 5% to 10% of body weight significantly improve health, and individuals in programs that modify diet and lifestyle typically achieve weight losses of this magnitude. Unfortunately, the great majority of people cannot maintain the loss. Regular exercise is crucial to the maintenance of weight loss, but most individuals have problems with adherence due to a variety of barriers to exercise. Typical barriers are lack of time, lack of childcare, and lack of access to facilities. The goal of the proposed research is to improve the maintenance of weight loss by increasing physical activity in a low-income, primarily African American population that participates in a community-based behavioral weight loss program. All participants (n=152) will be treated with a 20-week weight reduction program followed by 52 weeks of maintenance. At the outset of the study, subjects will be randomized to one of two physical activity conditions. The research has two specific aims: The first is to compare at week 72 the maintenance of weight loss and physical activity adherence in individuals who are prescribed a standard structured exercise program of walking (Condition 1) versus a lifestyle activity intervention self-monitored via pedometer (Condition 2). Adherence will be determined by obtaining a common measure of physical activity across both conditions using accelerometers. The second aim is to compare short- (week 20) and long-term (week 72) differences between the two conditions in measures of physical (serum lipids, glucose/insulin ratio, interleukin-6, Creactive protein, resting blood pressure, cardiorespiratory fitness) and psychosocial health (mood, quality of life). This study has been selected to further develop the investigator's knowledge of the treatment of obesity using principles of community health nursing, and the training has been designed to facilitate the investigator's development as an independent clinical scientist studying innovative ways of reducing cardiovascular risks within urban communities. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: SOCIAL DETERMINANTS OF OBESITY AND RISK OF STROKE Principal Investigator & Institution: Dubowitz, Tamara; Maternal and Child Health; Harvard University (Sch of Public Hlth) Public Health Campus Boston, MA 02460 Timing: Fiscal Year 2003; Project Start 01-APR-2003; Project End 31-MAR-2006 Summary: (provided by applicant): Stroke is the third leading cause of death in the United States, and a leading cause of long-term disability. The risk for stroke varies by race/ethnicity; stroke incidence is greater among African Americans at younger ages, contributing to a mortality rate 80 percent greater than that of Caucasians (Keppel et al 2002; DHHS 2000; Stroke Progress Review Group, NINDS 2002). Limited understanding exists concerning the etiology and variations of subtypes of stroke incidence in different populations and geographic locations over time (Stroke Progress Review Group, NINDS 2002). Obesity, which results in part from a complex pathway of numerous lifestyle precursors, is a strong predictor of cerebrovascular disease such as stroke and other cardiovascular disease (WHO, 2000). Moreover, dietary intake and physical activity contribute to energy imbalances that result in obesity and independently predict stroke (AICR 1997; USDA/USDHHS 2000; USDHHS 1996; 2000; Krebs-Smith SM. 2001). Few studies consider both biological and social determinants of intermediate outcomes of cerebrovascular disease from a multileveled perspective. This application considers longitudinal measures of social and biological variables to investigate the independent effect of social disparities to the development of obesity among low-income multi-ethnic postpartum women at increased risk of stroke and other comorbidities. As women face particular biological and social transition during the postpartum period, the proposed research seeks to measure social determinants of pregnancy-related weight gain over time, adjusting for diet, physical and biological predictors of obesity and stroke. Research findings from the proposed work can inform the design of future interventions to reduce risk of stroke in women of reproductive age in low income, racial/ethnic subpopulations at highest risk of obesity and its sequelae. Specific aims include examination of: (1) individual and household social determinants pregnancy-related weight change and obesity; (2) social disparity in dietary intake and nutritional status and its relation to pregnancy-related weight change and obesity; and (3) neighborhood characteristics that influence the development of obesity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: THE 4 CORNERS BREAST AND ENDOMETRIAL CANCER STUDY Principal Investigator & Institution: Baumgartner, Kathy B.; Phd; Internal Medicine; University of New Mexico Albuquerque Controller's Office Albuquerque, NM 87131 Timing: Fiscal Year 2001; Project Start 30-SEP-1999; Project End 31-JUL-2004 Summary: (Adapted from Applicant's Abstract) The incidence of breast and endometrial cancers varies almost three-fold between non-Hispanic white populations and Native American and Hispanic populations living in the 4-Corners area of the United States (Arizona, New Mexico, Colorado, and Utah). Interestingly, although American Indian and Hispanic women have higher prevalences of many risk factors for breast and endometrial cancer identified in non-Hispanic white women (e.g., obesity, low levels of vigorous physical activity, low intakes of fruits and vegetables, high rates of insulin resistance) they have lower cancer incidence rates. In this study the investigators focus on the metabolic factors of obesity/weight changes and indicators of insulin status as they relate to breast and endometrial cancers. Obesity is associated both with estrogen and insulin by two interrelated disease pathways. Insulin may influence cancer risk directly through its effects on insulin-like growth factor (IGF) and its binding proteins
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(IGFBPs) and well as indirectly through its effect on estrogen levels. The investigators propose focusing on the insulin pathway because of the high levels of insulin pathway dysfunction in this population. A multi-center case-control study is proposed that targets women living in the 4-Corners area; the study will consist of a 2.5 hour in-person interview and a blood draw. Over a three-year case ascertainment period, the study will enroll 3000 breast cancer cases, 450 endometrial cancer cases and 3000 controls, half of whom will be Hispanic/Native American and half of whom will be non-Hispanic white women between the ages of 25 and 79. Molecular variants of genes that influence obesity and insulin (androgen receptor gene (AR), vitamin D receptor gene(VDR), insulin receptor (ADRB3)) will be examined both independently and in conjunction with metabolic factors to determine differences in genetic susceptibility in the population. Because of the diverse population (Hispanics, Native American, and non-Hispanic white women), the investigators propose to evaluate ethnic background and genetic admixture in relationship to gene markers, environmental factors, and breast and endometrial cancer risk. Genetic admixture (Ameridian to European genetic mixture) is a novel and innovative way to study the continuum of ethnic diversity. C-peptide, glycosylated hemoglobin, IGF-1, and IGFBP3 will be evaluated with respect to breast and endometrial cancer in a subset of women. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: THE EPIDEMIOLOGY OF BODY MASS INDEX REBOUND Principal Investigator & Institution: Daniels, Stephen R.; Professor of Pediatrics and Environment; Children's Hospital Med Ctr (Cincinnati) 3333 Burnet Ave Cincinnati, OH 45229 Timing: Fiscal Year 2001; Project Start 17-AUG-2000; Project End 31-JUL-2005 Summary: (Adapted from the Investigator's Abstract) Obesity is the most obesity which are present prior to the onset of excess weight gain has been problematic. Recently, it has been shown that the timing of body mass index (BMI) rebound may be a predictor of future obesity. BMI increases during the first year of life. It then declines until it reaches a minimum value during childhood and subsequently increases into adolescence and adulthood. The nadir of BMI is called BMI rebound. Studies have shown that BMI rebound at a younger age is associated with increased risk of obesity later in life. Currently, very little is known about the epidemiology of BMI rebound. The purpose of the proposed investigation is to precisely determine the age of BMI rebound and evaluate the body composition changes which occur during this time to determine if BMI rebound corresponds to a rebound in adiposity. In addition, determinants of the changes in body composition, such as diet and physical activity, will be investigated. Finally, the relationship of the timing of BMI rebound to body composition and cardiovascular risk factor status will be studied. The proposed investigation is a cohort study designed to follow 320 children from age three age seven years. Subjects will be evaluated every four months during the period of the study. Data will be collected on height, weight, body composition, diet and physical activity. At age seven years, the level of adiposity, the distribution of body fat, and cardiovascular risk factors will be studied. The investigators note that better understanding of the epidemiology of BMI rebound could lead to improved identification of children at high risk of future obesity prior to excess weight gain. They further note that elucidation of the determinants of the timing of BMI rebound could lead to the development of clinical and public health strategies to prevent the development of obesity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: TREATMENT FOR OBESITY AND BINGE EATING DISORDER Principal Investigator & Institution: Grilo, Carlos M.; Associate Professor; Psychiatry; Yale University 47 College Street, Suite 203 New Haven, CT 065208047 Timing: Fiscal Year 2002; Project Start 01-AUG-1996; Project End 31-JUL-2007 Summary: (provided by applicant): This application seeks funds to conduct a study of cognitive behavioral and behavioral weight loss treatments for obese patients with binge eating disorder (BED). The proposed study builds directly upon the findings of the initial project that examined the efficacy of fluoxetine treatment and cognitive behavioral therapy (CBT) and the relative efficacy of the treatments alone and in combination for patients with BED (balanced 2 x 2 factorial design). CBT produced significant and clinically meaningful improvements in the behavioral (binge eating), cognitive (attitudinal features of eating disorders), and associated psychological (depression) features of BED, but not for the physical problem of obesity. In the 2 x 2 factorial design: (1) CBT was superior to treatment without CBT, treatment with fluoxetine was not superior to treatment without fluoxetine, and no interaction between treatments occurred; (2) Specific comparisons among specifc treatments revealed that fluoxetine was not superior to placebo, CBT + Placebo and CBT + Fluoxetine were similar, and CBT + Placebo and CBT + Fluoxetine were superior to Fluoxetine-only and Placebo-only. Findings suggest that CBT has efficacy for the behavioral, cognitive, associated psychological features of BED. The strong association between BED and obesity, and the major health risks associated with obesity highlight the need for developing interventions that also reduce weight. It remains uncertain whether behavioral weight loss (BWL) has efficacy for producing weight loss in BED or for reducing binge eating and its associated features. The proposed study involves a comparison of three treatment conditions: (1) CBT; (2) BWL, and (3) a sequential (twopart) treatment consisting of CBT followed by BWL. Assessments will occur at baseline, bimonthly during treatment, and 6-and 12-months post-treatment. The primary specific aim is to test the relative efficacy of CBT, BWL, and a sequential treatment consisting of CBT followed by BWL. Secondary aims are to (1) explore predictors and processes of change during the acute treatment and follow-up period, and (2) examine whether (a) BWL ("dieting") after the CBT produces weight loss, and (b) weight regain (if it occurs following BWL) is accompanied/followed by reoccurrence of binge eating, attitudinal features of eating disorders, psychological distress, or psychiatric disturbances. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: TREATMENT OF OBESITY IN UNDERSERVED RURAL SETTINGSTOURS Principal Investigator & Institution: Perri, Michael G.; Professor; Medicine; University of Florida Gainesville, FL 32611 Timing: Fiscal Year 2003; Project Start 01-JUN-2003; Project End 31-MAY-2007 Summary: (provided by applicant): Higher rates of obesity, sedentary lifestyle, and coronary heart disease are observed in rural than non-rural areas of the U.S., yet the treatment of obesity in the rural population has received little research attention. Efficacy studies, typically conducted in urban settings, show that lifestyle interventions produce clinically significant weight reductions, but a regaining of lost weight commonly follows the conclusion of treatment. Recent studies have demonstrated that clinic-based, extended-care programs can improve the maintenance of lost weight. Thus, the next logical steps in this line of research are (a) to extend these studies to community settings with underserved populations and (b) to test alternative and potentially more
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efficient methods of providing extended care, such as through the use of telephonebased rather than clinic-based maintenance programs. The primary objective of TOURS is to test the effectiveness of weight-loss maintenance programs in a randomized controlled trial, conducted in medically underserved rural settings. Obese women (N=300), ages 50-75 years, from six medically underserved rural counties will be randomly assigned to one of three 18- months long obesity treatment programs. Each treatment condition will include an initial 6-month lifestyle intervention followed by one of three 12-month follow-up programs: (A) an Office-based Maintenance Program, (B) a Telephone-Based Maintenance Program, or (C) an Education Control Condition. Dependent variables to be assessed at baseline, 6 months, and 18 months will include body weight, as well as a selected Array of health-related indicators and quality of life measures. It is hypothesized that participants assigned to either of the experimental programs will exhibit better maintenance of lost weight compared with those assigned to the control condition. Potential mediators and moderators of the intervention program-weight change relationship will be examined, and exploratory analyses of the costs and cost effectiveness of the interventions will be conducted. This trial will contribute important public health information regarding methods for improving obesity management in an underserved population at high risk for weight-related chronic diseases and disability. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: UAB CLINICAL NUTRITION RESEARCH UNIT Principal Investigator & Institution: Allison, David B.; Professor; Nutrition Sciences; University of Alabama at Birmingham Uab Station Birmingham, AL 35294 Timing: Fiscal Year 2003; Project Start 01-JUN-2000; Project End 31-MAY-2005 Summary: (adapted from the application) The proposed UAB Clinical Nutrition Research Unit (CNRU) will foster a multidisciplinary approach to basic, clinical and translational research with an emphasis on understanding the metabolic factors, environmental influences, and associated genetic traits underlying nutrition and obesity-related health problems. The University of Alabama at Birmingham (UAB) provides an ideal academic environment for interdisciplinary research centers. With a 50-year history of pioneering research, the Department of Nutrition Sciences currently includes 18 primary research faculty and $8.3 million in total direct cost funding (80% federal). In addition, the Department coordinates all of the extensive nutrition training and service programs at UAB. To complement its well-established nutrition research program, in 1990, the Department initiated a campus-wide effort to strengthen obesity research. Institutional support of $1.96 million enabled development of the Energy Metabolism Research Laboratory and recruitment of an outstanding team of scientists. The result was rapid growth in new/peer-reviewed funding and interdisciplinary collaborations, such that in 1996 UAB established an intramurally-funded UniversityWide Obesity Nutrition Research Center which, with NIH funding, will evolve into the proposed CNRU. The CNRU research base comprises 60 investigators from 18 academic units, with total direct funding of $44 million for nutrition/obesity research (88% federal; 11 R01s). Of the 77 funded nutrition/obesity studies and approved P/F projects, 65 (84%) will use CNRU Cores. The Energy Metabolism/Body Composition Core will support metabolic studies in humans and small animals; Genetics Core will focus on research related to gene expression, polymorphism detection, and genetic animal models; Nutrient Analysis Core will provide an array of nutrient analyses and new methods development; and the Biostatistics Core will support study design and data analysis. The CNRU will also support three P/F studies, a New Investigator, and an
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Enrichment Program. With exceptional institutional support and an ideal academic infrastructure, UAB has established a strong base of obesity/nutrition research and is now poised to greatly expand this effort through creation of a CNRU. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: UCLA TRAINING PROGRAM IN NUTRITION AND OBESITY Principal Investigator & Institution: Heber, David; Professor/Chief; Medicine; University of California Los Angeles 10920 Wilshire Blvd., Suite 1200 Los Angeles, CA 90024 Timing: Fiscal Year 2003; Project Start 30-SEP-1992; Project End 31-MAR-2008 Summary: This proposal requests renewed support for the UCLA Nutrition and Obesity Training Program in order to continue to train diverse and highly trained clinical and basic scientists in nutrition and obesity research. Through stipends and educational support of four postdoctoral M.D. or Ph.D. trainees, this program seeks to develop a new generation of scientists and physician-scientists capable of translating advances in the understanding of gene-nutrient interactions relevant to obesity and obesity-related diseases to clinical medicine and community health both nationally and internationally. Obesity-related diseases account for 300,000 deaths per year and one of 9 health care dollars are spent on over 30 obesity-related diseases. This program was established in 1992, and has since developed a cadre of dedicated faculty, a clear record of accomplishment among nutrition fellows who have advanced their careers to become competitively funded investigators in nutrition and obesity-related research areas. Since the last renewal, the UCLA Center for Human Nutrition has grown considerably with the funding in 1999 of the UCLA P50 Center for Dietary Supplements Research:Botanicals (CDSRB), and the NCI -funded P30 Clinical Nutrition Research (CNRU) which was competitively renewed for five years in 2002. All of these programs are housed in the Center for Human Nutrition which also is the site of successful clinical programs integrated into the research training of both basic and clinical scientists including the University Obesity Center, the Surgical Obesity Program, the Primary Care Network, and Community Outreach Programs in the Venice Family Clinic and Martin Luther King Medical Center. The Administrative Unit of the Center will administer the training program and foster the growth of the trainees. The training program will be directed by a Steering Committee including Principal Training Faculty from six broad areas: 1 ) The Genetics of Obesity; 2) Adipocyte and Lipid Metabolism; 3) Neuroregulation and Satiety; 4) Eating Disorders and Behavioral Medicine; 5) Clinical Research and Biostatistics; and 6) Minority and International Nutrition Research. The UCLA Center for Human Nutrition including the Nutrition Research Laboratories and the Scientific Core Laboratories of the CNRU and the CDSRB will provide laboratory resources and faculty expertise. Trainees in basic and clinical sciences training side by side will be prepared for the research agenda mandated by the growing epidemic of obesity through the acquisition of skills in molecular biology, genetics and neurosciences while critically understanding their translation to the clinical and public health challenges of the epidemic of obesity. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: VALIDATION OF HMGI-C AS A DRUG TARGET IN OBESITY Principal Investigator & Institution: Chouinard, Roland A.; Hmgene, Inc. 1308 Centennial Ave, #140 Piscataway, NJ 08854 Timing: Fiscal Year 2001; Project Start 15-AUG-1999; Project End 31-JUL-2003
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Summary: The unique, novel approach of HMGene to obesity treatment is to develop drugs that act directly on adipose tissue. The goal of Phase II will be to further validate HMGI-C, an architectural transcription factor which regulates gene expression in adipogenesis, as a drug target in obesity. In Phase I, it was shown that inactivation of HMGI-C reverses the obesity induced by leptin deficiency. Phase II will extend those studies to show that the same holds true for diet induced obesity which is a more physiological model and more closely parallels the human disease. As HMGI-C is a transcriptional regulator and sits at the apex of a genomic cascade, DNA microarray and RNA differential display technology will be used to identify genes in the HMGI-C genomic pathway which will provide novel drug targets. Finally, as the ultimate goal is to develop a safe, effective therapeutic for the treatment of obesity, both biochemical and cellular based assays will be developed in order to screen for small molecule inhibitors of HMGI-C which may be useful in the treatment of obesity. PROPOSED COMMERCIAL APPLICATIONS: Successful completion of this project would open up new prospects of the discovery of effective, clinically valuable anti-obesity drugs, which would have an enormous commercial potential. It is estimated that the U.S. mark for a prescription anti-obesity drug is approximately $ 1 billion in annual sales. For an overthe-counter drug, potential market is believed to be $10 billion. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: VISCREAL ADIPOSITY: GENETIC AND ENVIRONMENTAL INFLUENCES Principal Investigator & Institution: Demerath, Ellen W.; Assistant Professor; Community Health; Wright State University Colonel Glenn Hwy Dayton, OH 45435 Timing: Fiscal Year 2003; Project Start 20-SEP-2003; Project End 31-JUL-2008 Summary: (provided by applicant): The goal of the proposed study is to understand the genetic architecture underlying visceral obesity and its associated physiological components. Accumulation of fat deep within the abdomen (i.e., visceral adipose tissue) is known to play a pivotal role in the development of non-insulin dependent diabetes mellitus and cardiovascular disease (CVD). In our proposed study, we aim to disentangle the genetic and environmental factors that explain human variation in visceral adiposity by viewing it as a component of a phenotypic complex that also includes insulin resistance, vascular inflammation, and hormonal variations (the "visceral obesity complex"). The proposed study is built upon an existing study of 1,000 individuals in five large multi-generational kindreds, in which whole-genome genotyping and disease risk factor phenotyping are already underway. The proposed study has three specific aims. In Specific Aim 1 we will phenotype the study population using MRI and dual energy x-ray absorptiometry to measure the amount and distribution of visceral and subcutaneous adipose tissue, using ELISA to assay concentration of adipocyte-derived hormones, and using a repeated 24-hour dietary recall protocol to characterize current energy and macronutrient intake. In Specific Aim 2 we will use variance components-based quantitative genetic methods for extended pedigrees to estimate the heritability of the independent components of the visceral obesity complex, identify key environmental variables and covariates (i.e., sex, age, diet, physical activity, hormone usage, smoking and alcohol consumption) that influence the visceral obesity complex alone or in interaction with genetic factors, and examine the extent to which common genetic factors underlie this complex of closely related traits. In Specific Aim 3, we will use variance components-based linkage methods to identify quantitative trait loci (QTL) harboring genes that influence variation in constituent components of the visceral obesity complex. We also will examine gene-by-
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environment, gene-by-sex, and gene-by-age interactions in these traits. Fine mapping procedures will be used further localize QTL that are identified. At the conclusion of the proposed study, we will have identified particular genetic loci that influence the visceral obesity complex, and will better understand how particular genotypes may, when confronted with particular environments, predispose individuals to the accumulation of visceral adipose tissue, thereby putting them at increased future risk for developing diabetes and CVD. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen •
Project Title: WEIGHT GAIN IN AFRICAN-AMERICAN GIRLS Principal Investigator & Institution: Rochon, James; Research Professor; Statistics; George Washington University 2121 I St Nw Washington, DC 20052 Timing: Fiscal Year 2001; Project Start 01-AUG-1999; Project End 31-MAY-2002 Summary: According to NHANES data, the prevalence of obesity in the U.S. population has increased from 25 percent to 33 percent over the past 10 years. Obesity is well accepted as a risk factor for coronary heart disease and type 2 diabetes, and it exacerbates many chronic conditions such as hypertension and dyslipidemia. Not surprisingly, the economic costs of obesity are staggering and amount to approximately 100 billion dollars annually. The prevalence of obesity appears to be proportionately greater in certain minority populations. Almost twice as many African-American women are overweight compared to Caucasians. Moreover, the disproportionate levels of obesity in African-American women may have their origins in childhood and adolescence. Approximately 30 percent of African-American girls between the ages of 6 and 17 years are overweight, compared to only 22 percent for all other youth as a whole. Large prevention trials, most notably, the Child and Adolescent Trial for Cardiovascular Health (CATCH) and the Dietary Intervention Study in Children (DISC), have been largely unsuccessful in producing reductions in dietary fat, body weight or BMI. Thus, the NHLBI has proposed a research program to develop and test interventions to prevent weight gain in preadolescent African-American girls. The Biostatistics Center of the George Washington University proposes to serve as the Coordinating Center for this project. In this role, we will attend to the following functions. (1) Study Coordination and Planning: We will help establish an efficient organizational structure to ensure that all activities advance in a coordinated fashion. (2) Data Management Activities: We will apply our Distributed Data Entry system for on-going data collection and generate periodic reports summarizing the execution of the trial. (3) Statistical Analysis: We will provide statistical leadership in the design of the study, and perform interim and final analyses in an expeditious and timely manner. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
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Project Title: WISE MIND: ENVIRONMENTAL APPROACH FOR OBESITY PREVENTION Principal Investigator & Institution: Williamson, Donald A.; Professor; None; Lsu Pennington Biomedical Research Ctr 6400 Perkins Rd Baton Rouge, LA 70808 Timing: Fiscal Year 2002; Project Start 30-SEP-2002; Project End 31-JUL-2005 Summary: (provided by applicant): In this pilot study, we propose a two-arm primary prevention trial to test the efficacy of an environmental approach for the prevention of obesity in children who are in the second through sixth grades. An attention-placebo control group will receive an environmental approach for the prevention of alcohol drug tobacco use and abuse. This test of an environmental approach targets a school system
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for change. Four schools with a total of approximately 1,040 students will be the participants in the study. The four schools will be randomly assigned to one of the two treatment arms. The prevention study will be conducted across two consecutive academic years. The primary endpoint will be body mass index. The primary aim of the study is to test the efficacy of the obesity program for the prevention of weight gain in children. Changes in dietary intake and physical activity will be tested as mediators of changes in body mass index. Also, age of the child, initial body mass index, and gender will be tested as factors that are associated with differential outcomes related to the prevention of weight gain. Secondary endpoints include: body composition, waist circumference, physical activity, dietary intake, body image, mood, and self-esteem. The environmental program for the prevention of obesity will have multiple components that are designed to alter automatic/habitual decision making by students. The results of this pilot study will guide the development of full-scale investigations in a larger set of schools. The findings of the study will have significant impact upon public health policy regarding prevention of obesity. Several innovations are utilized in the study, including novel applications of the internet to provide environmental prompts to parents and families, and the use of a new method, called digital photography of foods, for measurement of the food selections and food intake of individual students, in school cafeterias. Website: http://crisp.cit.nih.gov/crisp/Crisp_Query.Generate_Screen
E-Journals: PubMed Central3 PubMed Central (PMC) is a digital archive of life sciences journal literature developed and managed by the National Center for Biotechnology Information (NCBI) at the U.S. National Library of Medicine (NLM).4 Access to this growing archive of e-journals is free and unrestricted.5 To search, go to http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=Pmc, and type “obesity” (or synonyms) into the search box. This search gives you access to fulltext articles. The following is a sample of items found for obesity in the PubMed Central database: •
11[beta]-Hydroxysteroid dehydrogenase type 1 knockout mice show attenuated glucocorticoid-inducible responses and resist hyperglycemia on obesity or stress. by Kotelevtsev Y, Holmes MC, Burchell A, Houston PM, Schmoll D, Jamieson P, Best R, Brown R, Edwards CR, Seckl JR, Mullins JJ. 1997 Dec 23; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=25139
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A metabolic defect promotes obesity in mice lacking melanocortin-4 receptors. by Ste. Marie L, Miura GI, Marsh DJ, Yagaloff K, Palmiter RD. 2000 Oct 24; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=17343
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A new class of obesity genes encodes leukocyte adhesion receptors. by Dong ZM, Gutierrez-Ramos JC, Coxon A, Mayadas TN, Wagner DD. 1997 Jul 8; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=23855
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Adapted from the National Library of Medicine: http://www.pubmedcentral.nih.gov/about/intro.html.
With PubMed Central, NCBI is taking the lead in preservation and maintenance of open access to electronic literature, just as NLM has done for decades with printed biomedical literature. PubMed Central aims to become a world-class library of the digital age. 5 The value of PubMed Central, in addition to its role as an archive, lies in the availability of data from diverse sources stored in a common format in a single repository. Many journals already have online publishing operations, and there is a growing tendency to publish material online only, to the exclusion of print.
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Abnormal regulation of the leptin gene in the pathogenesis of obesity. by Ioffe E, Moon B, Connolly E, Friedman JM. 1998 Sep 29; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=21729
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Adrenalectomy stimulates hypothalamic proopiomelanocortin expression but does not correct diet-induced obesity. by Makimura H, Mizuno TM, Beasley J, Silverstein JH, Mobbs CV. 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=165436
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Alteration of the Leptin Network in Late Morbid Obesity Induced in Mice by Brain Infection with Canine Distemper Virus. by Bernard A, Cohen R, Khuth ST, Vedrine B, Verlaeten O, Akaoka H, Giraudon P, Belin MF. 1999 Sep; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=104257
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An agouti mutation lacking the basic domain induces yellow pigmentation but not obesity in transgenic mice. by Miltenberger RJ, Mynatt RL, Bruce BD, Wilkison WO, Woychik RP, Michaud EJ. 1999 Jul 20; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=17559
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Aromatase-deficient (ArKO) mice have a phenotype of increased adiposity. by Jones ME, Thorburn AW, Britt KL, Hewitt KN, Wreford NG, Proietto J, Oz OK, Leury BJ, Robertson KM, Yao S, Simpson ER. 2000 Nov 7; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=18833
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Association between postnatal catch-up growth and obesity in childhood: prospective cohort study. by Ong KK, Ahmed ML, Emmett PM, Preece MA, Dunger DB. 2000 Apr 8; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=27335
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Beneficial effects of leptin on obesity, T cell hyporesponsiveness, and neuroendocrine/metabolic dysfunction of human congenital leptin deficiency. by Farooqi IS, Matarese G, Lord GM, Keogh JM, Lawrence E, Agwu C, Sanna V, Jebb SA, Perna F, Fontana S, Lechler RI, DePaoli AM, O'Rahilly S. 2002 Oct 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=150795
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Breast feeding and obesity: cross sectional study. by von Kries R, Koletzko B, Sauerwald T, von Mutius E, Barnert D, Grunert V, von Voss H. 1999 Jul 17; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=28161
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Breast is best for avoiding obesity. by Kerr C. 2002 Aug 6; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=117486
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C75 increases peripheral energy utilization and fatty acid oxidation in diet-induced obesity. by Thupari JN, Landree LE, Ronnett GV, Kuhajda FP. 2002 Jul 9; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=123169
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Central overweight and obesity in British youth aged 11-16 years: cross sectional surveys of waist circumference. by McCarthy HD, Ellis SM, Cole TJ. 2003 Mar 22; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=151972
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Ciliary neurotrophic factor activates leptin-like pathways and reduces body fat, without cachexia or rebound weight gain, even in leptin-resistant obesity. by Lambert PD, Anderson KD, Sleeman MW, Wong V, Tan J, Hijarunguru A, Corcoran TL, Murray JD, Thabet KE, Yancopoulos GD, Wiegand SJ. 2001 Apr 10; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=31889
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Ciliary neurotrophic factor corrects obesity and diabetes associated with leptin deficiency and resistance. by Gloaguen I, Costa P, Demartis A, Lazzaro D, Di Marco A, Graziani R, Paonessa G, Chen F, Rosenblum CI, Van der Ploeg LH, Cortese R, Ciliberto G, Laufer R. 1997 Jun 10; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=21071
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Combined effects of insulin treatment and adipose tissue-specific agouti expression on the development of obesity. by Mynatt RL, Miltenberger RJ, Klebig ML, Zemel MB, Wilkinson JE, Wilkison WO, Woychik RP. 1997 Feb 4; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=19614
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Correction of obesity and diabetes in genetically obese mice by leptin gene therapy. by Muzzin P, Eisensmith RC, Copeland KC, Woo SL. 1996 Dec 10; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=26217
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Corticotropin-releasing factor-binding protein ligand inhibitor blunts excessive weight gain in genetically obese Zucker rats and rats during nicotine withdrawal. by Heinrichs SC, Lapsansky J, Behan DP, Chan RK, Sawchenko PE, Lorang M, Ling N, Vale WW, De Souza EB. 1996 Dec 24; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=26429
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Decreased Food Intake does not Completely Account for Adiposity Reduction after ob Protein Infusion. by Levin N, Nelson C, Gurney A, Vandlen R, Sauvage FD. 1996 Feb 20; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=40010
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Diet-induced changes in uncoupling proteins in obesity-prone and obesity-resistant strains of mice. by Surwit RS, Wang S, Petro AE, Sanchis D, Raimbault S, Ricquier D, Collins S. 1998 Mar 31; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=19963
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Differential effects of a centrally acting fatty acid synthase inhibitor in lean and obese mice. by Kumar MV, Shimokawa T, Nagy TR, Lane MD. 2002 Feb 19; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=122295
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Do Plants Have a One-Way Ticket to Genomic Obesity? by Bennetzen JL, Kellogg EA. 1997 Sep; http://www.pubmedcentral.gov/picrender.fcgi?tool=pmcentrez&action=stream&blobt ype=pdf&artid=157029
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Ectopic Expression of the Agouti Gene in Transgenic Mice Causes Obesity, Features of Type II Diabetes, and Yellow Fur. by Klebig ML, Wilkinson JE, Geisler JG, Woychik RP. 1995 May 23; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=41780
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Effects of Greek orthodox christian church fasting on serum lipids and obesity. by Sarri KO, Tzanakis NE, Linardakis MK, Mamalakis GD, Kafatos AG. 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=156653
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Effects of peroxisome proliferator-activated receptor [delta] on placentation, adiposity, and colorectal cancer. by Barak Y, Liao D, He W, Ong ES, Nelson MC, Olefsky JM, Boland R, Evans RM. 2002 Jan 8; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=117556
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Establishing a standard definition for child overweight and obesity worldwide: international survey. by Cole TJ, Bellizzi MC, Flegal KM, Dietz WH. 2000 May 6; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=27365
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Evaluation of implementation and effect of primary school based intervention to reduce risk factors for obesity. by Sahota P, Rudolf MC, Dixey R, Hill AJ, Barth JH, Cade J. 2001 Nov 3; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=59380
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Evaluation of indices of obesity in men: descriptive study. by Pounder D, Carson D, Davison M, Orihara Y. 1998 May 9; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=28542
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Fatty acid-induced [beta] cell apoptosis: A link between obesity and diabetes. by Shimabukuro M, Zhou YT, Levi M, Unger RH. 1998 Mar 3; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=19389
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High penetrance, overweight, and glucocorticoid receptor variant: case-control study. by Lin RC, Wang WY, Morris BJ. 1999 Nov 20; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=28280
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Hormone replacement therapy use dramatically increases breast oestrogen receptor expression in obese postmenopausal women. by Lawson JS, Field AS, Tran DD, Houssami N. 2001; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=57804
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Hypothalamic growth hormone secretagogue receptor regulates growth hormone secretion, feeding, and adiposity. by Shuto Y, Shibasaki T, Otagiri A, Kuriyama H, Ohata H, Tamura H, Kamegai J, Sugihara H, Oikawa S, Wakabayashi I. 2002 Jun 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=150991
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Identification of the Promoter of the Mouse Obese Gene. by Brousse FC, Shan B, Chen J. 1996 Apr 30; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=39493
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Immediate and long term effects of weight reduction in obese people with asthma: randomised controlled study. by Stenius-Aarniala B, Poussa T, Kvarnstrom J, Gronlund EL, Ylikahri M, Mustajoki P. 2000 Mar 25; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=27319
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Impact of obesity on glucose and lipid profiles in adolescents at different age groups in relation to adulthood. by Plourde G. 2002; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=134463
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Implications of childhood obesity for adult health: findings from thousand families cohort study. by Wright CM, Parker L, Lamont D, Craft AW. 2001 Dec 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=60301
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Increased Energy Expenditure, Decreased Adiposity, and Tissue-Specific Insulin Sensitivity in Protein-Tyrosine Phosphatase 1B-Deficient Mice. by Klaman LD, Boss O, Peroni OD, Kim JK, Martino JL, Zabolotny JM, Moghal N, Lubkin M, Kim YB, Sharpe AH, Stricker-Krongrad A, Shulman GI, Neel BG, Kahn BB. 2000 Aug 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=85999
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Increasing prevalence of obesity in primary school children: cohort study. by Rudolf MC, Sahota P, Barth JH, Walker J. 2001 May 5; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=31260
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Insulin depletion leads to adipose-specific cell death in obese but not lean mice. by Loftus TM, Kuhajda FP, Lane MD. 1998 Nov 24; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=24345
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Lipotoxic heart disease in obese rats: Implications for human obesity. by Zhou YT, Grayburn P, Karim A, Shimabukuro M, Higa M, Baetens D, Orci L, Unger RH. 2000 Feb 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=26513
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Long-term correction of obesity and diabetes in genetically obese mice by a single intramuscular injection of recombinant adeno-associated virus encoding mouse leptin. by Murphy JE, Zhou S, Giese K, Williams LT, Escobedo JA, Dwarki VJ. 1997 Dec 9; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=28408
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Loss of stearoyl --CoA desaturase-1 function protects mice against adiposity. by Ntambi JM, Miyazaki M, Stoehr JP, Lan H, Kendziorski CM, Yandell BS, Song Y, Cohen P, Friedman JM, Attie AD. 2002 Aug 20; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=123282
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Major histocompatibility complex class I-restricted T cells are required for all but the end stages of diabetes development in nonobese diabetic mice and use a prevalent T cell receptor [alpha] chain gene rearrangement. by DiLorenzo TP, Graser RT, Ono T, Christianson GJ, Chapman HD, Roopenian DC, Nathenson SG, Serreze DV. 1998 Oct 13; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=22866
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Mice Lacking Paternally Expressed Pref-1/Dlk1 Display Growth Retardation and Accelerated Adiposity. by Moon YS, Smas CM, Lee K, Villena JA, Kim KH, Yun EJ, Sul HS. 2002 Aug; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=133956
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Muscle-specific PPAR[gamma]-deficient mice develop increased adiposity and insulin resistance but respond to thiazolidinediones. by Norris AW, Chen L, Fisher SJ, Szanto I, Ristow M, Jozsi AC, Hirshman MF, Rosen ED, Goodyear LJ, Gonzalez FJ, Spiegelman BM, Kahn CR. 2003 Aug 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=171387
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Mutations in the small heterodimer partner gene are associated with mild obesity in Japanese subjects. by Nishigori H, Tomura H, Tonooka N, Kanamori M, Yamada S, Sho K, Inoue I, Kikuchi N, Onigata K, Kojima I, Kohama T, Yamagata K, Yang Q, Matsuzawa Y, Miki T, Seino S, Kim MY, Choi HS, Lee YK, Moore DD, Takeda J. 2001 Jan 16; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=14629
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Obese gene expression at in vivo levels by fat pads derived from s.c. implanted 3T3F442A preadipocytes. by Mandrup S, Loftus TM, MacDougald OA, Kuhajda FP, Lane MD. 1997 Apr 29; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=20717
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Obese Gene Expression: Reduction by Fasting and Stimulation by Insulin and Glucose in Lean Mice, and Persistent Elevation in Acquired (Diet-Induced) and
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Genetic (Yellow Agouti) Obesity. by Mizuno TM, Bergen H, Funabashi T, Kleopoulos SP, Zhong Y, Bauman WA, Mobbs CV. 1996 Apr 16; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=39626 •
Obesity a heavy burden in Nova Scotia. by Moulton D. 2000 Nov 28; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=80435
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Obesity and hyperleptinemia in metallothionein (-I and -II) null mice. by Beattie JH, Wood AM, Newman AM, Bremner I, Choo KH, Michalska AE, Duncan JS, Trayhurn P. 1998 Jan 6; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=18223
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Obesity and mild hyperinsulinemia found in neuropeptide Y-Y1 receptor-deficient mice. by Kushi A, Sasai H, Koizumi H, Takeda N, Yokoyama M, Nakamura M. 1998 Dec 22; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=28100
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Obesity drug sibutramine (Meridia): hypertension and cardiac arrhythmias. by Wooltorton E. 2002 May 14; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=111085
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Obesity in Canadian children. by Auer R, Lau D, Reimer R. 2001 May 29; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=81101
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Obesity in Canadian children. by Katzmarzyk PT. 2001 May 29; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=81103
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Obesity in Canadian children. by Finkelstein M. 2001 May 29; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=81102
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Obesity in Canadian children. by Andersen R. 2001 May 29; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=81105
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Obesity in Canadian children. by Tremblay M, Willms JD. 2001 May 29; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=81104
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Obesity increases sensitivity to endotoxin liver injury: Implications for the pathogenesis of steatohepatitis. by Yang SQ, Lin HZ, Lane MD, Clemens M, Diehl AM. 1997 Mar 18; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=20127
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Obesity may soon be leading cause of preventable death in US. by Sibbald B. 2002 Mar 5; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=99423
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Obesity resistance and enhanced glucose metabolismin mice transplanted with white adipose tissue lackingacyl CoA:diacylglycerol acyltransferase 1. by Chen HC, Jensen DR, Myers HM, Eckel RH, Farese RV Jr. 2003 Jun 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=156099
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Overweight and obesity in relation to cardiovascular disease risk factors among medical students in Crete, Greece. by Bertsias G, Mammas I, Linardakis M, Kafatos A. 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=140012
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Paradoxical resistance to diet-induced obesity in UCP1-deficient mice. by Liu X, Rossmeisl M, McClaine J, Kozak LP. 2003 Feb 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=151850
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Perilipin ablation results in a lean mouse with aberrant adipocyte lipolysis, enhanced leptin production, and resistance to diet-induced obesity. by Tansey JT, Sztalryd C, Gruia-Gray J, Roush DL, Zee JV, Gavrilova O, Reitman ML, Deng CX, Li C, Kimmel AR, Londos C. 2001 May 22; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=33496
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Physiological response to long-term peripheral and central leptin infusion in lean and obese mice. by Halaas JL, Boozer C, Blair-West J, Fidahusein N, Denton DA, Friedman JM. 1997 Aug 5; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=23177
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Plasma interleukin 8 concentrations in obese subjects with impaired glucose tolerance.. by Straczkowski M, Kowalska I, Nikolajuk A, Dzienis-Straczkowska S, Szelachowska M, Kinalska I. 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=162167
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Prevalence and trends in overweight and obesity in three cross sectional studies of British children, 1974-94. by Chinn S, Rona RJ. 2001 Jan 6; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=26603
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Prevalence of attention deficit/hyperactivity disorder among adults in obesity treatment. by Altfas JR. 2002; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=130024
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Prevalence of overweight and obese children between 1989 and 1998: population based series of cross sectional studies. by Bundred P, Kitchiner D, Buchan I. 2001 Feb 10; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=26573
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Prevalence of overweight and obesity in British children: cohort study. by Reilly JJ, Dorosty AR, Emmett PM. 1999 Oct 16; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=32263
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Randomised controlled trial of primary school based intervention to reduce risk factors for obesity. by Sahota P, Rudolf MC, Dixey R, Hill AJ, Barth JH, Cade J. 2001 Nov 3; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=59381
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Rat Obesity Gene Fatty (fa) Maps to Chromosome 5: Evidence for Homology with the Mouse Gene Diabetes (db). by Truett GE, Bahary N, Friedman JM, Leibel RL. 1991 Sep 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=52392
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Regulated Expression of the Obese Gene Product (Leptin) in White Adipose Tissue and 3T3-L1 Adipocytes. by MacDougald OA, Hwang C, Fan H, Lane MD. 1995 Sep 26; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=abstr act&artid=40918
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Relation between obesity from childhood to adulthood and the metabolic syndrome: population based study. by Vanhala M, Vanhala P, Kumpusalo E, Halonen P, Takala J. 1998 Aug 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=28624
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Reversing adipocyte differentiation: Implications for treatment of obesity. by Zhou YT, Wang ZW, Higa M, Newgard CB, Unger RH. 1999 Mar 2; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=26794
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Targeted Deletion of the tub Mouse Obesity Gene Reveals that tubby Is a Loss-ofFunction Mutation. by Stubdal H, Lynch CA, Moriarty A, Fang Q, Chickering T, Deeds JD, Fairchild-Huntress V, Charlat O, Dunmore JH, Kleyn P, Huszar D, Kapeller R. 2000 Feb 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=85204
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Targeted disruption of H3 receptors results in changes in brain histamine tone leading to an obese phenotype. by Takahashi K, Suwa H, Ishikawa T, Kotani H. 2002 Dec 15; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=151650
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Targeted disruption of hormone-sensitive lipase results in male sterility and adipocyte hypertrophy, but not in obesity. by Osuga JI, Ishibashi S, Oka T, Yagyu H, Tozawa R, Fujimoto A, Shionoiri F, Yahagi N, Kraemer FB, Tsutsumi O, Yamada N. 2000 Jan 18; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=15409
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The Canadian obesity epidemic, 1985 --1998. by Katzmarzyk PT. 2002 Apr 16; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=100878
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The emerging science of body weight regulation and its impact on obesity treatment. by Korner J, Aronne LJ. 2003 Mar 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=151906
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The expression of adipogenic genes is decreased in obesity and diabetes mellitus. by Nadler ST, Stoehr JP, Schueler KL, Tanimoto G, Yandell BS, Attie AD. 2000 Oct 10; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=17207
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The G-308A variant of the Tumor Necrosis Factor-[alpha] (TNF-[alpha]) gene is not associated with obesity, insulin resistance and body fat distribution. by Romeo S, Sentinelli F, Capici F, Arca M, Berni A, Vecci E, Mario UD, Baroni MG. 2001; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=56593
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The relation of menarcheal age to obesity in childhood and adulthood: the Bogalusa heart study. by Freedman DS, Khan LK, Serdula MK, Dietz WH, Srinivasan SR, Berenson GS. 2003; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=156622
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The search for new ways to treat obesity. by Hirsch J. 2002 Jul 9; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=123098
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The spread of the childhood obesity epidemic. by Andersen RE. 2000 Nov 28; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&rendertype=exter nal&artid=80413
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Tissue factor gene expression in the adipose tissues of obese mice. by Samad F, Pandey M, Loskutoff DJ. 1998 Jun 23; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=22693
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Troglitazone prevents mitochondrial alterations, [beta] cell destruction, and diabetes in obese prediabetic rats. by Higa M, Zhou YT, Ravazzola M, Baetens D, Orci L, Unger RH. 1999 Sep 28; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=18065
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Tsp509I polymorphism in exon 2 of the glucocorticoid receptor gene in relation to obesity and cortisol secretion: cohort study. by Rosmond R, Bouchard C, Bjorntorp P. 2001 Mar 17; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=26546
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Tumor necrosis factor [alpha] is a key component in the obesity-linked elevation of plasminogen activator inhibitor 1. by Samad F, Uysal KT, Wiesbrock SM, Pandey M, Hotamisligil GS, Loskutoff DJ. 1999 Jun 8; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=22014
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Tumor necrosis factor [alpha] mediates apoptosis of brown adipocytes and defective brown adipocyte function in obesity. by Nisoli E, Briscini L, Giordano A, Tonello C, Wiesbrock SM, Uysal KT, Cinti S, Carruba MO, Hotamisligil GS. 2000 Jul 5; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=16665
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Yeast Vps55p, a Functional Homolog of Human Obesity Receptor Gene-related Protein, Is Involved in Late Endosome to Vacuole Trafficking. by Belgareh-Touze N, Avaro S, Rouille Y, Hoflack B, Haguenauer-Tsapis R. 2002 May 1; http://www.pubmedcentral.gov/articlerender.fcgi?tool=pmcentrez&artid=111137
The National Library of Medicine: PubMed One of the quickest and most comprehensive ways to find academic studies in both English and other languages is to use PubMed, maintained by the National Library of Medicine.6 The advantage of PubMed over previously mentioned sources is that it covers a greater number of domestic and foreign references. It is also free to use. If the publisher has a Web site that offers full text of its journals, PubMed will provide links to that site, as well as to sites offering other related data. User registration, a subscription fee, or some other type of fee may be required to access the full text of articles in some journals. To generate your own bibliography of studies dealing with obesity, simply go to the PubMed Web site at http://www.ncbi.nlm.nih.gov/pubmed. Type “obesity” (or synonyms) into the search box, and click “Go.” The following is the type of output you can expect from PubMed for obesity (hyperlinks lead to article summaries): •
A case-control study of the association of diet and obesity with gout in Taiwan. Author(s): Lyu LC, Hsu CY, Yeh CY, Lee MS, Huang SH, Chen CL. Source: The American Journal of Clinical Nutrition. 2003 October; 78(4): 690-701. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14522726&dopt=Abstract
PubMed was developed by the National Center for Biotechnology Information (NCBI) at the National Library of Medicine (NLM) at the National Institutes of Health (NIH). The PubMed database was developed in conjunction with publishers of biomedical literature as a search tool for accessing literature citations and linking to full-text journal articles at Web sites of participating publishers. Publishers that participate in PubMed supply NLM with their citations electronically prior to or at the time of publication.
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A clinical view of the obesity problem. Author(s): Pi-Sunyer X. Source: Science. 2003 February 7; 299(5608): 859-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12574620&dopt=Abstract
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A comparison of diet and exercise therapy versus laparoscopic Roux-en-Y gastric bypass surgery for morbid obesity: a decision analysis model. Author(s): Patterson EJ, Urbach DR, Swanstrom LL. Source: Journal of the American College of Surgeons. 2003 March; 196(3): 379-84. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12648689&dopt=Abstract
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A cost-analysis of adopting a healthful diet in a family-based obesity treatment program. Author(s): Raynor HA, Kilanowski CK, Esterlis I, Epstein LH. Source: Journal of the American Dietetic Association. 2002 May; 102(5): 645-56. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12008989&dopt=Abstract
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A cross-cultural analysis of 'motivation for eating' as a potential factor in the emergence of global obesity: Japan and the United States. Author(s): Hawks SR, Madanat HN, Merrill RM, Goudy MB, Miyagawa T. Source: Health Promotion International. 2003 June; 18(2): 153-62. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12746387&dopt=Abstract
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A dietary and behavioural programme for the treatment of obesity. A 4-year clinical trial and a long-term posttreatment follow-up. Author(s): Lantz H, Peltonen M, Agren L, Torgerson JS. Source: Journal of Internal Medicine. 2003 September; 254(3): 272-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12930237&dopt=Abstract
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A functional variant in the peroxisome proliferator-activated receptor gamma2 promoter is associated with predictors of obesity and type 2 diabetes in Pima Indians. Author(s): Muller YL, Bogardus C, Beamer BA, Shuldiner AR, Baier LJ. Source: Diabetes. 2003 July; 52(7): 1864-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12829658&dopt=Abstract
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A lifecourse study of risk for hyperinsulinaemia, dyslipidaemia and obesity (the central metabolic syndrome) at age 49-51 years. Author(s): Parker L, Lamont DW, Unwin N, Pearce MS, Bennett SM, Dickinson HO, White M, Mathers JC, Alberti KG, Craft AW. Source: Diabetic Medicine : a Journal of the British Diabetic Association. 2003 May; 20(5): 406-15. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12752491&dopt=Abstract
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A longitudinal evaluation of adolescent depression and adult obesity. Author(s): Richardson LP, Davis R, Poulton R, McCauley E, Moffitt TE, Caspi A, Connell F. Source: Archives of Pediatrics & Adolescent Medicine. 2003 August; 157(8): 739-45. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12912778&dopt=Abstract
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A low-carbohydrate as compared with a low-fat diet in severe obesity. Author(s): Samaha FF, Iqbal N, Seshadri P, Chicano KL, Daily DA, McGrory J, Williams T, Williams M, Gracely EJ, Stern L. Source: The New England Journal of Medicine. 2003 May 22; 348(21): 2074-81. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12761364&dopt=Abstract
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A meta-analysis of obesity and the risk of pancreatic cancer. Author(s): Berrington de Gonzalez A, Sweetland S, Spencer E. Source: British Journal of Cancer. 2003 August 4; 89(3): 519-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12888824&dopt=Abstract
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A new treatment for morbid obesity. Author(s): Offutt MR. Source: The Nurse Practitioner. 2003 August; 28(8): 54-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12902942&dopt=Abstract
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A perspective on obesity. Author(s): Johnson RW, Broadnax PA. Source: The Abnf Journal : Official Journal of the Association of Black Nursing Faculty in Higher Education, Inc. 2003 May-June; 14(3): 69-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12856445&dopt=Abstract
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A primer on early childhood obesity and parental influence. Author(s): Hodges EA. Source: Pediatric Nursing. 2003 January-February; 29(1): 13-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12630500&dopt=Abstract
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A programme of behaviour modification and nutrition counselling in the treatment of obesity: a randomised 2-y clinical trial. Author(s): Melin I, Karlstrom B, Lappalainen R, Berglund L, Mohsen R, Vessby B. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 September; 27(9): 1127-35. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12917721&dopt=Abstract
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A qualitative study of general practitioners' and practice nurses' attitudes to obesity management in primary care. Author(s): Mercer SW, Tessier S. Source: Health Bull (Edinb). 2001 July; 59(4): 248-53. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12664735&dopt=Abstract
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A randomized trial of a low-carbohydrate diet for obesity. Author(s): Foster GD, Wyatt HR, Hill JO, McGuckin BG, Brill C, Mohammed BS, Szapary PO, Rader DJ, Edman JS, Klein S. Source: The New England Journal of Medicine. 2003 May 22; 348(21): 2082-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12761365&dopt=Abstract
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A reduced-glycemic load diet in the treatment of adolescent obesity. Author(s): Ebbeling CB, Leidig MM, Sinclair KB, Hangen JP, Ludwig DS. Source: Archives of Pediatrics & Adolescent Medicine. 2003 August; 157(8): 773-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12912783&dopt=Abstract
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A war on obesity, not the obese. Author(s): Friedman JM. Source: Science. 2003 February 7; 299(5608): 856-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12574619&dopt=Abstract
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Abdominal obesity and risk of ischemic stroke: the Northern Manhattan Stroke Study. Author(s): Suk SH, Sacco RL, Boden-Albala B, Cheun JF, Pittman JG, Elkind MS, Paik MC; Northern Manhattan Stroke Study. Source: Stroke; a Journal of Cerebral Circulation. 2003 July; 34(7): 1586-92. Epub 2003 May 29. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12775882&dopt=Abstract
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Acupuncture for the treatment of obesity: a review of the evidence. Author(s): Lacey JM, Tershakovec AM, Foster GD. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 April; 27(4): 419-27. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12664074&dopt=Abstract
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Additional insight on childhood obesity article. Author(s): Landry D. Source: Pediatric Nursing. 2003 May-June; 29(3): 253. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12837005&dopt=Abstract
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Adiponectin expression from human adipose tissue: relation to obesity, insulin resistance, and tumor necrosis factor-alpha expression. Author(s): Kern PA, Di Gregorio GB, Lu T, Rassouli N, Ranganathan G. Source: Diabetes. 2003 July; 52(7): 1779-85. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12829646&dopt=Abstract
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Adipose tissue is a major source of interleukin-1 receptor antagonist: upregulation in obesity and inflammation. Author(s): Juge-Aubry CE, Somm E, Giusti V, Pernin A, Chicheportiche R, Verdumo C, Rohner-Jeanrenaud F, Burger D, Dayer JM, Meier CA. Source: Diabetes. 2003 May; 52(5): 1104-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12716739&dopt=Abstract
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Adolescent obesity, overt and relational peer victimization, and romantic relationships. Author(s): Pearce MJ, Boergers J, Prinstein MJ. Source: Obesity Research. 2002 May; 10(5): 386-93. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12006638&dopt=Abstract
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All obesity is not created equal. Author(s): Rosch PJ. Source: Science. 2003 September 5; 301(5638): 1325. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12958343&dopt=Abstract
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An after-school obesity prevention program for African-American girls: the Minnesota GEMS pilot study. Author(s): Story M, Sherwood NE, Himes JH, Davis M, Jacobs DR Jr, Cartwright Y, Smyth M, Rochon J. Source: Ethn Dis. 2003 Winter; 13(1 Suppl 1): S54-64. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12713211&dopt=Abstract
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An association between body mass index and markers of inflammation: is obesity the proinflammatory state in patients on peritoneal dialysis? Author(s): Stompor T, Sulowicz W, Dembinska-Kiec A, Janda K, Wojcik K, Zdzienicka A. Source: Perit Dial Int. 2003 January-February; 23(1): 79-83. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12691512&dopt=Abstract
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An obesity clinic model. Author(s): Munnelly P, Feehan S. Source: The Proceedings of the Nutrition Society. 2002 February; 61(1): 9-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12002800&dopt=Abstract
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Are physicians equipped to address the obesity epidemic? Knowledge and attitudes of internal medicine residents. Author(s): Block JP, DeSalvo KB, Fisher WP. Source: Preventive Medicine. 2003 June; 36(6): 669-75. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12744909&dopt=Abstract
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Are there long term protective effects of breast feeding against later obesity? Author(s): Koletzko B, von Kries R. Source: Nutr Health. 2001; 15(3-4): 225-36. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12003089&dopt=Abstract
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Associates of obesity and weight dissatisfaction among Finnish adolescents. Author(s): Mikkila V, Lahti-Koski M, Pietinen P, Virtanen SM, Rimpela M. Source: Public Health Nutrition. 2003 February; 6(1): 49-56. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12581465&dopt=Abstract
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Association between eating patterns and obesity in a free-living US adult population. Author(s): Ma Y, Bertone ER, Stanek EJ 3rd, Reed GW, Hebert JR, Cohen NL, Merriam PA, Ockene IS. Source: American Journal of Epidemiology. 2003 July 1; 158(1): 85-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12835290&dopt=Abstract
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Association of African genetic admixture with resting metabolic rate and obesity among women. Author(s): Fernandez JR, Shriver MD, Beasley TM, Rafla-Demetrious N, Parra E, Albu J, Nicklas B, Ryan AS, McKeigue PM, Hoggart CL, Weinsier RL, Allison DB. Source: Obesity Research. 2003 July; 11(7): 904-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12855761&dopt=Abstract
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Association of maternal obesity and depressive symptoms with television-viewing time in low-income preschool children. Author(s): Burdette HL, Whitaker RC, Kahn RS, Harvey-Berino J. Source: Archives of Pediatrics & Adolescent Medicine. 2003 September; 157(9): 894-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12963595&dopt=Abstract
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Association of polymorphisms in GPR10, the gene encoding the prolactin-releasing peptide receptor with blood pressure, but not obesity, in a U.K. Caucasian population. Author(s): Bhattacharyya S, Luan J, Challis B, Schmitz C, Clarkson P, Franks PW, Middelberg R, Keogh J, Farooqi IS, Montague C, Brennand J, Wareham NJ, O'Rahilly S. Source: Diabetes. 2003 May; 52(5): 1296-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12716769&dopt=Abstract
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Association of the mitochondrial DNA 15497G/A polymorphism with obesity in a middle-aged and elderly Japanese population. Author(s): Okura T, Koda M, Ando F, Niino N, Tanaka M, Shimokata H. Source: Human Genetics. 2003 October; 113(5): 432-6. Epub 2003 August 02. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12905068&dopt=Abstract
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Association of the TNF-alpha -308 G/A promoter polymorphism with insulin resistance in obesity. Author(s): Dalziel B, Gosby AK, Richman RM, Bryson JM, Caterson ID. Source: Obesity Research. 2002 May; 10(5): 401-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12006640&dopt=Abstract
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Austronesian-speaking people in Papua New Guinea have susceptibility to obesity and type 2 diabetes. Author(s): Sakaue M, Fuke Y, Katsuyama T, Kawabata M, Taniguchi H. Source: Diabetes Care. 2003 March; 26(3): 955-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12610072&dopt=Abstract
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Autonomic dysfunction of the beta-cell and the pathogenesis of obesity. Author(s): Lustig RH. Source: Reviews in Endocrine & Metabolic Disorders. 2003 March; 4(1): 23-32. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12618557&dopt=Abstract
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Bariatric surgery and long-term control of morbid obesity. Author(s): Brolin RE. Source: Jama : the Journal of the American Medical Association. 2002 December 11; 288(22): 2793-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12472304&dopt=Abstract
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Bariatric surgery for morbid obesity. Author(s): Duell PB. Source: Jama : the Journal of the American Medical Association. 2003 April 9; 289(14): 1779; Author Reply 1779. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12684352&dopt=Abstract
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Bariatric surgery for morbid obesity: why, who, when, how, where, and then what? Author(s): Choban PS, Jackson B, Poplawski S, Bistolarides P. Source: Cleve Clin J Med. 2002 November; 69(11): 897-903. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12430975&dopt=Abstract
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Bariatric surgery for severe obesity. Author(s): Sugerman HJ. Source: J Assoc Acad Minor Phys. 2001 July; 12(3): 129-36. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11851201&dopt=Abstract
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Behavior therapy and sibutramine for the treatment of adolescent obesity: a randomized controlled trial. Author(s): Berkowitz RI, Wadden TA, Tershakovec AM, Cronquist JL. Source: Jama : the Journal of the American Medical Association. 2003 April 9; 289(14): 1805-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12684359&dopt=Abstract
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Beneficial effects of leptin on obesity, T cell hyporesponsiveness, and neuroendocrine/metabolic dysfunction of human congenital leptin deficiency. Author(s): Farooqi IS, Matarese G, Lord GM, Keogh JM, Lawrence E, Agwu C, Sanna V, Jebb SA, Perna F, Fontana S, Lechler RI, DePaoli AM, O'Rahilly S. Source: The Journal of Clinical Investigation. 2002 October; 110(8): 1093-103. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12393845&dopt=Abstract
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Beneficial role of dietary phytoestrogens in obesity and diabetes. Author(s): Bhathena SJ, Velasquez MT. Source: The American Journal of Clinical Nutrition. 2002 December; 76(6): 1191-201. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12450882&dopt=Abstract
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Benefits of sustained moderate weight loss in obesity. Author(s): Pasanisi F, Contaldo F, de Simone G, Mancini M. Source: Nutr Metab Cardiovasc Dis. 2001 December; 11(6): 401-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12055705&dopt=Abstract
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Beta(2)-adrenergic receptor mutation and abdominal obesity risk: effect modification by gender and HDL-cholesterol. Author(s): Corbalan MS, Marti A, Forga L, Martinez-Gonzalez MA, Martinez JA. Source: European Journal of Nutrition. 2002 June; 41(3): 114-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12111048&dopt=Abstract
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Beta-Adrenergic receptors, diet-induced thermogenesis, and obesity. Author(s): Lowell BB, Bachman ES. Source: The Journal of Biological Chemistry. 2003 August 8; 278(32): 29385-8. Epub 2003 June 04. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12788929&dopt=Abstract
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Binge eating disorder in extreme obesity. Author(s): Hsu LK, Mulliken B, McDonagh B, Krupa Das S, Rand W, Fairburn CG, Rolls B, McCrory MA, Saltzman E, Shikora S, Dwyer J, Roberts S. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2002 October; 26(10): 1398-403. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12355338&dopt=Abstract
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Biocultural aspects of obesity in young Mexican schoolchildren. Author(s): Brewis A. Source: American Journal of Human Biology : the Official Journal of the Human Biology Council. 2003 May-June; 15(3): 446-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12704721&dopt=Abstract
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Biological and environmental determinants of childhood obesity. Author(s): Blass EM. Source: Nutrition in Clinical Care : an Official Publication of Tufts University. 2003 January-April; 6(1): 13-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12841426&dopt=Abstract
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Biomarkers and functional foods for obesity and diabetes. Author(s): Hill JO, Peters JC. Source: The British Journal of Nutrition. 2002 November; 88 Suppl 2: S213-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12495462&dopt=Abstract
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Blood pressure, lipids, and obesity are associated with retinopathy: the hoorn study. Author(s): van Leiden HA, Dekker JM, Moll AC, Nijpels G, Heine RJ, Bouter LM, Stehouwer CD, Polak BC. Source: Diabetes Care. 2002 August; 25(8): 1320-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12145228&dopt=Abstract
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Bodily characteristics and lifestyle of Czech children aged 7.00 to 10.99 years, incidence of childhood obesity. Author(s): Kovarova M, Vignerova J, Blaha P, Osancova K. Source: Cent Eur J Public Health. 2002 December; 10(4): 169-73. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12528392&dopt=Abstract
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Body composition and prognosis in chronic systolic heart failure: the obesity paradox. Author(s): Lavie CJ, Osman AF, Milani RV, Mehra MR. Source: The American Journal of Cardiology. 2003 April 1; 91(7): 891-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12667583&dopt=Abstract
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Body composition assessment in extreme obesity and after massive weight loss induced by gastric bypass surgery. Author(s): Das SK, Roberts SB, Kehayias JJ, Wang J, Hsu LK, Shikora SA, Saltzman E, McCrory MA. Source: American Journal of Physiology. Endocrinology and Metabolism. 2003 June; 284(6): E1080-8. Epub 2003 February 25. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12604503&dopt=Abstract
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Body fat percentages measured by dual-energy X-ray absorptiometry corresponding to recently recommended body mass index cutoffs for overweight and obesity in children and adolescents aged 3-18 y. Author(s): Taylor RW, Jones IE, Williams SM, Goulding A. Source: The American Journal of Clinical Nutrition. 2002 December; 76(6): 1416-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12450911&dopt=Abstract
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Body image disturbance in obese outpatients before and after weight loss in relation to race, gender, binge eating, and age of onset of obesity. Author(s): Sorbara M, Geliebter A. Source: The International Journal of Eating Disorders. 2002 May; 31(4): 416-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11948646&dopt=Abstract
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Body mass and survival in patients with chronic heart failure without cachexia: the importance of obesity. Author(s): Davos CH, Doehner W, Rauchhaus M, Cicoira M, Francis DP, Coats AJ, Clark AL, Anker SD. Source: Journal of Cardiac Failure. 2003 February; 9(1): 29-35. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12612870&dopt=Abstract
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Body mass index and mortality in asian populations: implications for obesity cutpoints. Author(s): Stevens J, Nowicki EM. Source: Nutrition Reviews. 2003 March; 61(3): 104-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12723643&dopt=Abstract
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Body mass index in 7-9-y-old French children: frequency of obesity, overweight and thinness. Author(s): Rolland-Cachera MF, Castetbon K, Arnault N, Bellisle F, Romano MC, Lehingue Y, Frelut ML, Hercberg S. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2002 December; 26(12): 1610-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12461677&dopt=Abstract
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Body mass index measurements and prevalence of overweight and obesity in schoolchildren living in the province of Belgian Limburg. Author(s): Massa G. Source: European Journal of Pediatrics. 2002 June; 161(6): 343-6. Epub 2002 April 26. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12029455&dopt=Abstract
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Body mass index, overweight and obesity in married and never married men and women in Poland. Author(s): Lipowicz A, Gronkiewicz S, Malina RM. Source: American Journal of Human Biology : the Official Journal of the Human Biology Council. 2002 July-August; 14(4): 468-75. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12112568&dopt=Abstract
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Body weight and obesity in adults and self-reported abuse in childhood. Author(s): Williamson DF, Thompson TJ, Anda RF, Dietz WH, Felitti V. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2002 August; 26(8): 1075-82. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12119573&dopt=Abstract
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Body weight regulation and obesity. Author(s): Kaplan LM. Source: Journal of Gastrointestinal Surgery : Official Journal of the Society for Surgery of the Alimentary Tract. 2003 May-June; 7(4): 443-51. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12763397&dopt=Abstract
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Bombesin and its family of peptides: prospects for the treatment of obesity. Author(s): Yamada K, Wada E, Santo-Yamada Y, Wada K. Source: European Journal of Pharmacology. 2002 April 12; 440(2-3): 281-90. Review. Erratum In: Eur J Pharmacol. 2002 July 19; 448(2-3): 269. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12007542&dopt=Abstract
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Both fasting-induced leptin reduction and GH increase are blunted in Cushing's syndrome and in simple obesity. Author(s): Grottoli S, Gauna C, Tassone F, Aimaretti G, Corneli G, Wu Z, Strasburger CJ, Dieguez C, Casanueva FF, Ghigo E, Maccario M. Source: Clinical Endocrinology. 2003 February; 58(2): 220-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12580939&dopt=Abstract
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Both under-nutrition and obesity increase morbidity following liver transplantation. Author(s): Hade AM, Shine AM, Kennedy NP, McCormick PA. Source: Ir Med J. 2003 May; 96(5): 140-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12846275&dopt=Abstract
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Breastfeeding and lowering the risk of childhood obesity. Author(s): Armstrong J, Reilly JJ; Child Health Information Team. Source: Lancet. 2002 June 8; 359(9322): 2003-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12076560&dopt=Abstract
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Breast-feeding and obesity. Author(s): Gillman MW. Source: The Journal of Pediatrics. 2002 December; 141(6): 749-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12461485&dopt=Abstract
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Cardiac autonomic neuropathy in diabetic patients: influence of diabetes duration, obesity, and microangiopathic complications--the French multicenter study. Author(s): Valensi P, Paries J, Attali JR; French Group for Research and Study of Diabetic Neuropathy. Source: Metabolism: Clinical and Experimental. 2003 July; 52(7): 815-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12870154&dopt=Abstract
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Cardiac function and obesity. Author(s): Vasan RS. Source: Heart (British Cardiac Society). 2003 October; 89(10): 1127-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12975393&dopt=Abstract
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Cardiovascular outcomes for obesity and metabolic syndrome. Author(s): Vega GL. Source: Obesity Research. 2002 November; 10 Suppl 1: 27S-32S. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12446855&dopt=Abstract
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Cardiovascular risks in obesity. Author(s): Uchegbu EC, Kopelman PG. Source: J Endocrinol Invest. 2002 November; 25(10): 915-8. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12508955&dopt=Abstract
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Cashing in on obesity? Author(s): Victoroff MS. Source: Manag Care. 2002 December; 11(12): 18-20. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12536953&dopt=Abstract
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CCK1R agonists: a promising target for the pharmacological treatment of obesity. Author(s): Szewczyk JR, Laudeman C. Source: Current Topics in Medicinal Chemistry. 2003; 3(8): 837-54. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12678836&dopt=Abstract
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Central overweight and obesity in British youth aged 11-16 years: cross sectional surveys of waist circumference. Author(s): McCarthy HD, Ellis SM, Cole TJ. Source: Bmj (Clinical Research Ed.). 2003 March 22; 326(7390): 624. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12649234&dopt=Abstract
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Central pre-proglucagon derived peptides: opportunities for treatment of obesity. Author(s): Larsen PJ, Vrang N, Tang-Christensen M. Source: Current Pharmaceutical Design. 2003; 9(17): 1373-82. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12769729&dopt=Abstract
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Chemical toxins: a hypothesis to explain the global obesity epidemic. Author(s): Baillie-Hamilton PF. Source: Journal of Alternative and Complementary Medicine (New York, N.Y.). 2002 April; 8(2): 185-92. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12006126&dopt=Abstract
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Chief medical officer's report on the nation's health: concerted action is needed to fight obesity, says chief medical officer. Author(s): Kmietowicz Z. Source: Bmj (Clinical Research Ed.). 2003 July 12; 327(7406): 69. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12855501&dopt=Abstract
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Child to adult socioeconomic conditions and obesity in a national cohort. Author(s): Power C, Manor O, Matthews S. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 September; 27(9): 1081-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12917714&dopt=Abstract
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Childhood obesity in Canada: a review of prevalence estimates and risk factors for cardiovascular diseases and type 2 diabetes. Author(s): Ball GD, McCargar LJ. Source: Canadian Journal of Applied Physiology = Revue Canadienne De Physiologie Appliquee. 2003 February; 28(1): 117-40. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12671200&dopt=Abstract
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Childhood obesity in Kuwait--prevalence and trends. Author(s): Sorkhou I, Al-Qallaf K, Al-Shamali N, Hajia A, Al-Qallaf B. Source: Family Medicine. 2003 July-August; 35(7): 463-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12861451&dopt=Abstract
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Childhood obesity, a modern plague. A gray-haired pediatrician's perspective. Author(s): Willson CF. Source: N C Med J. 2002 November-December; 63(6): 300-1. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12970977&dopt=Abstract
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Childhood obesity: a challenge for the anaesthetist? Author(s): Smith HL, Meldrum DJ, Brennan LJ. Source: Paediatric Anaesthesia. 2002 November; 12(9): 750-61. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12519133&dopt=Abstract
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Childhood obesity: modernity's scourge. Author(s): Waters EB, Baur LA. Source: The Medical Journal of Australia. 2003 May 5; 178(9): 422-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12720504&dopt=Abstract
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Childhood obesity--a public health problem. Author(s): Belfield J. Source: School Nurse News. 2003 January; 20(1): 20, 22, 24. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12616765&dopt=Abstract
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Childhood obesity--why should we be worried? Author(s): Roche EF. Source: Ir Med J. 2003 April; 96(4): 100-2. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12793468&dopt=Abstract
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Childhood social class and adulthood obesity: findings from the Glasgow Alumni Cohort. Author(s): Okasha M, McCarron P, McEwen J, Durnin J, Davey Smith G. Source: Journal of Epidemiology and Community Health. 2003 July; 57(7): 508-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12821695&dopt=Abstract
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CHO intake alters obesity risk associated with Pro12Ala polymorphism of PPARgamma gene. Author(s): Marti A, Corbalan MS, Martinez-Gonzalez MA, Forga L, Martinez JA. Source: J Physiol Biochem. 2002 December; 58(4): 219-20. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12744304&dopt=Abstract
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Cidea-deficient mice have lean phenotype and are resistant to obesity. Author(s): Zhou Z, Yon Toh S, Chen Z, Guo K, Ng CP, Ponniah S, Lin SC, Hong W, Li P. Source: Nature Genetics. 2003 September; 35(1): 49-56. Epub 2003 August 10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12910269&dopt=Abstract
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Circumferential abdominoplasty for sequential treatment after morbid obesity. Author(s): Modolin M, Cintra W Jr, Gobbi CI, Ferreira MC. Source: Obesity Surgery : the Official Journal of the American Society for Bariatric Surgery and of the Obesity Surgery Society of Australia and New Zealand. 2003 February; 13(1): 95-100. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12630621&dopt=Abstract
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Clinical obesity issues from an internist's perspective. Author(s): Klein S. Source: Obesity Research. 2002 November; 10 Suppl 1: 87S-88S. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12446867&dopt=Abstract
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Clinical predictors of leak after laparoscopic Roux-en-Y gastric bypass for morbid obesity. Author(s): Hamilton EC, Sims TL, Hamilton TT, Mullican MA, Jones DB, Provost DA. Source: Surgical Endoscopy. 2003 May; 17(5): 679-84. Epub 2003 March 07. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12618940&dopt=Abstract
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Clinical spectrum of obesity and mutations in the melanocortin 4 receptor gene. Author(s): Farooqi IS, Keogh JM, Yeo GS, Lank EJ, Cheetham T, O'Rahilly S. Source: The New England Journal of Medicine. 2003 March 20; 348(12): 1085-95. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12646665&dopt=Abstract
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Coagulation and fibrinolysis abnormalities in obesity. Author(s): De Pergola G, Pannacciulli N. Source: J Endocrinol Invest. 2002 November; 25(10): 899-904. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12508953&dopt=Abstract
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Coexistence of social inequalities in undernutrition and obesity in preschool children: population based cross sectional study. Author(s): Armstrong J, Dorosty AR, Reilly JJ, Emmett PM; Child Health Information Team. Source: Archives of Disease in Childhood. 2003 August; 88(8): 671-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12876159&dopt=Abstract
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Cognitive interference due to food cues in childhood obesity. Author(s): Braet C, Crombez G. Source: Journal of Clinical Child and Adolescent Psychology : the Official Journal for the Society of Clinical Child and Adolescent Psychology, American Psychological Association, Division 53. 2003 March; 32(1): 32-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12573930&dopt=Abstract
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Cognitive-behavioral approaches in the management of obesity. Author(s): Wisotsky W, Swencionis C. Source: Adolescent Medicine (Philadelphia, Pa.). 2003 February; 14(1): 37-48. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12529189&dopt=Abstract
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Comment on "Obesity and the environment: where do we go from here?". Author(s): Butte NF, Ellis KJ. Source: Science. 2003 August 1; 301(5633): 598; Author Reply 598. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12893926&dopt=Abstract
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Comparison between different methods to assess the prevalence of obesity in a sample of Italian children. Author(s): Valerio G, Scalfi L, De Martino C, Franzese A, Tenore A, Contaldo F. Source: J Pediatr Endocrinol Metab. 2003 February; 16(2): 211-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12713259&dopt=Abstract
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Complex haplotypes of IRS2 gene are associated with severe obesity and reveal heterogeneity in the effect of Gly1057Asp mutation. Author(s): Lautier C, El Mkadem SA, Renard E, Brun JF, Gris JC, Bringer J, Grigorescu F. Source: Human Genetics. 2003 July; 113(1): 34-43. Epub 2003 April 10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12687350&dopt=Abstract
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Confusing food with obesity. Author(s): Lupien JR. Source: Science. 2003 May 16; 300(5622): 1091. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12750499&dopt=Abstract
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Consensus view on the role of dietary fat and obesity. Author(s): Foreyt JP, Poston WS. Source: The American Journal of Medicine. 2002 December 30; 113 Suppl 9B: 60S-62S. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12566140&dopt=Abstract
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Contemporary surgical management of obesity. Author(s): McNatt SS, Howard-McNatt M. Source: W V Med J. 2002 November-December; 98(6): 273-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12645282&dopt=Abstract
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Correlates of overweight and obesity among lesbian and bisexual women. Author(s): Yancey AK, Cochran SD, Corliss HL, Mays VM. Source: Preventive Medicine. 2003 June; 36(6): 676-83. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12744910&dopt=Abstract
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Could elevated C-reactive protein in patients with obstructive sleep apnea be due to obesity per se? Author(s): Cheng TO. Source: Circulation. 2003 January 7; 107(1): E9; Author Reply E9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12515763&dopt=Abstract
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C-reactive protein and gestational diabetes: the central role of maternal obesity. Author(s): Retnakaran R, Hanley AJ, Raif N, Connelly PW, Sermer M, Zinman B. Source: The Journal of Clinical Endocrinology and Metabolism. 2003 August; 88(8): 3507-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12915627&dopt=Abstract
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Cryptic terminal deletion of chromosome 9q34: a novel cause of syndromic obesity in childhood? Author(s): Cormier-Daire V, Molinari F, Rio M, Raoul O, de Blois MC, Romana S, Vekemans M, Munnich A, Colleaux L. Source: Journal of Medical Genetics. 2003 April; 40(4): 300-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12676904&dopt=Abstract
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Current management strategies for coexisting diabetes mellitus and obesity. Author(s): Scheen AJ. Source: Drugs. 2003; 63(12): 1165-84. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12790691&dopt=Abstract
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DASH diet lowers blood pressure and lipid-induced oxidative stress in obesity. Author(s): Lopes HF, Martin KL, Nashar K, Morrow JD, Goodfriend TL, Egan BM. Source: Hypertension. 2003 March; 41(3): 422-30. Epub 2003 February 03. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12623938&dopt=Abstract
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Data management for clinical research in obesity. Author(s): Einbinder JS. Source: Obesity Research. 2002 November; 10 Suppl 1: 6S-9S. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12446851&dopt=Abstract
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De novo MECP2 frameshift mutation in a boy with moderate mental retardation, obesity and gynaecomastia. Author(s): Kleefstra T, Yntema HG, Oudakker AR, Romein T, Sistermans E, Nillessen W, van Bokhoven H, de Vries BB, Hamel BC. Source: Clinical Genetics. 2002 May; 61(5): 359-62. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12081720&dopt=Abstract
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Defective melanocortin 4 receptors in hyperphagia and morbid obesity. Author(s): List JF, Habener JF. Source: The New England Journal of Medicine. 2003 March 20; 348(12): 1160-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12646673&dopt=Abstract
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Deficit in the discrimination of nonverbal emotions in children with obesity and their mothers. Author(s): Baldaro B, Rossi N, Caterina R, Codispoti M, Balsamo A, Trombini G. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 February; 27(2): 191-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12586998&dopt=Abstract
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Defining childhood obesity: fiddling whilst Rome burns? Author(s): Poskitt EM. Source: Acta Paediatrica (Oslo, Norway : 1992). 2001 December; 90(12): 1361-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11853327&dopt=Abstract
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Demographics and trends in overweight and obesity in patients at time of kidney transplantation. Author(s): Friedman AN, Miskulin DC, Rosenberg IH, Levey AS. Source: American Journal of Kidney Diseases : the Official Journal of the National Kidney Foundation. 2003 February; 41(2): 480-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12552513&dopt=Abstract
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Depression and obesity treatments are life saving. Author(s): Licinio J, Wong ML. Source: Nature Medicine. 2002 December; 8(12): 1336; Author Reply 1336. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12457157&dopt=Abstract
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Depression and obesity. Author(s): Stunkard AJ, Faith MS, Allison KC. Source: Biological Psychiatry. 2003 August 1; 54(3): 330-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12893108&dopt=Abstract
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Depression in diabetes and obesity: racial/ethnic/gender issues in older adults. Author(s): Blazer DG, Moody-Ayers S, Craft-Morgan J, Burchett B. Source: Journal of Psychosomatic Research. 2002 October; 53(4): 913-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12377303&dopt=Abstract
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Dermatological complications of obesity. Author(s): Garcia Hidalgo L. Source: American Journal of Clinical Dermatology. 2002; 3(7): 497-506. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12180897&dopt=Abstract
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Detection of cardiovascular risk factors by indices of obesity obtained from anthropometry and dual-energy X-ray absorptiometry in Japanese individuals. Author(s): Ito H, Nakasuga K, Ohshima A, Maruyama T, Kaji Y, Harada M, Fukunaga M, Jingu S, Sakamoto M. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 February; 27(2): 232-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12587004&dopt=Abstract
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Developing health messages: qualitative studies with children, parents, and teachers help identify communications opportunities for healthful lifestyles and the prevention of obesity. Author(s): Borra ST, Kelly L, Shirreffs MB, Neville K, Geiger CJ. Source: Journal of the American Dietetic Association. 2003 June; 103(6): 721-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12778044&dopt=Abstract
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Development and future of gastroplasties for morbid obesity. Author(s): Mason EE. Source: Archives of Surgery (Chicago, Ill. : 1960). 2003 April; 138(4): 361-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12686521&dopt=Abstract
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Development of novel medications for use in the treatment of obesity in children will be directed by delineating controls of energy homeostasis. Author(s): Sherman PM, Zlotkin SH. Source: Archives of Pediatrics & Adolescent Medicine. 2003 August; 157(8): 721. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12912773&dopt=Abstract
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Diabetes and hypertension in severe obesity and effects of gastric bypass-induced weight loss. Author(s): Sugerman HJ, Wolfe LG, Sica DA, Clore JN. Source: Annals of Surgery. 2003 June; 237(6): 751-6; Discussion 757-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12796570&dopt=Abstract
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Diabetes contributes to cholesterol metabolism regardless of obesity. Author(s): Simonen PP, Gylling HK, Miettinen TA. Source: Diabetes Care. 2002 September; 25(9): 1511-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12196419&dopt=Abstract
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Diabetes mellitus and obesity. Author(s): Roth A. Source: Primary Care. 2002 June; 29(2): 279-95. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12391712&dopt=Abstract
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Diabetes, obesity, and Acrp30/adiponectin. Author(s): Hug C, Lodish HF. Source: Biotechniques. 2002 September; 33(3): 654, 656, 658 Passim. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12238775&dopt=Abstract
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Diet and physical activity for obesity: how effective are they? Author(s): Womble LG, Clark VL, Wadden TA. Source: J Endocrinol Invest. 2002 November; 25(10): 922-4. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12508957&dopt=Abstract
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Diet, exercise, and the challenge of combating obesity in primary care. Author(s): McInnis KJ. Source: The Journal of Cardiovascular Nursing. 2003 April-June; 18(2): 93-100; Quiz 1012. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12680567&dopt=Abstract
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Diet, obesity and reflux in the etiology of adenocarcinomas of the esophagus and gastric cardia in humans. Author(s): Mayne ST, Navarro SA. Source: The Journal of Nutrition. 2002 November; 132(11 Suppl): 3467S-3470S. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12421872&dopt=Abstract
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Diet, obesity, and cardiovascular risk. Author(s): Bonow RO, Eckel RH. Source: The New England Journal of Medicine. 2003 May 22; 348(21): 2057-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12761363&dopt=Abstract
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Dietary fat is a major player in obesity--but not the only one. Author(s): Astrup A. Source: Obesity Reviews : an Official Journal of the International Association for the Study of Obesity. 2002 May; 3(2): 57-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12120420&dopt=Abstract
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Dietary fat plays a major role in obesity: no. Author(s): Willett WC. Source: Obesity Reviews : an Official Journal of the International Association for the Study of Obesity. 2002 May; 3(2): 59-68. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12120421&dopt=Abstract
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Diet-dependent obesity and hypercholesterolemia in the New Zealand obese mouse: identification of a quantitative trait locus for elevated serum cholesterol on the distal mouse chromosome 5. Author(s): Giesen K, Plum L, Kluge R, Ortlepp J, Joost HG. Source: Biochemical and Biophysical Research Communications. 2003 May 16; 304(4): 812-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12727230&dopt=Abstract
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Differences in oral temperature and body shape in two populations with different propensities for obesity. Author(s): Vozarova B, Weyer C, Bogardus C, Ravussin E, Tataranni PA. Source: Annals of the New York Academy of Sciences. 2002 June; 967: 516-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12079882&dopt=Abstract
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Differences in overweight and obesity among Australian schoolchildren of low and middle/high socioeconomic status. Author(s): O'Dea JA. Source: The Medical Journal of Australia. 2003 July 7; 179(1): 63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12831394&dopt=Abstract
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Differences in the relation of obesity to serum triacylglycerol and VLDL subclass concentrations between black and white children: the Bogalusa Heart Study. Author(s): Freedman DS, Bowman BA, Otvos JD, Srinivasan SR, Berenson GS. Source: The American Journal of Clinical Nutrition. 2002 May; 75(5): 827-33. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11976155&dopt=Abstract
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Differentiation between obesity and insulin resistance in the association with Creactive protein. Author(s): McLaughlin T, Abbasi F, Lamendola C, Liang L, Reaven G, Schaaf P, Reaven P. Source: Circulation. 2002 December 3; 106(23): 2908-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12460870&dopt=Abstract
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Discovery and optimization of a series of carbazole ureas as NPY5 antagonists for the treatment of obesity. Author(s): Block MH, Boyer S, Brailsford W, Brittain DR, Carroll D, Chapman S, Clarke DS, Donald CS, Foote KM, Godfrey L, Ladner A, Marsham PR, Masters DJ, Mee CD, O'Donovan MR, Pease JE, Pickup AG, Rayner JW, Roberts A, Schofield P, Suleman A, Turnbull AV. Source: Journal of Medicinal Chemistry. 2002 August 1; 45(16): 3509-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12139462&dopt=Abstract
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Disease severity at time of referral for pediatric failure to thrive and obesity: time for a paradigm shift? Author(s): Miller LA, Grunwald GK, Johnson SL, Krebs NF. Source: The Journal of Pediatrics. 2002 July; 141(1): 121-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12091862&dopt=Abstract
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Do stress reactions cause abdominal obesity and comorbidities? Author(s): Bjorntorp P. Source: Obesity Reviews : an Official Journal of the International Association for the Study of Obesity. 2001 May; 2(2): 73-86. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12119665&dopt=Abstract
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Does metformin provide a new approach to the management of obesity? Author(s): Rivlin RS. Source: Heart Disease. 2001 September-October; 3(5): 283-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11975806&dopt=Abstract
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Dopamine transporter genotype as a risk factor for obesity in African-American smokers. Author(s): Epstein LH, Jaroni JL, Paluch RA, Leddy JJ, Vahue HE, Hawk L, Wileyto EP, Shields PG, Lerman C. Source: Obesity Research. 2002 December; 10(12): 1232-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12490667&dopt=Abstract
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Dopamine, hypertension and obesity. Author(s): Contreras F, Fouillioux C, Bolivar A, Simonovis N, Hernandez-Hernandez R, Armas-Hernandez MJ, Velasco M. Source: Journal of Human Hypertension. 2002 March; 16 Suppl 1: S13-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11986886&dopt=Abstract
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Dopaminergic tone and obesity: an insight from prolactinomas treated with bromocriptine. Author(s): Doknic M, Pekic S, Zarkovic M, Medic-Stojanoska M, Dieguez C, Casanueva F, Popovic V. Source: European Journal of Endocrinology / European Federation of Endocrine Societies. 2002 July; 147(1): 77-84. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12088923&dopt=Abstract
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Drug strategies for the treatment of obesity. Author(s): Alemany M, Remesar X, Fernandez-Lopez JA. Source: Idrugs. 2003 June; 6(6): 566-72. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12811679&dopt=Abstract
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Dusting off the epidemiological triad: could it work with obesity? Author(s): Egger G, Swinburn B, Rossner S. Source: Obesity Reviews : an Official Journal of the International Association for the Study of Obesity. 2003 May; 4(2): 115-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12760446&dopt=Abstract
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Dysfunctional immune-privilege in morbid obesity: implications and effect of gastric bypass surgery. Author(s): Cottam DR, Schaefer PA, Shaftan GW, Angus LD. Source: Obesity Surgery : the Official Journal of the American Society for Bariatric Surgery and of the Obesity Surgery Society of Australia and New Zealand. 2003 February; 13(1): 49-57. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12630613&dopt=Abstract
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Early life risk factors in cancer: the relation of birth weight to adult obesity. Author(s): Leong NM, Mignone LI, Newcomb PA, Titus-Ernstoff L, Baron JA, TrenthamDietz A, Stampfer MJ, Willett WC, Egan KM. Source: International Journal of Cancer. Journal International Du Cancer. 2003 March 1; 103(6): 789-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12516100&dopt=Abstract
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Early prevention of obesity and cardiovascular diseases. Author(s): Merker N, Wagner N, Kirch W, Muller MJ. Source: Deutsche Medizinische Wochenschrift. 2002 December 13; 127(50): 2661-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12481235&dopt=Abstract
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Eating disorders and obesity. Author(s): Reslewic S. Source: Science. 2003 May 16; 300(5622): 1091. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12750498&dopt=Abstract
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Eating patterns and obesity in children. The Bogalusa Heart Study. Author(s): Nicklas TA, Yang SJ, Baranowski T, Zakeri I, Berenson G. Source: American Journal of Preventive Medicine. 2003 July; 25(1): 9-16. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12818304&dopt=Abstract
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Economic and psychological implications of the obesity epidemic. Author(s): Kottke TE, Wu LA, Hoffman RS. Source: Mayo Clinic Proceedings. 2003 January; 78(1): 92-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12528882&dopt=Abstract
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Effect of family history, obesity and exercise on breast cancer risk among postmenopausal women. Author(s): Carpenter CL, Ross RK, Paganini-Hill A, Bernstein L. Source: International Journal of Cancer. Journal International Du Cancer. 2003 August 10; 106(1): 96-102. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12794763&dopt=Abstract
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Effect of obesity and/or sleep apnea on chemosensitivity: differences between men and women. Author(s): Buyse B, Markous N, Cauberghs M, Van Klaveren R, Muls E, Demedts M. Source: Respiratory Physiology & Neurobiology. 2003 February 19; 134(1): 13-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12573877&dopt=Abstract
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Effect of obesity on health-related quality of life among Appalachian elderly. Author(s): Goins RT, Spencer SM, Krummel DA. Source: Southern Medical Journal. 2003 June; 96(6): 552-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12938781&dopt=Abstract
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Effect of obesity on recombinant follicle-stimulating hormone absorption: subcutaneous versus intramuscular administration. Author(s): Steinkampf MP, Hammond KR, Nichols JE, Slayden SH. Source: Fertility and Sterility. 2003 July; 80(1): 99-102. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12849809&dopt=Abstract
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Effect of subclinical hypothyroidism and obesity on whole-body and regional bone mineral content. Author(s): Bertoli A, Fusco A, Andreoli A, Magnani A, Tulli A, Lauro D, De Lorenzo A. Source: Hormone Research. 2002; 57(3-4): 79-84. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12006702&dopt=Abstract
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Effect of television viewing on pediatric obesity. Author(s): Ma GS, Li YP, Hu XQ, Ma WJ, Wu J. Source: Biomed Environ Sci. 2002 December; 15(4): 291-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12642985&dopt=Abstract
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Effect of the factor VII R353Q missense mutation on plasma apolipoprotein B levels: impact of visceral obesity. Author(s): Berthier MT, Houde A, Bergeron J, Prud'homme D, Despres JP, Vohl MC. Source: Journal of Human Genetics. 2003; 48(7): 367-73. Epub 2003 July 08. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12851844&dopt=Abstract
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Effect of weight loss on VLDL-triglyceride and apoB-100 kinetics in women with abdominal obesity. Author(s): Mittendorfer B, Patterson BW, Klein S. Source: American Journal of Physiology. Endocrinology and Metabolism. 2003 March; 284(3): E549-56. Epub 2002 December 10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12475754&dopt=Abstract
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Effective management of obesity. Author(s): Shepherd TM. Source: The Journal of Family Practice. 2003 January; 52(1): 34-42. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12540311&dopt=Abstract
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Effects of growth hormone administration in human obesity. Author(s): Shadid S, Jensen MD. Source: Obesity Research. 2003 February; 11(2): 170-5. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12582210&dopt=Abstract
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Effects of hypertension and obesity on endometrial thickness. Author(s): Serdar Serin I, Ozcelik B, Basbug M, Ozsahin O, Yilmazsoy A, Erez R. Source: European Journal of Obstetrics, Gynecology, and Reproductive Biology. 2003 July 1; 109(1): 72-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12818448&dopt=Abstract
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Effects of isolated obesity on systolic and diastolic left ventricular function. Author(s): Pascual M, Pascual DA, Soria F, Vicente T, Hernandez AM, Tebar FJ, Valdes M. Source: Heart (British Cardiac Society). 2003 October; 89(10): 1152-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12975404&dopt=Abstract
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Effects of obesity and weight loss on soluble CD40L levels. Author(s): Desideri G, Ferri C. Source: Jama : the Journal of the American Medical Association. 2003 April 9; 289(14): 1781-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12684355&dopt=Abstract
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Effects of obesity on morbidity in children and adolescents. Author(s): Must A, Anderson SE. Source: Nutrition in Clinical Care : an Official Publication of Tufts University. 2003 January-April; 6(1): 4-12. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12841425&dopt=Abstract
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Enhanced erythrocyte adhesiveness/aggregation in obesity corresponds to low-grade inflammation. Author(s): Samocha-Bonet D, Lichtenberg D, Tomer A, Deutsch V, Mardi T, Goldin Y, Abu-Abeid S, Shenkerman G, Patshornik H, Shapira I, Berliner S. Source: Obesity Research. 2003 March; 11(3): 403-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12634437&dopt=Abstract
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Enhanced fat oxidation through physical activity is associated with improvements in insulin sensitivity in obesity. Author(s): Goodpaster BH, Katsiaras A, Kelley DE. Source: Diabetes. 2003 September; 52(9): 2191-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12941756&dopt=Abstract
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Epidemic obesity and the metabolic syndrome. Author(s): Haffner S, Taegtmeyer H. Source: Circulation. 2003 September 30; 108(13): 1541-5. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14517149&dopt=Abstract
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Epidemiology and consequences of obesity. Author(s): Stevens J, Truesdale KP. Source: Journal of Gastrointestinal Surgery : Official Journal of the Society for Surgery of the Alimentary Tract. 2003 May-June; 7(4): 438-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12763396&dopt=Abstract
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Establishing body composition in obesity. Author(s): Pietrobelli A, Heymsfield SB. Source: J Endocrinol Invest. 2002 November; 25(10): 884-92. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12508951&dopt=Abstract
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Evaluation and treatment of obesity. Author(s): Azar ST, Zantout MS. Source: J Med Liban. 2000 September-October; 48(5): 310-4. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12489585&dopt=Abstract
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Evidence for distinct genetic effects on obesity and lipid-related CVD risk factors in diabetic compared to nondiabetic American Indians: the Strong Heart Family Study. Author(s): North KE, MacCluer JW, Williams JT, Welty TK, Best LG, Lee ET, Fabsitz RR, Howard BV. Source: Diabetes/Metabolism Research and Reviews. 2003 March-April; 19(2): 140-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12673782&dopt=Abstract
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Evolution of operative procedures for the management of morbid obesity 1950-2000. Author(s): Buchwald H, Buchwald JN. Source: Obesity Surgery : the Official Journal of the American Society for Bariatric Surgery and of the Obesity Surgery Society of Australia and New Zealand. 2002 October; 12(5): 705-17. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12448398&dopt=Abstract
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Exercise and diet in obesity treatment: an integrative system dynamics perspective. Author(s): Abdel-Hamid TK. Source: Medicine and Science in Sports and Exercise. 2003 March; 35(3): 400-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12618569&dopt=Abstract
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Exercise considerations in hypertension, obesity, and dyslipidemia. Author(s): MacKnight JM. Source: Clinics in Sports Medicine. 2003 January; 22(1): 101-21, Vii. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12613089&dopt=Abstract
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Experimental drugs take aim at obesity. Author(s): Vastag B. Source: Jama : the Journal of the American Medical Association. 2003 April 9; 289(14): 1763-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12684341&dopt=Abstract
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Exploring the association between body weight, stigma of obesity, and health care avoidance. Author(s): Drury CA, Louis M. Source: Journal of the American Academy of Nurse Practitioners. 2002 December; 14(12): 554-61. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12567923&dopt=Abstract
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Expression of 11beta-hydroxysteroid dehydrogenase type 1 in adipose tissue is not increased in human obesity. Author(s): Tomlinson JW, Sinha B, Bujalska I, Hewison M, Stewart PM. Source: The Journal of Clinical Endocrinology and Metabolism. 2002 December; 87(12): 5630-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12466364&dopt=Abstract
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Facing the problem of obesity: a call to action. Author(s): Mina WC. Source: Mo Med. 2003 May-June; 100(3): 176-7. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12847860&dopt=Abstract
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Factorial study of the effects of atorvastatin and fish oil on dyslipidaemia in visceral obesity. Author(s): Chan DC, Watts GF, Mori TA, Barrett PH, Beilin LJ, Redgrave TG. Source: European Journal of Clinical Investigation. 2002 June; 32(6): 429-36. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12059988&dopt=Abstract
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Factors associated with overweight/obesity in economically active South African populations. Author(s): Senekal M, Steyn NP, Nel JH. Source: Ethn Dis. 2003 Winter; 13(1): 109-16. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12723019&dopt=Abstract
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Familial approach to the treatment of childhood obesity: conceptual mode. Author(s): Golan M, Weizman A. Source: Journal of Nutrition Education. 2001 March-April; 33(2): 102-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12031190&dopt=Abstract
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Familial clustering of obesity and the role of nutrition: Tehran Lipid and Glucose Study. Author(s): Mirmiran P, Mirbolooki M, Azizi F. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2002 December; 26(12): 1617-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12461678&dopt=Abstract
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Familial combined hyperlipidemia (FCHL) in children: the significance of early development of hyperapoB lipoproteinemia, obesity and aging. Author(s): Kuromori Y, Okada T, Iwata F, Hara M, Noto N, Harada K. Source: J Atheroscler Thromb. 2002; 9(6): 314-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12560593&dopt=Abstract
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Familial isolated growth hormone deficiency is associated with increased systolic blood pressure, central obesity, and dyslipidemia. Author(s): Barreto-Filho JA, Alcantara MR, Salvatori R, Barreto MA, Sousa AC, Bastos V, Souza AH, Pereira RM, Clayton PE, Gill MS, Aguiar-Oliveira MH. Source: The Journal of Clinical Endocrinology and Metabolism. 2002 May; 87(5): 2018-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11994335&dopt=Abstract
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Family history of prostate cancer and obesity in relation to high-grade disease and extraprostatic extension in young men with prostate cancer. Author(s): Rohrmann S, Roberts WW, Walsh PC, Platz EA. Source: The Prostate. 2003 May 1; 55(2): 140-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12661039&dopt=Abstract
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Family-based interventions for the treatment of childhood obesity. Author(s): St Jeor ST, Perumean-Chaney S, Sigman-Grant M, Williams C, Foreyt J. Source: Journal of the American Dietetic Association. 2002 May; 102(5): 640-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12008987&dopt=Abstract
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Fast food and obesity in China. Author(s): Cheng TO. Source: Journal of the American College of Cardiology. 2003 August 20; 42(4): 773. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12932622&dopt=Abstract
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Fasting and daylong triglycerides in obesity with and without type 2 diabetes. Author(s): van Wijk JP, Halkes CJ, Erkelens DW, Castro Cabezas M. Source: Metabolism: Clinical and Experimental. 2003 August; 52(8): 1043-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12898471&dopt=Abstract
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Fat accumulation in the liver is associated with defects in insulin suppression of glucose production and serum free fatty acids independent of obesity in normal men. Author(s): Seppala-Lindroos A, Vehkavaara S, Hakkinen AM, Goto T, Westerbacka J, Sovijarvi A, Halavaara J, Yki-Jarvinen H. Source: The Journal of Clinical Endocrinology and Metabolism. 2002 July; 87(7): 3023-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12107194&dopt=Abstract
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Fat versus carbohydrate in insulin resistance, obesity, diabetes and cardiovascular disease. Author(s): Hung T, Sievenpiper JL, Marchie A, Kendall CW, Jenkins DJ. Source: Current Opinion in Clinical Nutrition and Metabolic Care. 2003 March; 6(2): 16576. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12589186&dopt=Abstract
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Feeding our children to death: the tragedy of childhood obesity in America. Author(s): Freeman-Fobbs P. Source: Journal of the National Medical Association. 2003 February; 95(2): 119. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12760606&dopt=Abstract
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Fetal environment and subsequent obesity: a study of maternal smoking. Author(s): Power C, Jefferis BJ. Source: International Journal of Epidemiology. 2002 April; 31(2): 413-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11980805&dopt=Abstract
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Fibrin glue as a sealant for high-risk anastomosis in surgery for morbid obesity. Author(s): Liu CD, Glantz GJ, Livingston EH. Source: Obesity Surgery : the Official Journal of the American Society for Bariatric Surgery and of the Obesity Surgery Society of Australia and New Zealand. 2003 February; 13(1): 45-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12630612&dopt=Abstract
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Fighting childhood obesity with university-community partnerships. Author(s): Thompson LS, Grey M. Source: Nurs Leadersh Forum. 2002 Fall; 7(1): 20-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12683028&dopt=Abstract
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Fighting fat. New drugs against obesity in the pipeline. Author(s): Brower V. Source: Embo Reports. 2002 July; 3(7): 601-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12101089&dopt=Abstract
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Five-year results of laparoscopic vertical banded gastroplasty in the treatment of massive obesity. Author(s): Magnusson M, Freedman J, Jonas E, Stockeld D, Granstrom L, Naslund E. Source: Obesity Surgery : the Official Journal of the American Society for Bariatric Surgery and of the Obesity Surgery Society of Australia and New Zealand. 2002 December; 12(6): 826-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12568189&dopt=Abstract
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Focus issue: the signaling skinny on obesity. Author(s): Chong LD, Adler EM, Ray LB. Source: Science's Stke [electronic Resource] : Signal Transduction Knowledge Environment. 2003 February 11; 2003(169): Eg2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12582198&dopt=Abstract
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Food insecurity is associated with increased risk of obesity in California women. Author(s): Adams EJ, Grummer-Strawn L, Chavez G. Source: The Journal of Nutrition. 2003 April; 133(4): 1070-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12672921&dopt=Abstract
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Food stamp program participation is positively related to obesity in low income women. Author(s): Gibson D. Source: The Journal of Nutrition. 2003 July; 133(7): 2225-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12840184&dopt=Abstract
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For the patient. Are vegetarians at less risk for obesity, diabetes, and hypertension? Obesity, diabetes, hypertension, and vegetarian status among Seventh-Day Adventists in Barbados: preliminary results. Author(s): Brathwaite N, Fraser HS, Modeste N, Broome H, King R. Source: Ethn Dis. 2003 Winter; 13(1): 148. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12723025&dopt=Abstract
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For the patient. What lifestyle choices place people at-risk of obesity? Factors associated with overweight/obesity in economically active South African populations. Author(s): Senekal M, Steyn NP, Nel JH. Source: Ethn Dis. 2003 Winter; 13(1): 153. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12723030&dopt=Abstract
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Free fatty acids in obesity and type 2 diabetes: defining their role in the development of insulin resistance and beta-cell dysfunction. Author(s): Boden G, Shulman GI. Source: European Journal of Clinical Investigation. 2002 June; 32 Suppl 3: 14-23. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12028371&dopt=Abstract
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Functional characterization of melanocortin-4 receptor mutations associated with childhood obesity. Author(s): Tao YX, Segaloff DL. Source: Endocrinology. 2003 October; 144(10): 4544-51. Epub 2003 June 19. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12959994&dopt=Abstract
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Further evidence for the association between obesity-related traits and the apolipoprotein A-IV gene. Author(s): Fiegenbaum M, Hutz MH. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 April; 27(4): 484-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12664082&dopt=Abstract
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Future of obesity and chronic-disease management in health care: the employer perspective. Author(s): Walters GA. Source: Obesity Research. 2002 November; 10 Suppl 1: 84S-86S. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12446866&dopt=Abstract
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Future of obesity and chronic-disease management in health care: the HMO perspective. Author(s): Hyatt JD. Source: Obesity Research. 2002 November; 10 Suppl 1: 79S-81S. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12446864&dopt=Abstract
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Future of obesity and disease management in health care: the government perspective. Author(s): Primack A. Source: Obesity Research. 2002 November; 10 Suppl 1: 82S-83S. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12446865&dopt=Abstract
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Galanin/GALP and galanin receptors: role in central control of feeding, body weight/obesity and reproduction? Author(s): Gundlach AL. Source: European Journal of Pharmacology. 2002 April 12; 440(2-3): 255-68. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12007540&dopt=Abstract
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Gastric bypass for morbid obesity in patients 50 years or older: is laparoscopic technique safer? Author(s): Gonzalez R, Lin E, Mattar SG, Venkatesh KR, Smith CD. Source: The American Surgeon. 2003 July; 69(7): 547-53; Discussion 553-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12889614&dopt=Abstract
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Gastric bypass is an effective treatment for obstructive sleep apnea in patients with clinically significant obesity. Author(s): Rasheid S, Banasiak M, Gallagher SF, Lipska A, Kaba S, Ventimiglia D, Anderson WM, Murr MM. Source: Obesity Surgery : the Official Journal of the American Society for Bariatric Surgery and of the Obesity Surgery Society of Australia and New Zealand. 2003 February; 13(1): 58-61. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12630614&dopt=Abstract
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Gastric bypass surgery for obesity. Author(s): Buechner JS. Source: Medicine and Health, Rhode Island. 2003 March; 86(3): 81-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12703143&dopt=Abstract
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Gastric bypass surgery for severe obesity. Author(s): Sugerman HJ. Source: Semin Laparosc Surg. 2002 June; 9(2): 79-85. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12152150&dopt=Abstract
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Gastric dilatation in a girl with former obesity and atypical anorexia nervosa. Author(s): Holtkamp K, Mogharrebi R, Hanisch C, Schumpelick V, Herpertz-Dahlmann B. Source: The International Journal of Eating Disorders. 2002 November; 32(3): 372-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12210653&dopt=Abstract
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Gastric restrictive procedures to treat obesity: reasons for failure and long-term evaluation of the results of operative revision. Author(s): Kaminski DL. Source: International Journal of Surgical Investigation. 2001; 2(5): 413-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12678546&dopt=Abstract
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Gastro-oesophageal reflux disease in obesity: pathophysiological and therapeutic considerations. Author(s): Barak N, Ehrenpreis ED, Harrison JR, Sitrin MD. Source: Obesity Reviews : an Official Journal of the International Association for the Study of Obesity. 2002 February; 3(1): 9-15. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12119661&dopt=Abstract
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Gender, obesity and health. Author(s): Heitmann BL. Source: Sb Lek. 2002; 103(4): 465-70. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12688160&dopt=Abstract
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Genetic and environmental contributions to obesity and binge eating. Author(s): Bulik CM, Sullivan PF, Kendler KS. Source: The International Journal of Eating Disorders. 2003 April; 33(3): 293-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12655626&dopt=Abstract
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Genetic predisposition to obesity in bulimia nervosa: a mutation screen of the melanocortin-4 receptor gene. Author(s): Hebebrand J, Fichter M, Gerber G, Gorg T, Hermann H, Geller F, Schafer H, Remschmidt H, Hinney A. Source: Molecular Psychiatry. 2002; 7(6): 647-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12140789&dopt=Abstract
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Genetic variability in responses to caloric restriction in animals and in regulation of metabolism and obesity in humans. Author(s): Allison DB, Miller RA, Austad SN, Bouchard C, Leibel R, Klebanov S, Johnson T, Harrison DE. Source: The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences. 2001 March; 56 Spec No 1: 55-65. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12088213&dopt=Abstract
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Genetic variation in the small heterodimer partner gene and young-onset type 2 diabetes, obesity, and birth weight in U.K. subjects. Author(s): Mitchell SM, Weedon MN, Owen KR, Shields B, Wilkins-Wall B, Walker M, McCarthy MI, Frayling TM, Hattersley AT. Source: Diabetes. 2003 May; 52(5): 1276-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12716764&dopt=Abstract
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Genetics and pathophysiology of human obesity. Author(s): Cummings DE, Schwartz MW. Source: Annual Review of Medicine. 2003; 54: 453-71. Epub 2001 December 03. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12414915&dopt=Abstract
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Genetics of obesity and type 2 diabetes: tracking pathogenic traits during the predisease period. Author(s): Bougneres P. Source: Diabetes. 2002 December; 51 Suppl 3: S295-303. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12475766&dopt=Abstract
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Genetics of obesity. Author(s): Clement K, Boutin P, Froguel P. Source: American Journal of Pharmacogenomics : Genomics-Related Research in Drug Development and Clinical Practice. 2002; 2(3): 177-87. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12383024&dopt=Abstract
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Genome scan for childhood and adolescent obesity in German families. Author(s): Saar K, Geller F, Ruschendorf F, Reis A, Friedel S, Schauble N, Nurnberg P, Siegfried W, Goldschmidt HP, Schafer H, Ziegler A, Remschmidt H, Hinney A, Hebebrand J. Source: Pediatrics. 2003 February; 111(2): 321-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12563058&dopt=Abstract
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Genotype, obesity and cardiovascular disease--has technical and social advancement outstripped evolution? Author(s): Zimmet P, Thomas CR. Source: Journal of Internal Medicine. 2003 August; 254(2): 114-25. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12859692&dopt=Abstract
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Genotype-by-smoking interaction for leptin levels in the Metabolic Risk Complications of Obesity Genes project. Author(s): Martin LJ, Kissebah AH, Sonnenberg GE, Blangero J, Comuzzie AG; Metabolic Risk Complications of Obesity Genes Project. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 March; 27(3): 334-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12629560&dopt=Abstract
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Ghrelin and the hyposomatotropism of obesity. Author(s): Lindeman JH, Pijl H, Van Dielen FM, Lentjes EG, Van Leuven C, Kooistra T. Source: Obesity Research. 2002 November; 10(11): 1161-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12429880&dopt=Abstract
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Ghrelin as a potential anti-obesity target. Author(s): Horvath TL, Castaneda T, Tang-Christensen M, Pagotto U, Tschop MH. Source: Current Pharmaceutical Design. 2003; 9(17): 1383-95. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12769730&dopt=Abstract
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Ghrelin, growth and obesity. Author(s): Ukkola O, Poykko S. Source: Annals of Medicine. 2002; 34(2): 102-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12108573&dopt=Abstract
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Girls health Enrichment Multi-site Studies (GEMS): new approaches to obesity prevention among young African-American girls. Author(s): Obarzanek E, Pratt CA. Source: Ethn Dis. 2003 Winter; 13(1 Suppl 1): S1-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12713206&dopt=Abstract
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Glucagon administration elicits blunted GH but exaggerated ACTH response in obesity. Author(s): Tassone F, Grottoli S, Rossetto R, Maccagno B, Gauna C, Giordano R, Ghigo E, Maccario M. Source: J Endocrinol Invest. 2002 June; 25(6): 551-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12109628&dopt=Abstract
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Glucose transport and phosphorylation in skeletal muscle in obesity: insight from a muscle-specific positron emission tomography model. Author(s): Williams KV, Bertoldo A, Mattioni B, Price JC, Cobelli C, Kelley DE. Source: The Journal of Clinical Endocrinology and Metabolism. 2003 March; 88(3): 12719. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12629118&dopt=Abstract
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Glucose-dependent insulinotropic polypeptide analogues and their therapeutic potential for the treatment of obesity-diabetes. Author(s): Gault VA, Flatt PR, O'Harte FP. Source: Biochemical and Biophysical Research Communications. 2003 August 22; 308(2): 207-13. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12901855&dopt=Abstract
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Glycemic index and obesity. Author(s): Brand-Miller JC, Holt SH, Pawlak DB, McMillan J. Source: The American Journal of Clinical Nutrition. 2002 July; 76(1): 281S-5S. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12081852&dopt=Abstract
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Gourmand savants and environmental determinants of obesity. Author(s): Myslobodsky M. Source: Obesity Reviews : an Official Journal of the International Association for the Study of Obesity. 2003 May; 4(2): 121-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12760447&dopt=Abstract
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Guidance on surgery for morbid obesity. Author(s): Cooper R. Source: Br J Perioper Nurs. 2002 October; 12(10): 340. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12400389&dopt=Abstract
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Guidelines for childhood obesity prevention programs: promoting healthy weight in children. Author(s): Berg F, Buechner J, Parham E; Weight Realities Division of the Society for Nutrition Education. Source: Journal of Nutrition Education and Behavior. 2003 January-February; 35(1): 1-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12596730&dopt=Abstract
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Hand-assisted laparoscopic gastric bypass does not improve outcome and increases costs when compared to open gastric bypass for the surgical treatment of obesity. Author(s): DeMaria EJ, Schweitzer MA, Kellum JM, Meador J, Wolfe L, Sugerman HJ. Source: Surgical Endoscopy. 2002 October; 16(10): 1452-5. Epub 2002 June 14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12063573&dopt=Abstract
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Harry Potter and obesity. Author(s): Adami GF. Source: Obesity Surgery : the Official Journal of the American Society for Bariatric Surgery and of the Obesity Surgery Society of Australia and New Zealand. 2002 April; 12(2): 298. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11975235&dopt=Abstract
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Health consequences of obesity in youth: childhood predictors of adult disease. Author(s): Dietz WH. Source: Pediatrics. 1998 March; 101(3 Pt 2): 518-25. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12224658&dopt=Abstract
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Health consequences of obesity. Author(s): Reilly JJ, Methven E, McDowell ZC, Hacking B, Alexander D, Stewart L, Kelnar CJ. Source: Archives of Disease in Childhood. 2003 September; 88(9): 748-52. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12937090&dopt=Abstract
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Healthy Eating and Activity Together (HEAT): weapons against obesity. Author(s): Gottesman MM. Source: Journal of Pediatric Health Care : Official Publication of National Association of Pediatric Nurse Associates & Practitioners. 2003 July-August; 17(4): 210-5. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12847433&dopt=Abstract
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Herbal simulation of ephedrine and caffeine in treatment of obesity. Author(s): Dulloo AG. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2002 May; 26(5): 590-2. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12032740&dopt=Abstract
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High circulating ghrelin: a potential cause for hyperphagia and obesity in praderwilli syndrome. Author(s): DelParigi A, Tschop M, Heiman ML, Salbe AD, Vozarova B, Sell SM, Bunt JC, Tataranni PA. Source: The Journal of Clinical Endocrinology and Metabolism. 2002 December; 87(12): 5461-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12466337&dopt=Abstract
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High prevalence of obesity in asthmatic patients on sick leave. Author(s): Nathell L, Jensen I, Larsson K. Source: Respiratory Medicine. 2002 August; 96(8): 642-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12195847&dopt=Abstract
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High serum concentrations of soluble E-selectin correlate with obesity but not fat distribution in patients with type 2 diabetes mellitus. Author(s): Matsumoto K, Sera Y, Abe Y, Tominaga T, Horikami K, Hirao K, Ueki Y, Miyake S. Source: Metabolism: Clinical and Experimental. 2002 July; 51(7): 932-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12077744&dopt=Abstract
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High-insulinogenic nutrition--an etiologic factor for obesity and the metabolic syndrome? Author(s): Kopp W. Source: Metabolism: Clinical and Experimental. 2003 July; 52(7): 840-4. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12870158&dopt=Abstract
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Highlights from the annual scientific assembly: mechanisms to stop the epidemic of obesity: surgical therapy for obesity. Author(s): Sugerman HJ. Source: Southern Medical Journal. 2002 June; 95(6): 657-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12081225&dopt=Abstract
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Hip-Hop to Health Jr., an obesity prevention program for minority preschool children: baseline characteristics of participants. Author(s): Stolley MR, Fitzgibbon ML, Dyer A, Van Horn L, KauferChristoffel K, Schiffer L. Source: Preventive Medicine. 2003 March; 36(3): 320-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12634023&dopt=Abstract
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Histologic findings of gallbladder mucosa in 87 patients with morbid obesity without gallstones compared to 87 control subjects. Author(s): Csendes A, Burdiles P, Smok G, Csendes P, Burgos A, Recio M. Source: Journal of Gastrointestinal Surgery : Official Journal of the Society for Surgery of the Alimentary Tract. 2003 May-June; 7(4): 547-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12763414&dopt=Abstract
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Historical perspective: visceral obesity and related comorbidity in Joannes Baptista Morgagni's 'De sedibus et causis morborum per anatomen indagata'. Author(s): Enzi G, Busetto L, Inelmen EM, Coin A, Sergi G. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 April; 27(4): 534-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12664088&dopt=Abstract
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Homocysteine and psychological traits: a study in obesity. Author(s): Marchesini G, Manini R, Bianchi G, Sassi S, Natale S, Chierici S, Visani F, Baraldi L, Forlani G, Melchionda N. Source: Nutrition (Burbank, Los Angeles County, Calif.). 2002 May; 18(5): 403-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11985945&dopt=Abstract
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Hormonal regulation of human adipocytes at the cross-roads between obesity and hypertension. Author(s): Tikhonoff V, Staessen JA. Source: Journal of Hypertension. 2002 May; 20(5): 839-41. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12011640&dopt=Abstract
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Hormonal regulation of the human adipose-tissue renin-angiotensin system: relationship to obesity and hypertension. Author(s): Gorzelniak K, Engeli S, Janke J, Luft FC, Sharma AM. Source: Journal of Hypertension. 2002 May; 20(5): 965-73. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12011658&dopt=Abstract
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Human leptin administered intraperitoneally stimulates natriuresis and decreases renal medullary Na+, K+-ATPase activity in the rat -- impaired effect in dietaryinduced obesity. Author(s): Beltowski J, W jcicka G, Gorny D, Marciniak A. Source: Medical Science Monitor : International Medical Journal of Experimental and Clinical Research. 2002 June; 8(6): Br221-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12070427&dopt=Abstract
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Human obesity and type 2 diabetes are associated with alterations in SREBP1 isoform expression that are reproduced ex vivo by tumor necrosis factor-alpha. Author(s): Sewter C, Berger D, Considine RV, Medina G, Rochford J, Ciaraldi T, Henry R, Dohm L, Flier JS, O'Rahilly S, Vidal-Puig AJ. Source: Diabetes. 2002 April; 51(4): 1035-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11916923&dopt=Abstract
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Hunter-gatherers win profit-sharing deal for obesity drug. Author(s): Wise J. Source: Bulletin of the World Health Organization. 2003; 81(5): 382. Epub 2003 July 07. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12856057&dopt=Abstract
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Hyperglycaemic siblings of Type II (non-insulin-dependent) diabetic patients have increased PAI-1, central obesity and insulin resistance compared with their paired normoglycaemic sibling. Author(s): Herlihy OM, Barrow BA, Grant PJ, Levy JC. Source: Diabetologia. 2002 May; 45(5): 635-41. Epub 2002 April 26. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12107743&dopt=Abstract
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Hyperinsulinemia, dyslipidemia, and obesity as risk factors for hospitalized gallbladder disease. A prospective study. Author(s): Boland LL, Folsom AR, Rosamond WD; Atherosclerosis Risk in Communities (ARIC) Study Investigators. Source: Annals of Epidemiology. 2002 February; 12(2): 131-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11880221&dopt=Abstract
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Hyperinsulinism and overgrowth without obesity. Author(s): Srinivasan S, Waters MJ, Rowland JE, Baxter RC, Verge CF. Source: Archives of Disease in Childhood. 2003 April; 88(4): 332-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12651761&dopt=Abstract
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Hypertension and obesity after the menopause. Author(s): Rappelli A. Source: Journal of Hypertension. 2002 May; 20 Suppl 2: S26-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12183846&dopt=Abstract
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Hypertension and obesity. Author(s): Najman DM, Kapoor P, Serrano A, Tckachenko D. Source: Archives of Internal Medicine. 2003 May 12; 163(9): 1114-5; Author Reply 1115-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12742816&dopt=Abstract
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Hypertension and obesity. Author(s): Diaz ME. Source: Journal of Human Hypertension. 2002 March; 16 Suppl 1: S18-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11986887&dopt=Abstract
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Hypertension in obesity. Author(s): Redon J. Source: Nutr Metab Cardiovasc Dis. 2001 October; 11(5): 344-53. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11887431&dopt=Abstract
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Hypertension, obesity, and the renin-angiotensin system: a tale of tight associations. Author(s): Sibley S. Source: Minn Med. 2003 January; 86(1): 46-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12585560&dopt=Abstract
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Hypothalamic growth hormone-releasing hormone (GHRH) cell number is increased in human illness, but is not reduced in Prader-Willi syndrome or obesity. Author(s): Goldstone AP, Unmehopa UA, Swaab DF. Source: Clinical Endocrinology. 2003 June; 58(6): 743-55. Erratum In: Clin Endocrinol (Oxf). 2003 August; 59(2): 266. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12780752&dopt=Abstract
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Hypothalamic obesity in humans: what do we know and what can be done? Author(s): Pinkney J, Wilding J, Williams G, MacFarlane I. Source: Obesity Reviews : an Official Journal of the International Association for the Study of Obesity. 2002 February; 3(1): 27-34. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12119657&dopt=Abstract
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Images in cardiology: Massive epicardial adipose tissue indicating severe visceral obesity. Author(s): Iacobellis G, Leonetti F, Di Mario U. Source: Clin Cardiol. 2003 May; 26(5): 237. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12769252&dopt=Abstract
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Immunohistochemical identification of the beta(3)-adrenoceptor in intact human adipocytes and ventricular myocardium: effect of obesity and treatment with ephedrine and caffeine. Author(s): De Matteis R, Arch JR, Petroni ML, Ferrari D, Cinti S, Stock MJ. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2002 November; 26(11): 1442-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12439645&dopt=Abstract
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Impaired glucose tolerance: obesity and inactivity as modifiable risk factors. Author(s): Taylor K. Source: Adv Nurse Pract. 2001 December; 9(12): 59-61. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12400355&dopt=Abstract
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Implications of the prevalence of stunting, overweight and obesity amongst South African primary school children: a possible nutritional transition? Author(s): Jinabhai CC, Taylor M, Sullivan KR. Source: European Journal of Clinical Nutrition. 2003 February; 57(2): 358-65. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12571672&dopt=Abstract
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Increased abdominal obesity, insulin and glucose levels in nondiabetic subjects with a T29C polymorphism of the transforming growth factor-beta1 gene. Author(s): Rosmond R, Chagnon M, Bouchard C, Bjorntorp P. Source: Hormone Research. 2003; 59(4): 191-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12649573&dopt=Abstract
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Increased adrenal androgen levels in patients with Prader-Willi syndrome are associated with insulin, IGF-I, and leptin, but not with measures of obesity. Author(s): L'Allemand D, Eiholzer U, Rousson V, Girard J, Blum W, Torresani T, Gasser T. Source: Hormone Research. 2002; 58(5): 215-22. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12401940&dopt=Abstract
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Increased oxidative stress and hypozincemia in male obesity. Author(s): Ozata M, Mergen M, Oktenli C, Aydin A, Sanisoglu SY, Bolu E, Yilmaz MI, Sayal A, Isimer A, Ozdemir IC. Source: Clinical Biochemistry. 2002 November; 35(8): 627-31. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12498997&dopt=Abstract
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Increasing portion sizes in American diets: more calories, more obesity. Author(s): Nestle M. Source: Journal of the American Dietetic Association. 2003 January; 103(1): 39-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12525791&dopt=Abstract
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Increasing prevalence of type 2 diabetes mellitus in Thai children and adolescents associated with increasing prevalence of obesity. Author(s): Likitmaskul S, Kiattisathavee P, Chaichanwatanakul K, Punnakanta L, Angsusingha K, Tuchinda C. Source: J Pediatr Endocrinol Metab. 2003 January; 16(1): 71-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12585343&dopt=Abstract
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India sees parallel rise in malnutrition and obesity. Author(s): Chatterjee P. Source: Lancet. 2002 December 14; 360(9349): 1948. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12493270&dopt=Abstract
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Indices of obesity, dyslipidemia, and insulin resistance in apparently healthy Caribbean subjects. Author(s): Ezenwaka CE, Kalloo R. Source: Journal of Clinical Laboratory Analysis. 2003; 17(1): 6-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12526016&dopt=Abstract
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Infant feeding and obesity through the lifecourse. Author(s): Parsons TJ, Power C, Manor O. Source: Archives of Disease in Childhood. 2003 September; 88(9): 793-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12937101&dopt=Abstract
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Influence of depressive mood on the association of CRP and obesity in 3205 middle aged healthy men. Author(s): Ladwig KH, Marten-Mittag B, Lowel H, Doring A, Koenig W. Source: Brain, Behavior, and Immunity. 2003 August; 17(4): 268-75. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12831829&dopt=Abstract
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Influencing the childhood behaviors that lead to obesity: role of the pediatrician and health care professional. Author(s): Rivara FP, Whitaker R, Sherman PM, Cuttler L. Source: Archives of Pediatrics & Adolescent Medicine. 2003 August; 157(8): 719-20. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12912772&dopt=Abstract
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Insulin resistance in type 2 diabetes: association with truncal obesity, impaired fitness, and atypical malonyl coenzyme A regulation. Author(s): Bavenholm PN, Kuhl J, Pigon J, Saha AK, Ruderman NB, Efendic S. Source: The Journal of Clinical Endocrinology and Metabolism. 2003 January; 88(1): 82-7. Erratum In: J Clin Endocrinol Metab. 2003 May; 88(5): 2036. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12519834&dopt=Abstract
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Insulin resistance, impaired postprandial lipid metabolism and abdominal obesity. A deadly triad. Author(s): Frayn KN. Source: Medical Principles and Practice : International Journal of the Kuwait University, Health Science Centre. 2002; 11 Suppl 2: 31-40. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12444308&dopt=Abstract
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Insulin-stimulated protein kinase C lambda/zeta activity is reduced in skeletal muscle of humans with obesity and type 2 diabetes: reversal with weight reduction. Author(s): Kim YB, Kotani K, Ciaraldi TP, Henry RR, Kahn BB. Source: Diabetes. 2003 August; 52(8): 1935-42. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12882908&dopt=Abstract
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Interacting genetic loci on chromosomes 20 and 10 influence extreme human obesity. Author(s): Dong C, Wang S, Li WD, Li D, Zhao H, Price RA. Source: American Journal of Human Genetics. 2003 January; 72(1): 115-24. Epub 2002 December 11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12478478&dopt=Abstract
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Intermediate results following laparoscopic adjustable gastric banding for morbid obesity. Author(s): Victorzon M, Tolonen P. Source: Digestive Surgery. 2002; 19(5): 354-7; Discussion 358. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12435905&dopt=Abstract
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Inter-relationships between lifestyle and diabetes mellitus, overweight/obesity and hypertension in Nigeria. Author(s): Abidoye RO, Izunwa RD, Akinkuade FO, Abidoye GO. Source: Nutr Health. 2002; 16(3): 203-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12418804&dopt=Abstract
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Interventions for treating obesity in children. Author(s): Summerbell CD, Ashton V, Campbell KJ, Edmunds L, Kelly S, Waters E. Source: Cochrane Database Syst Rev. 2003; (3): Cd001872. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12917914&dopt=Abstract
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Intra-abdominal obesity and metabolic risk factors: a study of young adults. Author(s): von Eyben FE, Mouritsen E, Holm J, Montvilas P, Dimcevski G, Suciu G, Helleberg I, Kristensen L, von Eyben R. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 August; 27(8): 941-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12861235&dopt=Abstract
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Intracellular retention is a common characteristic of childhood obesity-associated MC4R mutations. Author(s): Lubrano-Berthelier C, Durand E, Dubern B, Shapiro A, Dazin P, Weill J, Ferron C, Froguel P, Vaisse C. Source: Human Molecular Genetics. 2003 January 15; 12(2): 145-53. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12499395&dopt=Abstract
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Is maternal obesity a predictor of shoulder dystocia? Author(s): Robinson H, Tkatch S, Mayes DC, Bott N, Okun N. Source: Obstetrics and Gynecology. 2003 January; 101(1): 24-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12517641&dopt=Abstract
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Is obesity a disease of the blood-brain barrier? Physiological, pathological, and evolutionary considerations. Author(s): Banks WA. Source: Current Pharmaceutical Design. 2003; 9(10): 801-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12678879&dopt=Abstract
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Is obesity a risk factor for cirrhosis-related death or hospitalization? A populationbased cohort study. Author(s): Ioannou GN, Weiss NS, Kowdley KV, Dominitz JA. Source: Gastroenterology. 2003 October; 125(4): 1053-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14517789&dopt=Abstract
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Is obesity associated with early sexual maturation? A comparison of the association in American boys versus girls. Author(s): Wang Y. Source: Pediatrics. 2002 November; 110(5): 903-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12415028&dopt=Abstract
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Is oxidant stress a connection between obesity and atherosclerosis? Author(s): Morrow JD. Source: Arteriosclerosis, Thrombosis, and Vascular Biology. 2003 March 1; 23(3): 368-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12639824&dopt=Abstract
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Is the Canadian childhood obesity epidemic related to physical inactivity? Author(s): Tremblay MS, Willms JD. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 September; 27(9): 1100-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12917717&dopt=Abstract
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Is the gender difference in LDL size explained by the metabolic complications of visceral obesity? Author(s): Lemieux I, Pascot A, Lamarche B, Prud'homme D, Nadeau A, Bergeron J, Despres JP. Source: European Journal of Clinical Investigation. 2002 December; 32(12): 909-17. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12534450&dopt=Abstract
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JAMA patient page. Obesity. Author(s): Torpy JM, Lynm C, Glass RM. Source: Jama : the Journal of the American Medical Association. 2003 April 9; 289(14): 1880. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12684367&dopt=Abstract
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Jejunoileal bypass in the treatment of morbid obesity: a 25-year follow-up study of 36 patients. Author(s): Vage V, Solhaug JH, Berstad A, Svanes K, Viste A. Source: Obesity Surgery : the Official Journal of the American Society for Bariatric Surgery and of the Obesity Surgery Society of Australia and New Zealand. 2002 June; 12(3): 312-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12082879&dopt=Abstract
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Laparoscopic adjustable gastric banding for morbid obesity. Author(s): Ferraro DR. Source: Aorn Journal. 2003 May; 77(5): 923-40; Quiz 942-4. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12769325&dopt=Abstract
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Laparoscopic adjustable gastric banding in the treatment of morbid obesity. Author(s): O'Brien PE, Dixon JB. Source: Archives of Surgery (Chicago, Ill. : 1960). 2003 April; 138(4): 376-82. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12686523&dopt=Abstract
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Laparoscopic adjustable gastric banding with duodenal switch for morbid obesity: technique and preliminary results. Author(s): Gagner M, Steffen R, Biertho L, Horber F. Source: Obesity Surgery : the Official Journal of the American Society for Bariatric Surgery and of the Obesity Surgery Society of Australia and New Zealand. 2003 June; 13(3): 444-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12841909&dopt=Abstract
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Laparoscopic era of operations for morbid obesity. Author(s): Cottam DR, Mattar SG, Schauer PR. Source: Archives of Surgery (Chicago, Ill. : 1960). 2003 April; 138(4): 367-75. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12686522&dopt=Abstract
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Laparoscopic gastric banding: a minimally invasive surgical treatment for morbid obesity: prospective study of 500 consecutive patients. Author(s): Zinzindohoue F, Chevallier JM, Douard R, Elian N, Ferraz JM, Blanche JP, Berta JL, Altman JJ, Safran D, Cugnenc PH. Source: Annals of Surgery. 2003 January; 237(1): 1-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12496523&dopt=Abstract
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Laparoscopic gastric bypass for morbid obesity with linear gastroenterostomy. Author(s): Korenkov M, Goh P, Yucel N, Troidl H. Source: Obesity Surgery : the Official Journal of the American Society for Bariatric Surgery and of the Obesity Surgery Society of Australia and New Zealand. 2003 June; 13(3): 360-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12841894&dopt=Abstract
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Laparoscopic management of complications following laparoscopic Roux-en-Y gastric bypass for morbid obesity. Author(s): Papasavas PK, Caushaj PF, McCormick JT, Quinlin RF, Hayetian FD, Maurer J, Kelly JJ, Gagne DJ. Source: Surgical Endoscopy. 2003 April; 17(4): 610-4. Epub 2003 February 17. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12582772&dopt=Abstract
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Laser acupuncture and low-calorie diet during visceral obesity therapy after menopause. Author(s): Wozniak P, Stachowiak G, Pieta-Dolinska A, Oszukowski P. Source: Acta Obstetricia Et Gynecologica Scandinavica. 2003 January; 82(1): 69-73. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12580844&dopt=Abstract
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Left atrial size in children with hypertension: the influence of obesity, blood pressure, and left ventricular mass. Author(s): Daniels SR, Witt SA, Glascock B, Khoury PR, Kimball TR. Source: The Journal of Pediatrics. 2002 August; 141(2): 186-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12183712&dopt=Abstract
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Legal interest expands from tobacco to obesity. Author(s): Willensky D. Source: Bulletin of the World Health Organization. 2003; 81(4): 309-10. Epub 2003 May 16. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12764502&dopt=Abstract
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Leisure-time activity is an important determinant of long-term weight maintenance after weight loss in the Sibutramine Trial on Obesity Reduction and Maintenance (STORM trial). Author(s): van Baak MA, van Mil E, Astrup AV, Finer N, Van Gaal LF, Hilsted J, Kopelman PG, Rossner S, James WP, Saris WH; STORM Study Group. Source: The American Journal of Clinical Nutrition. 2003 August; 78(2): 209-14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12885699&dopt=Abstract
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Leptin and the central neural mechanisms of obesity hypertension. Author(s): Rahmouni K, G Haynes W. Source: Drugs Today (Barc). 2002 December; 38(12): 807-17. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12582470&dopt=Abstract
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Leptin and the treatment of obesity: its current status. Author(s): Eur J Pharmacol. 2002 Aug 16;450(1):93-109 Source: European Journal of Pharmacology. 2002 April 12; 440(2-3): 129-39. Review. /entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12176114
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Leptin: a novel link between obesity, diabetes, cardiovascular risk, and ventricular hypertrophy. Author(s): Sader S, Nian M, Liu P. Source: Circulation. 2003 August 12; 108(6): 644-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12912793&dopt=Abstract
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Letting the "Gini" out of the bottle: social causation and the obesity epidemic. Author(s): Goodman E. Source: The Journal of Pediatrics. 2003 March; 142(3): 228-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12640364&dopt=Abstract
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Leukocytosis and hyperleptinemia in obesity: is there a link? Author(s): Perfetto F, Mancuso F, Tarquini R. Source: Haematologica. 2002 May; 87(5): Elt25. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12010685&dopt=Abstract
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Lifestyle factors, obesity and the risk of chronic kidney disease. Author(s): Stengel B, Tarver-Carr ME, Powe NR, Eberhardt MS, Brancati FL. Source: Epidemiology (Cambridge, Mass.). 2003 July; 14(4): 479-87. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12843775&dopt=Abstract
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Lifestyle modification in the management of obesity. Author(s): Wadden TA, McGuckin BG, Rothman RA, Sargent SL. Source: Journal of Gastrointestinal Surgery : Official Journal of the Society for Surgery of the Alimentary Tract. 2003 May-June; 7(4): 452-63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12763398&dopt=Abstract
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Linkage and linkage disequilibrium mapping of genes influencing human obesity in chromosome region 7q22.1-7q35. Author(s): Li WD, Li D, Wang S, Zhang S, Zhao H, Price RA. Source: Diabetes. 2003 June; 52(6): 1557-61. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12765970&dopt=Abstract
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Links between body mass index, total body fat, cholesterol, high-density lipoprotein, and insulin sensitivity in patients with obesity related to depression, anger, and anxiety. Author(s): Laederach-Hofmann K, Kupferschmid S, Mussgay L. Source: The International Journal of Eating Disorders. 2002 July; 32(1): 58-71. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12183947&dopt=Abstract
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Liver volume and visceral obesity in women with hepatic steatosis undergoing gastric banding. Author(s): Busetto L, Tregnaghi A, De Marchi F, Segato G, Foletto M, Sergi G, Favretti F, Lise M, Enzi G. Source: Obesity Research. 2002 May; 10(5): 408-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12006641&dopt=Abstract
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Local and systemic impact of transcriptional up-regulation of 11beta-hydroxysteroid dehydrogenase type 1 in adipose tissue in human obesity. Author(s): Wake DJ, Rask E, Livingstone DE, Soderberg S, Olsson T, Walker BR. Source: The Journal of Clinical Endocrinology and Metabolism. 2003 August; 88(8): 3983-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12915696&dopt=Abstract
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Localized lichen myxoedematosus (papular mucinosis) associated with morbid obesity: report of two cases. Author(s): Saez-Rodriguez M, Garcia-Bustinduy M, Lopez-Alba A, Noda-Cabrera A, Guimera-Martin-Neda F, Dorta-Alom S, Escoda-Garcia M, Fagundo-Gonzalez E, Sanchez-Gonzalez R, Martin-Herrera A, Garcia-Montelongo R. Source: The British Journal of Dermatology. 2003 January; 148(1): 165-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12534614&dopt=Abstract
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Longitudinal analysis of changes in indices of obesity from age 8 years to age 18 years. Project HeartBeat! Author(s): Dai S, Labarthe DR, Grunbaum JA, Harrist RB, Mueller WH. Source: American Journal of Epidemiology. 2002 October 15; 156(8): 720-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12370160&dopt=Abstract
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Long-term and recent time trends in the prevalence of obesity among Dutch men and women. Author(s): Visscher TL, Kromhout D, Seidell JC. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2002 September; 26(9): 1218-24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12187399&dopt=Abstract
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Long-term data indicate a progressive loss in efficacy of adjustable silicone gastric banding for the surgical treatment of morbid obesity. Author(s): Doherty C, Maher JW, Heitshusen DS. Source: Surgery. 2002 October; 132(4): 724-7; Discussion 727-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12407358&dopt=Abstract
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Long-term results of laparoscopic adjustable gastric banding for the treatment of morbid obesity. Author(s): Belachew M, Belva PH, Desaive C. Source: Obesity Surgery : the Official Journal of the American Society for Bariatric Surgery and of the Obesity Surgery Society of Australia and New Zealand. 2002 August; 12(4): 564-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12194552&dopt=Abstract
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Low adiponectin levels in adolescent obesity: a marker of increased intramyocellular lipid accumulation. Author(s): Weiss R, Dufour S, Groszmann A, Petersen K, Dziura J, Taksali SE, Shulman G, Caprio S. Source: The Journal of Clinical Endocrinology and Metabolism. 2003 May; 88(5): 2014-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12727947&dopt=Abstract
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Low circulating IGF-II concentrations predict weight gain and obesity in humans. Author(s): Sandhu MS, Gibson JM, Heald AH, Dunger DB, Wareham NJ. Source: Diabetes. 2003 June; 52(6): 1403-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12765950&dopt=Abstract
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Low plasma antioxidants and normal plasma B vitamins and homocysteine in patients with severe obesity. Author(s): Reitman A, Friedrich I, Ben-Amotz A, Levy Y. Source: Isr Med Assoc J. 2002 August; 4(8): 590-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12183861&dopt=Abstract
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Management and treatment of obesity. Author(s): Zizza CA. Source: Southern Medical Journal. 2003 June; 96(6): 537-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12938777&dopt=Abstract
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Management of obesity as a chronic disease: nonpharmacologic, pharmacologic, and surgical options. Author(s): Fujioka K. Source: Obesity Research. 2002 December; 10 Suppl 2: 116S-123S. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12490660&dopt=Abstract
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Managing obesity. Author(s): Rabinowitz E. Source: Healthplan. 2003 January-February; 44(1): 40-2, 44-5. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12611252&dopt=Abstract
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Managing overweight and obesity in women. Author(s): Klauer J, Aronne LJ. Source: Clinical Obstetrics and Gynecology. 2002 December; 45(4): 1080-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12438886&dopt=Abstract
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Maternal gestational diabetes, birth weight, and adolescent obesity. Author(s): Gillman MW, Rifas-Shiman S, Berkey CS, Field AE, Colditz GA. Source: Pediatrics. 2003 March; 111(3): E221-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12612275&dopt=Abstract
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Maternal obesity and breast-feeding practices. Author(s): Li R, Jewell S, Grummer-Strawn L. Source: The American Journal of Clinical Nutrition. 2003 April; 77(4): 931-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12663294&dopt=Abstract
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Maternal obesity and pregnancy outcomes. Author(s): Castro LC, Avina RL. Source: Current Opinion in Obstetrics & Gynecology. 2002 December; 14(6): 601-6. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12441699&dopt=Abstract
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Maternal obesity and risk for birth defects. Author(s): Watkins ML, Rasmussen SA, Honein MA, Botto LD, Moore CA. Source: Pediatrics. 2003 May; 111(5 Part 2): 1152-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12728129&dopt=Abstract
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Measurement of sleep apnea during obesity treatment. Author(s): Billington CJ. Source: Obesity Research. 2002 November; 10 Suppl 1: 38S-41S. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12446857&dopt=Abstract
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Measuring food intake in studies of obesity. Author(s): Lissner L. Source: Public Health Nutrition. 2002 December; 5(6A): 889-92. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12638596&dopt=Abstract
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Medical and surgical options in the treatment of severe obesity. Author(s): Fisher BL, Schauer P. Source: American Journal of Surgery. 2002 December; 184(6B): 9S-16S. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12527344&dopt=Abstract
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Medical management of obesity: a clinical imperative? Author(s): Haynes WG. Source: Curr Diab Rep. 2003 February; 3(1): 1-3. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12643140&dopt=Abstract
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Medical management of obesity: present and future therapy. Author(s): Klein S. Source: Journal of Gastrointestinal Surgery : Official Journal of the Society for Surgery of the Alimentary Tract. 2003 May-June; 7(4): 464-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12763399&dopt=Abstract
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Melanocortin-3-receptor gene variants in morbid obesity. Author(s): Schalin-Jantti C, Valli-Jaakola K, Oksanen L, Martelin E, Laitinen K, Krusius T, Mustajoki P, Heikinheimo M, Kontula K. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 January; 27(1): 70-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12532156&dopt=Abstract
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Melanocortin-4 receptor gene: case-control study and transmission disequilibrium test confirm that functionally relevant mutations are compatible with a major gene effect for extreme obesity. Author(s): Hinney A, Hohmann S, Geller F, Vogel C, Hess C, Wermter AK, Brokamp B, Goldschmidt H, Siegfried W, Remschmidt H, Schafer H, Gudermann T, Hebebrand J. Source: The Journal of Clinical Endocrinology and Metabolism. 2003 September; 88(9): 4258-67. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12970296&dopt=Abstract
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Metabolic disturbances in obesity versus sleep apnoea: the importance of visceral obesity and insulin resistance. Author(s): Vgontzas AN, Bixler EO, Chrousos GP. Source: Journal of Internal Medicine. 2003 July; 254(1): 32-44. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12823641&dopt=Abstract
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Metabolic effects of the Gly1057Asp polymorphism in IRS-2 and interactions with obesity. Author(s): Stefan N, Kovacs P, Stumvoll M, Hanson RL, Lehn-Stefan A, Permana PA, Baier LJ, Tataranni PA, Silver K, Bogardus C. Source: Diabetes. 2003 June; 52(6): 1544-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12765968&dopt=Abstract
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Metabolic syndrome & obesity: co-epidemics could overwhelm home health care. Author(s): Pearce LC. Source: Caring. 2003 June; 22(6): 24-8, 30, 32-3; Quiz 34-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12905569&dopt=Abstract
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Methods of estimating years of life lost due to obesity. Author(s): Peeters A, Bonneux L, Barendregt J, Nusselder W. Source: Jama : the Journal of the American Medical Association. 2003 June 11; 289(22): 2941; Author Reply 2941-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12799399&dopt=Abstract
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Midface hypoplasia, obesity, developmental delay and neonatal hypotonia in two brothers. Author(s): Rozendaal L, Del Canho H, Waterham HR, Hennekam RC. Source: Clinical Dysmorphology. 2003 January; 12(1): 9-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12514359&dopt=Abstract
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Minireview: From anorexia to obesity--the yin and yang of body weight control. Author(s): Zigman JM, Elmquist JK. Source: Endocrinology. 2003 September; 144(9): 3749-56. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12933644&dopt=Abstract
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Minireview: human obesity-lessons from monogenic disorders. Author(s): O'Rahilly S, Farooqi IS, Yeo GS, Challis BG. Source: Endocrinology. 2003 September; 144(9): 3757-64. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12933645&dopt=Abstract
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Modifications of blood pressure and IGF-I levels after weight loss in obesity. Author(s): Dall'Aglio E, Salimbeni I, Rocci A, Mazzoni S, Corradi F, Cattadori E, Visioli S, Banchini A, Valenti G, Ceda GP. Source: J Endocrinol Invest. 2002; 25(10 Suppl): 107-9. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12508940&dopt=Abstract
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Molecular and genetic mechanisms of obesity: implications for future management. Author(s): Liu YJ, Araujo S, Recker RR, Deng HW. Source: Current Molecular Medicine. 2003 June; 3(4): 325-40. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12776988&dopt=Abstract
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Molecular genetics of human obesity-associated MC4R mutations. Author(s): Lubrano-Berthelier C, Cavazos M, Dubern B, Shapiro A, Stunff CL, Zhang S, Picart F, Govaerts C, Froguel P, Bougneres P, Clement K, Vaisse C. Source: Annals of the New York Academy of Sciences. 2003 June; 994: 49-57. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12851297&dopt=Abstract
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Morbid obesity and hypersomnolence in several members of an ancient royal family. Author(s): Michalopoulos A, Tzelepis G, Geroulanos S. Source: Thorax. 2003 March; 58(3): 281-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12612315&dopt=Abstract
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Morbid obesity and postoperative pulmonary atelectasis: an underestimated problem. Author(s): Eichenberger A, Proietti S, Wicky S, Frascarolo P, Suter M, Spahn DR, Magnusson L. Source: Anesthesia and Analgesia. 2002 December; 95(6): 1788-92, Table of Contents. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12456460&dopt=Abstract
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Morbid obesity: the disease and comorbidities. Author(s): Owens TM. Source: Critical Care Nursing Quarterly. 2003 April-June; 26(2): 162-5. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12744597&dopt=Abstract
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Muscle fiber type is associated with obesity and weight loss. Author(s): Tanner CJ, Barakat HA, Dohm GL, Pories WJ, MacDonald KG, Cunningham PR, Swanson MS, Houmard JA. Source: American Journal of Physiology. Endocrinology and Metabolism. 2002 June; 282(6): E1191-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12006347&dopt=Abstract
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Musculoskeletal pain in the obese: a comparison with a general population and longterm changes after conventional and surgical obesity treatment. Author(s): Peltonen M, Lindroos AK, Torgerson JS. Source: Pain. 2003 August; 104(3): 549-57. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12927627&dopt=Abstract
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Nasal continuous positive airway pressure improves quality of life in obesity hypoventilation syndrome. Author(s): Hida W, Okabe S, Tatsumi K, Kimura H, Akasiba T, Chin K, Ohi M, Nakayama H, Satoh M, Kuriyama T. Source: Sleep & Breathing = Schlaf & Atmung. 2003 March; 7(1): 3-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12712392&dopt=Abstract
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National and international strategies to prevent obesity and diabetes. Author(s): Reeder BA. Source: Advances in Experimental Medicine and Biology. 2001; 498: 393-400. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11900397&dopt=Abstract
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National Cholesterol Education Program Adult Treatment Panel III guidelines and obesity: implications for Canada. Author(s): Ardern CI, Katzmarzyk PT. Source: The Canadian Journal of Cardiology. 2003 September; 19(10): 1171-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14532943&dopt=Abstract
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Neonatal nutrition: metabolic programming of pancreatic islets and obesity. Author(s): Srinivasan M, Laychock SG, Hill DJ, Patel MS. Source: Experimental Biology and Medicine (Maywood, N.J.). 2003 January; 228(1): 1523. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12524468&dopt=Abstract
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Neuroendocrine and metabolic determinants of the adaptation of GH/IGF-I axis to obesity. Author(s): Maccario M, Tassone F, Grottoli S, Rossetto R, Gauna C, Ghigo E. Source: Annales D'endocrinologie. 2002 April; 63(2 Pt 1): 140-4. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11994678&dopt=Abstract
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Neuroendocrine and peripheral activities of ghrelin: implications in metabolism and obesity. Author(s): Muccioli G, Tschop M, Papotti M, Deghenghi R, Heiman M, Ghigo E. Source: European Journal of Pharmacology. 2002 April 12; 440(2-3): 235-54. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12007539&dopt=Abstract
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Neuroimaging and obesity: mapping the brain responses to hunger and satiation in humans using positron emission tomography. Author(s): Del Parigi A, Gautier JF, Chen K, Salbe AD, Ravussin E, Reiman E, Tataranni PA. Source: Annals of the New York Academy of Sciences. 2002 June; 967: 389-97. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12079866&dopt=Abstract
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Neuropeptide Y receptors as targets for anti-obesity drug development: perspective and current status. Author(s): Parker E, Van Heek M, Stamford A. Source: European Journal of Pharmacology. 2002 April 12; 440(2-3): 173-87. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12007534&dopt=Abstract
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New criteria for 'obesity disease' in Japan. Author(s): Examination Committee of Criteria for 'Obesity Disease' in Japan; Japan Society for the Study of Obesity. Source: Circulation Journal : Official Journal of the Japanese Circulation Society. 2002 November; 66(11): 987-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12419927&dopt=Abstract
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New insights in obesity. Author(s): Bloomgarden ZT. Source: Diabetes Care. 2002 April; 25(4): 789-95. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11919138&dopt=Abstract
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New Moves: a school-based obesity prevention program for adolescent girls. Author(s): Neumark-Sztainer D, Story M, Hannan PJ, Rex J. Source: Preventive Medicine. 2003 July; 37(1): 41-51. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12799128&dopt=Abstract
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New obesity center at WVU offering comprehensive program.. Author(s): Dino GA, Cohen D, Tessaro I, Ducatman A. Source: W V Med J. 2002 November-December; 98(6): 288-9. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12645285&dopt=Abstract
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New pharmacological tools for obesity. Author(s): Nisoli E, Carruba MO. Source: J Endocrinol Invest. 2002 November; 25(10): 905-14. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12508954&dopt=Abstract
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Nicotine, body weight and potential implications in the treatment of obesity. Author(s): Li MD, Kane JK, Konu O. Source: Current Topics in Medicinal Chemistry. 2003; 3(8): 899-919. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12678839&dopt=Abstract
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Night eating in obesity: a descriptive study. Author(s): Adami GF, Campostano A, Marinari GM, Ravera G, Scopinaro N. Source: Nutrition (Burbank, Los Angeles County, Calif.). 2002 July-August; 18(7-8): 5879. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12093435&dopt=Abstract
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No association found between the Ala54Thr polymorphism of FABP2 gene and obesity and obesity with dyslipidemia in Japanese schoolchildren. Author(s): Endo K, Yanagi H, Hirano C, Hayakawa Y, Hamaguchi H, Tomura S. Source: J Atheroscler Thromb. 2001; 8(3): 80-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11866034&dopt=Abstract
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No evidence for involvement of the calpain-10 gene 'high-risk' haplotype combination for non-insulin-dependent diabetes mellitus in early onset obesity. Author(s): Hinney A, Antwerpen B, Geller F, Schafer H, Siegfried W, Goldschmidt H, Remschmidt H, Ziegler A, Hebebrand J. Source: Molecular Genetics and Metabolism. 2002 June; 76(2): 152-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12083814&dopt=Abstract
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No influence of obesity on the pharmacokinetics and pharmacodynamics of melagatran, the active form of the oral direct thrombin inhibitor ximelagatran. Author(s): Sarich TC, Teng R, Peters GR, Wollbratt M, Homolka R, Svensson M, Eriksson UG. Source: Clinical Pharmacokinetics. 2003; 42(5): 485-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12739986&dopt=Abstract
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No linkage to obesity in candidate regions of chromosome 2 and 10 in a selected sample of Swedish twins. Author(s): Iliadou A, Lichtenstein P, Ahlberg S, Hoffstedt J, Arner P, Schalling M, Pedersen NL, Lavebratt C. Source: Twin Research : the Official Journal of the International Society for Twin Studies. 2003 April; 6(2): 162-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12724003&dopt=Abstract
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Non-communicable diseases (diabetes, obesity and hyperlipidaemia) in urban slums. Author(s): Misra A, Pandey RM, Sharma R. Source: Natl Med J India. 2002 July-August; 15(4): 242-4. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12296484&dopt=Abstract
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Nutrition for health promotion: phytochemicals, functional foods, and alternative approaches to combat obesity. Author(s): Bloch AS. Source: Dent Clin North Am. 2003 April; 47(2): 411-23, Viii-Ix. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12699239&dopt=Abstract
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Nutrition, physical activity, and obesity. Author(s): Jacobson MF. Source: Lancet. 2002 October 19; 360(9341): 1250. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12401275&dopt=Abstract
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Nutrition, physical activity, and obesity. Author(s): Summers JB, Kaminski JM. Source: Lancet. 2002 October 19; 360(9341): 1249. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12401274&dopt=Abstract
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Nutrition, physical activity, and obesity. Author(s): Kerr D, James J. Source: Lancet. 2002 October 19; 360(9341): 1249. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12401273&dopt=Abstract
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Nutrition, physical activity, and obesity. Author(s): Das UN, Meguid MM. Source: Lancet. 2002 October 19; 360(9341): 1249-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12401272&dopt=Abstract
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Nutritional advice for obesity management and health. Author(s): Hunking P. Source: British Journal of Community Nursing. 2002 May; 7(5): 246-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12048498&dopt=Abstract
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Nutritional risk assessment and obesity in rural older adults: a sex difference. Author(s): Ledikwe JH, Smiciklas-Wright H, Mitchell DC, Jensen GL, Friedmann JM, Still CD. Source: The American Journal of Clinical Nutrition. 2003 March; 77(3): 551-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12600842&dopt=Abstract
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Obesity - a global problem. Author(s): Siddiqui NI. Source: Mymensingh Med J. 2003 July; 12(2): 76-7. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12894035&dopt=Abstract
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Obesity and cancer. Author(s): Abu-Abid S, Szold A, Klausner J. Source: J Med. 2002; 33(1-4): 73-86. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12939106&dopt=Abstract
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Obesity and cancer. Author(s): Smith JA. Source: The New England Journal of Medicine. 2003 July 31; 349(5): 502-4; Author Reply 502-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12892104&dopt=Abstract
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Obesity and cancer. Author(s): Gaesser GA. Source: The New England Journal of Medicine. 2003 July 31; 349(5): 502-4; Author Reply 502-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12892103&dopt=Abstract
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Obesity and cancer. Author(s): Frankel PH. Source: The New England Journal of Medicine. 2003 July 31; 349(5): 502-4; Author Reply 502-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12892102&dopt=Abstract
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Obesity and cancer. Author(s): Flegal KM, Williamson DF, Graubard BI. Source: The New England Journal of Medicine. 2003 July 31; 349(5): 502-4; Author Reply 502-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12892101&dopt=Abstract
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Obesity and cancer. Author(s): Deutsch ME. Source: The New England Journal of Medicine. 2003 July 31; 349(5): 502-4; Author Reply 502-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12890851&dopt=Abstract
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Obesity and cardiovascular disease: the hippocrates paradox? Author(s): Lavie CJ, Milani RV. Source: Journal of the American College of Cardiology. 2003 August 20; 42(4): 677-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12932600&dopt=Abstract
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Obesity and diabetes in African American women. Author(s): Tilghman J. Source: The Abnf Journal : Official Journal of the Association of Black Nursing Faculty in Higher Education, Inc. 2003 May-June; 14(3): 66-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12856444&dopt=Abstract
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Obesity and hip osteoarthritis. Author(s): Lievense AM, Reijman M, Pols HA, Bierma-Zeinstra SM. Source: The American Journal of Medicine. 2003 September; 115(4): 329; Author Reply 329-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12967700&dopt=Abstract
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Obesity and its nurturing effect on hepatitis C. Author(s): McCullough AJ. Source: Hepatology (Baltimore, Md.). 2003 September; 38(3): 557-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12939581&dopt=Abstract
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Obesity and low back pain. Author(s): Bener A, Alwash R, Gaber T, Lovasz G. Source: Coll Antropol. 2003 June; 27(1): 95-104. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12974137&dopt=Abstract
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Obesity and overweight among adults in North Carolina. Author(s): Buescher PA. Source: N C Med J. 2002 November-December; 63(6): 287. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12970975&dopt=Abstract
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Obesity and pregnancy--the propagation of a viscous cycle? Author(s): Catalano PM. Source: The Journal of Clinical Endocrinology and Metabolism. 2003 August; 88(8): 3505-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12915626&dopt=Abstract
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Obesity and the heart: an ever-growing problem. Author(s): Lavie CJ, Milani RV, Messerli FH. Source: Southern Medical Journal. 2003 June; 96(6): 535-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12938776&dopt=Abstract
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Obesity and the risk of early and late mortality after coronary artery bypass graft surgery. Author(s): Kim J, Hammar N, Jakobsson K, Luepker RV, McGovern PG, Ivert T. Source: American Heart Journal. 2003 September; 146(3): 555-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12947378&dopt=Abstract
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Obesity and the risk of newly diagnosed asthma in school-age children. Author(s): Gilliland FD, Berhane K, Islam T, McConnell R, Gauderman WJ, Gilliland SS, Avol E, Peters JM. Source: American Journal of Epidemiology. 2003 September 1; 158(5): 406-15. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12936895&dopt=Abstract
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Obesity as a potential risk factor for adenocarcinomas and squamous cell carcinomas of the uterine cervix. Author(s): Lacey JV Jr, Swanson CA, Brinton LA, Altekruse SF, Barnes WA, Gravitt PE, Greenberg MD, Hadjimichael OC, McGowan L, Mortel R, Schwartz PE, Kurman RJ, Hildesheim A. Source: Cancer. 2003 August 15; 98(4): 814-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12910527&dopt=Abstract
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Obesity goes global. Author(s): Nash JM. Source: Time. 2003 August 25; 162(8): 53-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12964464&dopt=Abstract
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Obesity in 70-year-old subjects as a risk factor for 15-year coronary heart disease incidence. Author(s): Dey DK, Lissner L. Source: Obesity Research. 2003 July; 11(7): 817-27. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12855750&dopt=Abstract
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Obesity in African American women. Author(s): July FM. Source: The Abnf Journal : Official Journal of the Association of Black Nursing Faculty in Higher Education, Inc. 2003 May-June; 14(3): 55. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12856441&dopt=Abstract
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Obesity in general elective surgery. Author(s): McCarthy R, Leslie T, Williams DJ. Source: Lancet. 2003 August 16; 362(9383): 577; Author Reply 577-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12932397&dopt=Abstract
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Obesity in general elective surgery. Author(s): Slim K, Kwiatkowski F, Chipponi J. Source: Lancet. 2003 August 16; 362(9383): 577; Author Reply 577-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12932396&dopt=Abstract
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Obesity in general elective surgery. Author(s): Pravinkumar E. Source: Lancet. 2003 August 16; 362(9383): 576-7; Author Reply 577-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12932394&dopt=Abstract
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Obesity is associated with impaired platelet-inhibitory effect of acetylsalicylic acid in nondiabetic subjects. Author(s): Tamminen M, Lassila R, Westerbacka J, Vehkavaara S, Yki-Jarvinen H. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 August; 27(8): 907-11. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12861231&dopt=Abstract
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Obesity prevention in pediatric primary care: four behaviors to target. Author(s): Whitaker RC. Source: Archives of Pediatrics & Adolescent Medicine. 2003 August; 157(8): 725-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12912775&dopt=Abstract
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Obesity, tamoxifen use, and outcomes in women with estrogen receptor-positive early-stage breast cancer. Author(s): Dignam JJ, Wieand K, Johnson KA, Fisher B, Xu L, Mamounas EP. Source: Journal of the National Cancer Institute. 2003 October 1; 95(19): 1467-76. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14519753&dopt=Abstract
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Obesity: an epidemic. Author(s): Hamdy RC. Source: Southern Medical Journal. 2003 June; 96(6): 531-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12938774&dopt=Abstract
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Obesity: associations with acute mountain sickness. Author(s): Ri-Li G, Chase PJ, Witkowski S, Wyrick BL, Stone JA, Levine BD, Babb TG. Source: Annals of Internal Medicine. 2003 August 19; 139(4): 253-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12965980&dopt=Abstract
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Overweight and obesity prevalence rates among youth in the Carolinas. Author(s): Terrell DF. Source: N C Med J. 2002 November-December; 63(6): 281-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12970974&dopt=Abstract
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Pediatric obesity policy: the danger of skepticism. Author(s): Cuttler L, Whittaker JL, Kodish ED. Source: Archives of Pediatrics & Adolescent Medicine. 2003 August; 157(8): 722-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12912774&dopt=Abstract
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Peroxisome proliferator activated receptors and obesity. Author(s): Kersten S. Source: European Journal of Pharmacology. 2002 April 12; 440(2-3): 223-34. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12007538&dopt=Abstract
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Perspectives on childhood obesity. Author(s): Strauss R. Source: Current Gastroenterology Reports. 2002 June; 4(3): 244-50. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12010626&dopt=Abstract
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Pharmacoeconomics of obesity management in childhood and adolescence. Author(s): Kiess W, Bottner A, Bluher S, Raile K, Seidel B, Kapellen T, Keller E, Kratzsch J. Source: Expert Opinion on Pharmacotherapy. 2003 September; 4(9): 1471-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12943476&dopt=Abstract
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Pharmacological therapy of obesity: past, present, and future. Author(s): Weigle DS. Source: The Journal of Clinical Endocrinology and Metabolism. 2003 June; 88(6): 2462-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12788841&dopt=Abstract
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Pharmacotherapy of obesity: an update. Author(s): Schurgin S, Siegel RD. Source: Nutrition in Clinical Care : an Official Publication of Tufts University. 2003 January-April; 6(1): 27-37. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12841428&dopt=Abstract
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Photo quiz. Obesity and daytime sleepiness. Prader-Willi syndrome. Author(s): Baumgart DC, Gerl H. Source: American Family Physician. 2003 July 1; 68(1): 151-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12887122&dopt=Abstract
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Physical activity, obesity, and the incidence of type 2 diabetes in a high-risk population. Author(s): Kriska AM, Saremi A, Hanson RL, Bennett PH, Kobes S, Williams DE, Knowler WC. Source: American Journal of Epidemiology. 2003 October 1; 158(7): 669-75. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14507603&dopt=Abstract
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Physical inactivity, energy intake, obesity and the risk of rectal cancer in Canada. Author(s): Mao Y, Pan S, Wen SW, Johnson KC; Canadian Cancer Registries Epidemiology Research Group. Source: International Journal of Cancer. Journal International Du Cancer. 2003 July 20; 105(6): 831-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12767070&dopt=Abstract
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Plasmalemmal fatty acid transport is regulated in heart and skeletal muscle by contraction, insulin and leptin, and in obesity and diabetes. Author(s): Bonen A, Benton CR, Campbell SE, Chabowski A, Clarke DC, Han XX, Glatz JF, Luiken JJ. Source: Acta Physiologica Scandinavica. 2003 August; 178(4): 347-56. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12864739&dopt=Abstract
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Plasminogen activator inhibitor-1, inflammation, obesity, insulin resistance and vascular risk. Author(s): Juhan-Vague I, Alessi MC, Mavri A, Morange PE. Source: Journal of Thrombosis and Haemostasis : Jth. 2003 July; 1(7): 1575-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12871293&dopt=Abstract
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Poor cell surface expression of human melanocortin-4 receptor mutations associated with obesity. Author(s): Nijenhuis WA, Garner KM, van Rozen RJ, Adan RA. Source: The Journal of Biological Chemistry. 2003 June 20; 278(25): 22939-45. Epub 2003 April 09. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12690102&dopt=Abstract
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Possible lessons from the tobacco experience for obesity control. Author(s): Mercer SL, Green LW, Rosenthal AC, Husten CG, Khan LK, Dietz WH. Source: The American Journal of Clinical Nutrition. 2003 April; 77(4 Suppl): 1073S1082S. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12663321&dopt=Abstract
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Predicting obesity in early adulthood from childhood and parental obesity. Author(s): Magarey AM, Daniels LA, Boulton TJ, Cockington RA. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 April; 27(4): 505-13. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12664084&dopt=Abstract
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Prevalence of obesity and dyslipidemia in middle-aged men and women in Tanzania, Africa: relationship with resting energy expenditure and dietary factors. Author(s): Njelekela M, Kuga S, Nara Y, Ntogwisangu J, Masesa Z, Mashalla Y, Ikeda K, Mtabaji J, Yamori Y, Tsuda K. Source: J Nutr Sci Vitaminol (Tokyo). 2002 October; 48(5): 352-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12656207&dopt=Abstract
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Prevalence of obesity and its association with blood pressure, serum lipids and selected lifestyles in a Puerto Rican population of adolescents 12-16 years of age. Author(s): Venegas HL, Perez CM, Suarez EL, Guzman M. Source: P R Health Sci J. 2003 June; 22(2): 137-43. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12866137&dopt=Abstract
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Prevalence of obesity in children in Alabama and Texas participating in social programs. Author(s): Feese M, Franklin F, Murdock M, Harrington K, Brown-Binns M, Nicklas T, Hughes S, Morales M. Source: Jama : the Journal of the American Medical Association. 2003 April 9; 289(14): 1780-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12684354&dopt=Abstract
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Prevalence of overweight and obesity among Costa Rican elementary school children. Author(s): Nunez-Rivas HP, Monge-Rojas R, Leon H, Rosello M. Source: Revista Panamericana De Salud Publica = Pan American Journal of Public Health. 2003 January; 13(1): 24-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12744799&dopt=Abstract
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Prevalence of overweight and obesity in affluent adolescent girls in Chennai in 1981 and 1998. Author(s): Subramanyam V, Jayashree R, Rafi M. Source: Indian Pediatrics. 2003 August; 40(8): 775-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12956109&dopt=Abstract
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Prevalence of overweight and obesity in affluent adolescent girls in Chennai in 1981 and 1998. Author(s): Subramanyam V, R J, Rafi M. Source: Indian Pediatrics. 2003 April; 40(4): 332-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12736406&dopt=Abstract
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Prevalence of overweight, obesity, and associated diseases among outpatients in a public hospital. Author(s): Huang J, Marin E, Yu H, Carden D, Arnold C, Davis T, Banks D. Source: Southern Medical Journal. 2003 June; 96(6): 558-62. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12938782&dopt=Abstract
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Preventing obesity. Author(s): Kealy MM. Source: Awhonn Lifelines / Association of Women's Health, Obstetric and Neonatal Nurses. 2003 February-March; 7(1): 24-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12674056&dopt=Abstract
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Prevention of childhood obesity: sociocultural and familial factors. Author(s): Bruss MB, Morris J, Dannison L. Source: Journal of the American Dietetic Association. 2003 August; 103(8): 1042-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12891156&dopt=Abstract
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Prevention of obesity in young children: a critical challenge for medical professionals. Author(s): Sothern MS, Gordon ST. Source: Clinical Pediatrics. 2003 March; 42(2): 101-11. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12659382&dopt=Abstract
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Prevention of pediatric overweight and obesity. Author(s): Krebs NF, Jacobson MS; American Academy of Pediatrics Committee on Nutrition. Source: Pediatrics. 2003 August; 112(2): 424-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12897303&dopt=Abstract
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Principles and practices in the management of obesity. Author(s): Foster GD. Source: American Journal of Respiratory and Critical Care Medicine. 2003 August 1; 168(3): 274-80. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12888610&dopt=Abstract
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Prospective association between obesity and depression: evidence from the Alameda County Study. Author(s): Roberts RE, Deleger S, Strawbridge WJ, Kaplan GA. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 April; 27(4): 514-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12664085&dopt=Abstract
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Prospects for obesity treatment: MCH receptor antagonists. Author(s): Collins CA, Kym PR. Source: Curr Opin Investig Drugs. 2003 April; 4(4): 386-94. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12808876&dopt=Abstract
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Protein tyrosine phosphatase 1B: a novel target for type 2 diabetes and obesity. Author(s): Ramachandran C, Kennedy BP. Source: Current Topics in Medicinal Chemistry. 2003; 3(7): 749-57. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12678842&dopt=Abstract
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Proton magnetic resonance spectroscopy study of soleus muscle in non-obese healthy and Type 2 diabetic Asian Northern Indian males: high intramyocellular lipid content correlates with excess body fat and abdominal obesity. Author(s): Misra A, Sinha S, Kumar M, Jagannathan NR, Pandey RM. Source: Diabetic Medicine : a Journal of the British Diabetic Association. 2003 May; 20(5): 361-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12752484&dopt=Abstract
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Quality of life and obesity. Author(s): Kolotkin RL, Meter K, Williams GR. Source: Obesity Reviews : an Official Journal of the International Association for the Study of Obesity. 2001 November; 2(4): 219-29. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12119993&dopt=Abstract
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Quality of life following laparoscopic gastric banding in patients with morbid obesity. Author(s): Freys SM, Tigges H, Heimbucher J, Fuchs KH, Fein M, Thiede A. Source: Journal of Gastrointestinal Surgery : Official Journal of the Society for Surgery of the Alimentary Tract. 2001 July-August; 5(4): 401-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11985982&dopt=Abstract
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Quality of life in obesity hypoventilation syndrome. Author(s): Hida W. Source: Sleep & Breathing = Schlaf & Atmung. 2003 March; 7(1): 1-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12712391&dopt=Abstract
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Racial/ethnic differences in weight concerns: protective and risk factors for the development of eating disorders and obesity among adolescent females. Author(s): White MA, Kohlmaier JR, Varnado-Sullivan P, Williamson DA. Source: Eat Weight Disord. 2003 March; 8(1): 20-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12762621&dopt=Abstract
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Randomized controlled trial of the effect of n-3 fatty acid supplementation on the metabolism of apolipoprotein B-100 and chylomicron remnants in men with visceral obesity. Author(s): Chan DC, Watts GF, Mori TA, Barrett PH, Redgrave TG, Beilin LJ. Source: The American Journal of Clinical Nutrition. 2003 February; 77(2): 300-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12540386&dopt=Abstract
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Rapid weight gain during infancy and obesity in young adulthood in a cohort of African Americans. Author(s): Stettler N, Kumanyika SK, Katz SH, Zemel BS, Stallings VA. Source: The American Journal of Clinical Nutrition. 2003 June; 77(6): 1374-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12791612&dopt=Abstract
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Rapid weight gain during infancy as a predictor of adult obesity. Author(s): Yanovski JA. Source: The American Journal of Clinical Nutrition. 2003 June; 77(6): 1350-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12791608&dopt=Abstract
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Recent developments in the treatment of obesity-related hypertension. Author(s): Pischon T, Sharma AM. Source: Current Opinion in Nephrology and Hypertension. 2002 September; 11(5): 497502. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12187313&dopt=Abstract
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Recent tax changes may assist treatment of obesity. Author(s): Fitzner K, Caputo N, Trendell W, French MV, Bondi MA, Jennings C. Source: Manag Care Interface. 2003 January; 16(1): 47-51, 55. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12564405&dopt=Abstract
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Recruitment of African-American pre-adolescent girls into an obesity prevention trial: the GEMS pilot studies. Author(s): Story M, Sherwood NE, Obarzanek E, Beech BM, Baranowski JC, Thompson NS, Owens AS, Mitchell M, Rochon J. Source: Ethn Dis. 2003 Winter; 13(1 Suppl 1): S78-87. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12713213&dopt=Abstract
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Redefining type 2 diabetes: 'diabesity' or 'obesity dependent diabetes mellitus'? Author(s): Astrup A, Finer N. Source: Obesity Reviews : an Official Journal of the International Association for the Study of Obesity. 2000 October; 1(2): 57-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12119987&dopt=Abstract
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Reduction in obesity and coronary risk factors after high caloric exercise training in overweight coronary patients. Author(s): Savage PD, Brochu M, Poehlman ET, Ades PA. Source: American Heart Journal. 2003 August; 146(2): 317-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12891202&dopt=Abstract
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Regulation of PPARgamma and obesity by agouti/melanocortin signaling in adipocytes. Author(s): Mynatt RL, Stephens JM. Source: Annals of the New York Academy of Sciences. 2003 June; 994: 141-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12851309&dopt=Abstract
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Relation between physical activity and obesity. Author(s): Salbe AD, Weyer C, Harper I, Lindsay RS, Ravussin E, Tataranni PA. Source: The American Journal of Clinical Nutrition. 2003 July; 78(1): 193-4; Author Reply 194-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12816794&dopt=Abstract
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Relationship between juvenile obesity, dietary energy and fat intake and physical activity. Author(s): Gillis LJ, Kennedy LC, Gillis AM, Bar-Or O. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2002 April; 26(4): 458-63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12075571&dopt=Abstract
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Relationship between obesity and cardiovascular risk factors in elderly Chinese subjects. Author(s): Thomas GN, Zhao HL, Ma YQ, Ys Leung W, Cn Chan J, Tomlinson B, Ajh Critchley J. Source: Chin Med J (Engl). 2002 June; 115(6): 897-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12123561&dopt=Abstract
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Relationship between obesity and health-related quality of life in men. Author(s): Yancy WS Jr, Olsen MK, Westman EC, Bosworth HB, Edelman D. Source: Obesity Research. 2002 October; 10(10): 1057-64. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12376587&dopt=Abstract
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Relationship between obesity, insulin resistance, and coronary heart disease risk. Author(s): Abbasi F, Brown BW Jr, Lamendola C, McLaughlin T, Reaven GM. Source: Journal of the American College of Cardiology. 2002 September 4; 40(5): 937-43. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12225719&dopt=Abstract
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Relationship of beta2-adrenergic receptor polymorphism with obesity in type 2 diabetes. Author(s): van Tilburg JH, Wijmenga C, van Bakel H, Rozeman L, Pearson PL, van Haeften TW. Source: Diabetes Care. 2003 January; 26(1): 251-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12502697&dopt=Abstract
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Relationship of internalized racism to abdominal obesity and blood pressure in AfroCaribbean women. Author(s): Tull SE, Wickramasuriya T, Taylor J, Smith-Burns V, Brown M, Champagnie G, Daye K, Donaldson K, Solomon N, Walker S, Fraser H, Jordan OW. Source: Journal of the National Medical Association. 1999 August; 91(8): 447-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12656433&dopt=Abstract
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Relationship of urodynamic parameters and obesity in women with stress urinary incontinence. Author(s): Bai SW, Kang JY, Rha KH, Lee MS, Kim JY, Park KH. Source: J Reprod Med. 2002 July; 47(7): 559-63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12170533&dopt=Abstract
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Relationships of the systolic blood pressure response during exercise with insulin resistance, obesity, and endurance fitness in men with type 2 diabetes mellitus. Author(s): Kumagai S, Kai Y, Hanada H, Uezono K, Sasaki H. Source: Metabolism: Clinical and Experimental. 2002 October; 51(10): 1247-52. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12370842&dopt=Abstract
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Relative impact of insulin resistance and obesity on cardiovascular risk factors in polycystic ovary syndrome. Author(s): Goodarzi MO, Erickson S, Port SC, Jennrich RI, Korenman SG. Source: Metabolism: Clinical and Experimental. 2003 June; 52(6): 713-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12800096&dopt=Abstract
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Relevance of energy expenditure and energy intake to the etiology of obesity. Author(s): Chapelot D, Louis-Sylvestre J. Source: The American Journal of Clinical Nutrition. 2002 August; 76(2): 489; Author Reply 489-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12145028&dopt=Abstract
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Renal and cardiovascular considerations for the nonpharmacological and pharmacological therapies of obesity-hypertension. Author(s): Zhang R, Thakur V, Morse S, Reisin E. Source: Journal of Human Hypertension. 2002 December; 16(12): 819-27. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12522462&dopt=Abstract
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Research agenda for pediatric gastroenterology, hepatology and nutrition: nutrition and obesity. Report of the North American Society for Pediatric Gastroenterology, Hepatology and Nutrition for the Children's Digestive Health and Nutrition Foundation. Author(s): Baker SS, Motil KJ, Heyman MB. Source: Journal of Pediatric Gastroenterology and Nutrition. 2002; 35 Suppl 3: S281-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12394366&dopt=Abstract
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Researching new treatments for obesity: from neuroscience to inflammation. Author(s): Donnelly R. Source: Diabetes, Obesity & Metabolism. 2003 January; 5(1): 1-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12542719&dopt=Abstract
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Resistin - a mediator of obesity-associated insulin resistance or an innocent bystander? Author(s): Ukkola O. Source: European Journal of Endocrinology / European Federation of Endocrine Societies. 2002 November; 147(5): 571-4. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12444887&dopt=Abstract
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Risk factors for the development of obesity in children surviving brain tumors. Author(s): Lustig RH, Post SR, Srivannaboon K, Rose SR, Danish RK, Burghen GA, Xiong X, Wu S, Merchant TE. Source: The Journal of Clinical Endocrinology and Metabolism. 2003 February; 88(2): 611-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12574189&dopt=Abstract
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Risk stratification of obesity as a coronary risk factor. Author(s): Kannel WB, Wilson PW, Nam BH, D'Agostino RB. Source: The American Journal of Cardiology. 2002 October 1; 90(7): 697-701. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12356380&dopt=Abstract
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Role of ghrelin polymorphisms in obesity based on three different studies. Author(s): Ukkola O, Ravussin E, Jacobson P, Perusse L, Rankinen T, Tschop M, Heiman ML, Leon AS, Rao DC, Skinner JS, Wilmore JH, Sjostrom L, Bouchard C. Source: Obesity Research. 2002 August; 10(8): 782-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12181387&dopt=Abstract
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Role of obesity and leptin in the pubertal process and pubertal growth--a review. Author(s): Shalitin S, Phillip M. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 August; 27(8): 869-74. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12861226&dopt=Abstract
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Roux-en-Y gastric bypass for morbid obesity. Author(s): Barrow CJ. Source: Aorn Journal. 2002 October; 76(4): 590, 593-604; Quiz 606-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12382465&dopt=Abstract
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School-based obesity prevention: a blueprint for taming the epidemic. Author(s): Baranowski T, Cullen KW, Nicklas T, Thompson D, Baranowski J. Source: American Journal of Health Behavior. 2002 November-December; 26(6): 486-93. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12437023&dopt=Abstract
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Screening for childhood obesity: international vs population-specific definitions. Which is more appropriate? Author(s): Fu WP, Lee HC, Ng CJ, Tay YK, Kau CY, Seow CJ, Siak JK, Hong CY. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 September; 27(9): 1121-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12917720&dopt=Abstract
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Self-reported concern about food security associated with obesity--Washington, 19951999. Author(s): Centers for Disease Control and Prevention (CDC). Source: Mmwr. Morbidity and Mortality Weekly Report. 2003 September 5; 52(35): 8402. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12966359&dopt=Abstract
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Serum androgen concentrations in young men: a longitudinal analysis of associations with age, obesity, and race. The CARDIA male hormone study. Author(s): Gapstur SM, Gann PH, Kopp P, Colangelo L, Longcope C, Liu K. Source: Cancer Epidemiology, Biomarkers & Prevention : a Publication of the American Association for Cancer Research, Cosponsored by the American Society of Preventive Oncology. 2002 October; 11(10 Pt 1): 1041-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12376505&dopt=Abstract
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Severe metabolic bone disease as a long-term complication of obesity surgery. Author(s): Goldner WS, O'Dorisio TM, Dillon JS, Mason EE. Source: Obesity Surgery : the Official Journal of the American Society for Bariatric Surgery and of the Obesity Surgery Society of Australia and New Zealand. 2002 October; 12(5): 685-92. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12448393&dopt=Abstract
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Sex steroid hormones, upper body obesity, and insulin resistance. Author(s): Abate N, Haffner SM, Garg A, Peshock RM, Grundy SM. Source: The Journal of Clinical Endocrinology and Metabolism. 2002 October; 87(10): 4522-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12364429&dopt=Abstract
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Should we recommend low-fat diets for obesity? Author(s): Pirozzo S, Summerbell C, Cameron C, Glasziou P. Source: Obesity Reviews : an Official Journal of the International Association for the Study of Obesity. 2003 May; 4(2): 83-90. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12760443&dopt=Abstract
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Sibutramine in the management of obesity. Author(s): Brunton S. Source: The Journal of Family Practice. 2003 August; 52(8): 635. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12899819&dopt=Abstract
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Simple index for screening overweight and obesity. Author(s): Pruenglampoo S, Pruenglampoo B, Kingkeow C, Mongkalabrug A. Source: Public Health Nutrition. 2003 April; 6(2): 225-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12675966&dopt=Abstract
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Sizes and obesity pattern of South Iranian adolescent females. Author(s): Ayatollahi SM. Source: Annals of Human Biology. 2003 March-April; 30(2): 191-202. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12637194&dopt=Abstract
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Skeletal muscle triglyceride: marker or mediator of obesity-induced insulin resistance in type 2 diabetes mellitus? Author(s): Goodpaster BH, Kelley DE. Source: Curr Diab Rep. 2002 June; 2(3): 216-22. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12643176&dopt=Abstract
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Sleep apnea associated with antipsychotic-induced obesity. Author(s): Wirshing DA, Pierre JM, Wirshing WC. Source: The Journal of Clinical Psychiatry. 2002 April; 63(4): 369-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12000215&dopt=Abstract
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Social factors and obesity: an investigation of the role of health behaviours. Author(s): Ball K, Mishra GD, Crawford D. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 March; 27(3): 394-403. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12629569&dopt=Abstract
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Societal change to prevent obesity. Author(s): Weisberg SP. Source: Jama : the Journal of the American Medical Association. 2002 November 6; 288(17): 2176. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12413382&dopt=Abstract
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Socioeconomic aspects of spousal concordance for hypertension, obesity, and smoking in a community of Rio de Janeiro, Brazil. Author(s): Bloch KV, Klein CH, de Souza e Silva NA, Nogueira Ada R, Salis LH. Source: Arquivos Brasileiros De Cardiologia. 2003 February; 80(2): 179-86, 171-8. Epub 2003 February 25. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12640511&dopt=Abstract
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Some thoughts about childhood obesity. Author(s): Chambers S. Source: J Ark Med Soc. 2002 November; 99(5): 141. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12434622&dopt=Abstract
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Substrate oxidation, obesity and exercise training. Author(s): Blaak EE, Saris WH. Source: Best Practice & Research. Clinical Endocrinology & Metabolism. 2002 December; 16(4): 667-78. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12468414&dopt=Abstract
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Success of laparoscopic ovarian wedge resection is related to obesity, lipid profile, and insulin levels. Author(s): Duleba AJ, Banaszewska B, Spaczynski RZ, Pawelczyk L. Source: Fertility and Sterility. 2003 April; 79(4): 1008-14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12749446&dopt=Abstract
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Successes and challenges in treating obesity. Author(s): Elderkin AL, Bourbon A, Curtis LG, Dillard WC, Buskey RH, Nelson RL, Ulshafer C. Source: Jaapa. 2002 November; 15(11): 11-2, 15-6, 19 Passim. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12474429&dopt=Abstract
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Succinylcholine and morbid obesity. Author(s): Brodsky JB, Foster PE. Source: Obesity Surgery : the Official Journal of the American Society for Bariatric Surgery and of the Obesity Surgery Society of Australia and New Zealand. 2003 February; 13(1): 138-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12630630&dopt=Abstract
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Summary of the 2000 Surgeon General's listening session: toward a national action plan on overweight and obesity. Author(s): Jackson Y, Dietz WH, Sanders C, Kolbe LJ, Whyte JJ, Wechsler H, Schneider BS, McNally LA, Charles-Azure J, Vogel-Taylor M, Starke-Reed P, Hubbard VS, Johnson-Taylor WL, Troiano RP, Donato K, Yanovski S, Kuczmarski RJ, Haverkos L, McMurry K, Wykoff RF, Woo V, Noonan AS, Rowe J, McCarty K, Spain CB. Source: Obesity Research. 2002 December; 10(12): 1299-305. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12490675&dopt=Abstract
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Suppression of fibrinolytic activity and obesity in young patients with myocardial infarction. Author(s): Saigo M, Abe S, Ogawa M, Maruyama I, Tei C. Source: Thrombosis and Haemostasis. 2002 November; 88(5): 878-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12428113&dopt=Abstract
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Surgery for morbid obesity. Author(s): Colquitt J, Clegg A, Sidhu M, Royle P. Source: Cochrane Database Syst Rev. 2003; (2): Cd003641. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12804481&dopt=Abstract
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Surgery for obesity: demand soars amid scientific, ethical questions. Author(s): Mitka M. Source: Jama : the Journal of the American Medical Association. 2003 April 9; 289(14): 1761-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12684340&dopt=Abstract
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Surgical management of obesity. Author(s): Nehoda H. Source: Wiener Klinische Wochenschrift. 2002 September 30; 114(17-18): 744-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12416277&dopt=Abstract
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Surgical treatment of severe obesity with a low-pressure adjustable gastric band: experimental data and clinical results in 625 patients. Author(s): Ceelen W, Walder J, Cardon A, Van Renterghem K, Hesse U, El Malt M, Pattyn P. Source: Annals of Surgery. 2003 January; 237(1): 10-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12496524&dopt=Abstract
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Survey of physician attitudes and practices related to pediatric obesity. Author(s): Jelalian E, Boergers J, Alday CS, Frank R. Source: Clinical Pediatrics. 2003 April; 42(3): 235-45. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12739922&dopt=Abstract
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Sustaining dietary changes for preventing obesity and diabetes: lessons learned from the successes of other epidemic control programs. Author(s): Swinburn B. Source: Asia Pacific Journal of Clinical Nutrition. 2002; 11 Suppl 3: S598-606. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12492653&dopt=Abstract
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Sympathetic neural activation in visceral obesity. Author(s): Alvarez GE, Beske SD, Ballard TP, Davy KP. Source: Circulation. 2002 November 12; 106(20): 2533-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12427647&dopt=Abstract
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Symptom status and functional status outcomes: humanistic outcomes in obesity disease management. Author(s): Ropka ME. Source: Obesity Research. 2002 November; 10 Suppl 1: 42S-49S. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12446858&dopt=Abstract
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Television viewing and risk of obesity. Author(s): Redelmeier DA, Stanbrook MB. Source: Jama : the Journal of the American Medical Association. 2003 July 16; 290(3): 332; Author Reply 332. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12865370&dopt=Abstract
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Television watching and soft drink consumption: associations with obesity in 11- to 13-year-old schoolchildren. Author(s): Giammattei J, Blix G, Marshak HH, Wollitzer AO, Pettitt DJ. Source: Archives of Pediatrics & Adolescent Medicine. 2003 September; 157(9): 882-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12963593&dopt=Abstract
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Testosterone supplementation in men with type 2 diabetes, visceral obesity and partial androgen deficiency. Author(s): Boyanov MA, Boneva Z, Christov VG. Source: The Aging Male : the Official Journal of the International Society for the Study of the Aging Male. 2003 March; 6(1): 1-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12809074&dopt=Abstract
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The "big picture" in obesity research. Author(s): Muhlhausler B. Source: Science. 2003 May 16; 300(5622): 1091-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12750500&dopt=Abstract
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The association of dehydroepiandrosterone, obesity, waist-hip ratio and insulin resistance with fatty liver in postmenopausal women--a hyperinsulinemic euglycemic insulin clamp study. Author(s): Saruc M, Yuceyar H, Ayhan S, Turkel N, Tuzcuoglu I, Can M. Source: Hepatogastroenterology. 2003 May-June; 50(51): 771-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12828082&dopt=Abstract
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The effect of the -308A allele of the TNF-alpha gene on insulin action is dependent on obesity. Author(s): Pihlajamaki J, Ylinen M, Karhapaa P, Vauhkonen I, Laakso M. Source: Obesity Research. 2003 July; 11(7): 912-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12855762&dopt=Abstract
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The effects of weight loss on renal function in patients with severe obesity. Author(s): Chagnac A, Weinstein T, Herman M, Hirsh J, Gafter U, Ori Y. Source: Journal of the American Society of Nephrology : Jasn. 2003 June; 14(6): 1480-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12761248&dopt=Abstract
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The epidemic of childhood overweight and obesity. Extent of the problem and prospects for change. Author(s): Molloy M, Kovach K, Bors P, Caldwell D, Lebeuf JS. Source: N C Med J. 2002 November-December; 63(6): 291-7. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12970976&dopt=Abstract
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The etiology of obesity. Author(s): Gardner D. Source: Mo Med. 2003 May-June; 100(3): 242-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12847865&dopt=Abstract
156 Obesity
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The frequency of respiratory failure in patients with morbid obesity undergoing gastric bypass. Author(s): Blouw EL, Rudolph AD, Narr BJ, Sarr MG. Source: Aana Journal. 2003 February; 71(1): 45-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12776650&dopt=Abstract
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The influence of obesity on the frequency and distribution of medication. Author(s): Dzien A, Pfeiffer KP, Dzien-Bischinger C, Hoppichler F, Lechleitner M. Source: Acta Medica Austriaca. 2003; 30(2): 51-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12752089&dopt=Abstract
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The management of adult obesity. Author(s): Birmingham CL, Jones P, Hoffer LJ. Source: Eat Weight Disord. 2003 June; 8(2): 157-63. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12880194&dopt=Abstract
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The obesity charge. Author(s): Epperson S. Source: Time. 2003 September 8; 162(10): 100. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14509905&dopt=Abstract
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The obesity epidemic: can we turn the tide? Author(s): Campbell I. Source: Heart (British Cardiac Society). 2003 May; 89 Suppl 2: Ii22-4; Discussion Ii35-7. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12695431&dopt=Abstract
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The obesity epidemic--how states can trim the "fat". Author(s): Fierro MP. Source: N C Med J. 2002 November-December; 63(6): 304. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12970979&dopt=Abstract
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The physiology of obesity. Author(s): Montague MC. Source: The Abnf Journal : Official Journal of the Association of Black Nursing Faculty in Higher Education, Inc. 2003 May-June; 14(3): 56-60. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12856442&dopt=Abstract
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The prevalence of obesity and undernutrition in Scottish children: growth monitoring within the Child Health Surveillance Programme. Author(s): Armstrong J, Reilly JJ. Source: Scott Med J. 2003 May; 48(2): 32-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12774591&dopt=Abstract
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The public health burden of obesity in Missouri. Author(s): Kabeer NH, Simoes EJ. Source: Mo Med. 2003 May-June; 100(3): 236-41. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12847864&dopt=Abstract
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The relationship between obesity and breast cancer. Author(s): Adderley-Kelly B, Williams-Stephens E. Source: The Abnf Journal : Official Journal of the Association of Black Nursing Faculty in Higher Education, Inc. 2003 May-June; 14(3): 61-5. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12856443&dopt=Abstract
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The relationship of obesity to the metabolic syndrome. Author(s): Lebovitz HE. Source: Int J Clin Pract Suppl. 2003 March; (134): 18-27. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12793594&dopt=Abstract
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The role of the sympathetic nervous system in linking obesity with hypertension in white versus black Americans. Author(s): Eslami P, Tuck M. Source: Current Hypertension Reports. 2003 June; 5(3): 269-72. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12724061&dopt=Abstract
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The significance of elevated levels of parathyroid hormone in patients with morbid obesity before and after bariatric surgery. Author(s): Hamoui N, Kim K, Anthone G, Crookes PF. Source: Archives of Surgery (Chicago, Ill. : 1960). 2003 August; 138(8): 891-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12912749&dopt=Abstract
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The skinny on obesity and cancer. Obesity increases the risk of death from cancer, but being overweight isn't inescapable. Author(s): Blackburn GL. Source: Health News. 2003 June; 9(6): 3. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12793396&dopt=Abstract
158 Obesity
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The TNF-alpha gene NcoI polymorphism at position -308 of the promoter influences insulin resistance, and increases serum triglycerides after postprandial lipaemia in familiar obesity. Author(s): Wybranska I, Malczewska-Malec M, Niedbal S, Naskalski JW, DembinskaKiec A. Source: Clinical Chemistry and Laboratory Medicine : Cclm / Fescc. 2003 April; 41(4): 501-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12747594&dopt=Abstract
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The treatment of obesity. Author(s): Mina WC, Burns RW, Terry BE. Source: Mo Med. 2003 May-June; 100(3): 248-55. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12847866&dopt=Abstract
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Therapeutic role of peroxisome proliferator-activated receptors in obesity, diabetes and inflammation. Author(s): Ram VJ. Source: Prog Drug Res. 2003; 60: 93-132. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12790340&dopt=Abstract
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Treatment of obesity. Author(s): Sugerman HJ. Source: Journal of Gastrointestinal Surgery : Official Journal of the Society for Surgery of the Alimentary Tract. 2003 May-June; 7(4): 476-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12763401&dopt=Abstract
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Treatment of obesity: should we target the individual or society? Author(s): Tataranni PA. Source: Current Pharmaceutical Design. 2003; 9(15): 1151-63. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12769743&dopt=Abstract
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Trends and predictors of overweight and obesity in East German children. Author(s): Frye C, Heinrich J. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 August; 27(8): 963-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12861238&dopt=Abstract
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Tribunal clears obesity researcher of fraud. Author(s): Butler D. Source: Nature. 2003 July 3; 424(6944): 6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12840722&dopt=Abstract
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Uncoupling protein genes and racial differences in obesity. Author(s): Polednak AP. Source: The American Journal of Clinical Nutrition. 2003 June; 77(6): 1527-8; Author Reply 1528. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12791636&dopt=Abstract
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Uncoupling proteins, leptin, and obesity: an updated review. Author(s): Giacobino JP. Source: Annals of the New York Academy of Sciences. 2002 June; 967: 398-402. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12079867&dopt=Abstract
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Uncoupling proteins: a molecular basis for racial differences in energy expenditure (and obesity?). Author(s): Schonfeld-Warden NA, Warden CH. Source: The American Journal of Clinical Nutrition. 2002 April; 75(4): 607-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11916746&dopt=Abstract
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Underdiagnosis of obesity at a community health center. Author(s): Lemay CA, Cashman S, Savageau J, Fletcher K, Kinney R, Long-Middleton E. Source: The Journal of the American Board of Family Practice / American Board of Family Practice. 2003 January-February; 16(1): 14-21. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12583646&dopt=Abstract
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Understanding obesity and program participation in the context of poverty and food insecurity. Author(s): Frongillo EA. Source: The Journal of Nutrition. 2003 July; 133(7): 2117-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12840164&dopt=Abstract
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Understanding the complex journey to obesity in early adulthood. Author(s): Whitaker RC. Source: Annals of Internal Medicine. 2002 June 18; 136(12): 923-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12069566&dopt=Abstract
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Understanding the physiology of obesity: review of recent developments in obesity research. Author(s): Woods SC, Seeley RJ. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2002 December; 26 Suppl 4: S8-S10. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12457292&dopt=Abstract
160 Obesity
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Undertreatment of obesity. Author(s): Grizzard T. Source: Jama : the Journal of the American Medical Association. 2002 November 6; 288(17): 2177. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12413383&dopt=Abstract
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Unemployment and obesity among young adults in a northern Finland 1966 birth cohort. Author(s): Laitinen J, Power C, Ek E, Sovio U, Jarvelin MR. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2002 October; 26(10): 1329-38. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12355341&dopt=Abstract
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Untreated hypertension among Australian adults: the 1999-2000 Australian Diabetes, Obesity and Lifestyle Study (AusDiab). Author(s): Briganti EM, Shaw JE, Chadban SJ, Zimmet PZ, Welborn TA, McNeil JJ, Atkins RC; Australian Diabetes, Obesity and Lifestyle Study (AusDiab). Source: The Medical Journal of Australia. 2003 August 4; 179(3): 135-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12885281&dopt=Abstract
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Up to date. Gastroesophageal reflux disease (GERD) influence of obesity. Author(s): Chiocca JC. Source: Acta Gastroenterol Latinoam. 2002; 32(2): 95-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12553162&dopt=Abstract
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Upper abdominal obesity, insulin resistance and breast cancer risk. Author(s): Stoll BA. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2002 June; 26(6): 747-53. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12037643&dopt=Abstract
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Urologic and plastic surgical collaboration for continent diversion when urine leakage is complicated by pressure ulcers or obesity. Author(s): Sterbis JR, Lewis VL, Bushman W. Source: J Spinal Cord Med. 2003 Summer; 26(2): 124-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12828288&dopt=Abstract
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US paediatricians call for checks for childhood obesity. Author(s): Gottlieb S. Source: Bmj (Clinical Research Ed.). 2003 September 6; 327(7414): 518. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12958090&dopt=Abstract
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Use of beta-blockers in obesity hypertension: potential role of weight gain. Author(s): Pischon T, Sharma AM. Source: Obesity Reviews : an Official Journal of the International Association for the Study of Obesity. 2001 November; 2(4): 275-80. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12119998&dopt=Abstract
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Use of BMI as a measure of overweight and obesity in a field study on 5-7 year old children. Author(s): Mast M, Langnase K, Labitzke K, Bruse U, Preuss U, Muller MJ. Source: European Journal of Nutrition. 2002 April; 41(2): 61-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12083315&dopt=Abstract
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Use of somatostatin receptor ligands in obesity and diabetic complications. Author(s): Boehm BO, Lustig RH. Source: Best Practice & Research. Clinical Gastroenterology. 2002 June; 16(3): 493-509. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12079271&dopt=Abstract
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Use of the health and activities limitation index as a measure of quality of life in obesity. Author(s): Livingston EH, Ko CY. Source: Obesity Research. 2002 August; 10(8): 824-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12181392&dopt=Abstract
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Usefulness of anthropometrics and dual-energy x-ray absorptiometry for estimating abdominal obesity measured by magnetic resonance imaging in older men and women. Author(s): Stewart KJ, DeRegis JR, Turner KL, Bacher AC, Sung J, Hees PS, Shapiro EP, Tayback M, Ouyang P. Source: Journal of Cardiopulmonary Rehabilitation. 2003 March-April; 23(2): 109-14. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12668933&dopt=Abstract
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Using mouse models to dissect the genetics of obesity. Author(s): Brockmann GA, Bevova MR. Source: Trends in Genetics : Tig. 2002 July; 18(7): 367-76. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12127777&dopt=Abstract
162 Obesity
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Varicose veins of the lower limbs and venous capacitance in postmenopausal women: relationship with obesity. Author(s): Iannuzzi A, Panico S, Ciardullo AV, Bellati C, Cioffi V, Iannuzzo G, Celentano E, Berrino F, Rubba P. Source: Journal of Vascular Surgery : Official Publication, the Society for Vascular Surgery [and] International Society for Cardiovascular Surgery, North American Chapter. 2002 November; 36(5): 965-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12422106&dopt=Abstract
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Venlafaxine treatment of binge-eating disorder associated with obesity: a series of 35 patients. Author(s): Malhotra S, King KH, Welge JA, Brusman-Lovins L, McElroy SL. Source: The Journal of Clinical Psychiatry. 2002 September; 63(9): 802-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12363121&dopt=Abstract
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Vertical gastric banding for morbid obesity: a long-term follow-up study. Author(s): Waaddegaard P, Clemmesen T, Jess P. Source: The European Journal of Surgery = Acta Chirurgica. 2002; 168(4): 220-2. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12440759&dopt=Abstract
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Very low energy diets in the treatment of obesity. Author(s): Mustajoki P, Pekkarinen T. Source: Obesity Reviews : an Official Journal of the International Association for the Study of Obesity. 2001 February; 2(1): 61-72. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12119638&dopt=Abstract
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Virtual gastroduodenoscopy: a new look at the bypassed stomach and duodenum after laparoscopic Roux-en-Y gastric bypass for morbid obesity. Author(s): Silecchia G, Catalano C, Gentileschi P, Elmore U, Restuccia A, Gagner M, Basso N. Source: Obesity Surgery : the Official Journal of the American Society for Bariatric Surgery and of the Obesity Surgery Society of Australia and New Zealand. 2002 February; 12(1): 39-48. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11868296&dopt=Abstract
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Visceral fat and psychosocial stress in identical twins discordant for obesity. Author(s): Marniemi J, Kronholm E, Aunola S, Toikka T, Mattlar CE, Koskenvuo M, Ronnemaa T. Source: Journal of Internal Medicine. 2002 January; 251(1): 35-43. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11851863&dopt=Abstract
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Visceral obesity and hyperinsulinemia modulate the impact of the microsomal triglyceride transfer protein -493G/T polymorphism on plasma lipoprotein levels in men. Author(s): St-Pierre J, Lemieux I, Miller-Felix I, Prud'homme D, Bergeron J, Gaudet D, Nadeau A, Despres JP, Vohl MC. Source: Atherosclerosis. 2002 February; 160(2): 317-24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11849654&dopt=Abstract
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Visceral obesity and metabolic syndrome. Author(s): Bosello O, Zamboni M. Source: Obesity Reviews : an Official Journal of the International Association for the Study of Obesity. 2000 May; 1(1): 47-56. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12119645&dopt=Abstract
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Visceral obesity attenuates the effect of the hepatic lipase -514C>T polymorphism on plasma HDL-cholesterol levels in French-Canadian men. Author(s): St-Pierre J, Miller-Felix I, Paradis ME, Bergeron J, Lamarche B, Despres JP, Gaudet D, Vohl MC. Source: Molecular Genetics and Metabolism. 2003 January; 78(1): 31-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12559845&dopt=Abstract
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Visceral obesity is characterized by impaired nitric oxide-independent vasodilation. Author(s): Vigili de Kreutzenberg S, Kiwanuka E, Tiengo A, Avogaro A. Source: European Heart Journal. 2003 July; 24(13): 1210-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12831815&dopt=Abstract
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Visceral obesity, hepatic lipase activity, and dyslipidemia in type 1 diabetes. Author(s): Sibley SD, Palmer JP, Hirsch IB, Brunzell JD. Source: The Journal of Clinical Endocrinology and Metabolism. 2003 July; 88(7): 3379-84. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12843191&dopt=Abstract
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Vitamin A deficiency in a newborn resulting from maternal hypovitaminosis A after biliopancreatic diversion for the treatment of morbid obesity. Author(s): Huerta S, Rogers LM, Li Z, Heber D, Liu C, Livingston EH. Source: The American Journal of Clinical Nutrition. 2002 August; 76(2): 426-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12145017&dopt=Abstract
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VLDL-triglyceride kinetics during hyperglycemia-hyperinsulinemia: effects of sex and obesity. Author(s): Mittendorfer B, Patterson BW, Klein S, Sidossis LS. Source: American Journal of Physiology. Endocrinology and Metabolism. 2003 April; 284(4): E708-15. Epub 2002 December 10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12475756&dopt=Abstract
164 Obesity
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Waist circumference and obesity-associated risk factors among whites in the third National Health and Nutrition Examination Survey: clinical action thresholds. Author(s): Zhu S, Wang Z, Heshka S, Heo M, Faith MS, Heymsfield SB. Source: The American Journal of Clinical Nutrition. 2002 October; 76(4): 743-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12324286&dopt=Abstract
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Waist circumference, visceral obesity, and cardiovascular risk. Author(s): Poirier P, Despres JP. Source: Journal of Cardiopulmonary Rehabilitation. 2003 May-June; 23(3): 161-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12782898&dopt=Abstract
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Weighing in on obesity: America's growing health epidemic. Author(s): Grantmakers in Health, Washington, D.C., USA. Source: Issue Brief (Grantmakers Health). 2001 October 31; (11): 1-32. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14535290&dopt=Abstract
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Weight control and the management of obesity after menopause: the role of physical activity. Author(s): Dubnov G, Brzezinski A, Berry EM. Source: Maturitas. 2003 February 25; 44(2): 89-101. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12590004&dopt=Abstract
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Weight loss improves neurovascular and muscle metaboreflex control in obesity. Author(s): Trombetta IC, Batalha LT, Rondon MU, Laterza MC, Kuniyoshi FH, Gowdak MM, Barretto AC, Halpern A, Villares SM, Negrao CE. Source: American Journal of Physiology. Heart and Circulatory Physiology. 2003 September; 285(3): H974-82. Epub 2003 April 24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12714324&dopt=Abstract
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Weight loss increases circulating levels of ghrelin in human obesity. Author(s): Hansen TK, Dall R, Hosoda H, Kojima M, Kangawa K, Christiansen JS, Jorgensen JO. Source: Clinical Endocrinology. 2002 February; 56(2): 203-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11874411&dopt=Abstract
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Weight loss-induced plasticity of glucose transport and phosphorylation in the insulin resistance of obesity and type 2 diabetes. Author(s): Williams KV, Bertoldo A, Kinahan P, Cobelli C, Kelley DE. Source: Diabetes. 2003 July; 52(7): 1619-26. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12829624&dopt=Abstract
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Weight maintenance and relapse in obesity: a qualitative study. Author(s): Byrne S, Cooper Z, Fairburn C. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 August; 27(8): 955-62. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12861237&dopt=Abstract
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Weight reduction and long-term maintenance after 18 months treatment with orlistat for obesity. Author(s): Krempf M, Louvet JP, Allanic H, Miloradovich T, Joubert JM, Attali JR. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 May; 27(5): 591-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12704403&dopt=Abstract
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What are the most effective interventions to reduce childhood obesity? Author(s): Hill JC, Smith PC, Meadows SE. Source: The Journal of Family Practice. 2002 October; 51(10): 891. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12401163&dopt=Abstract
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What can we do about the "epidemic" of obesity. Author(s): Hall JE, Jones DW. Source: American Journal of Hypertension : Journal of the American Society of Hypertension. 2002 July; 15(7 Pt 1): 657-9. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12118917&dopt=Abstract
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What diets should we be recommending for obesity? Author(s): Hill JO, Astrup A. Source: Obesity Reviews : an Official Journal of the International Association for the Study of Obesity. 2003 May; 4(2): 77-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12760441&dopt=Abstract
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What do we do about the problem of overweight and obesity in the Americas? Author(s): Teelucksingh S. Source: Revista Panamericana De Salud Publica = Pan American Journal of Public Health. 2003 May; 13(5): 275-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12846232&dopt=Abstract
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What will it take to stop obesity? Author(s): Potteiger CE, Still CD. Source: J Am Osteopath Assoc. 2003 April; 103(4): 168. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12733545&dopt=Abstract
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Which aspects of socioeconomic status are related to obesity among men and women? Author(s): Ball K, Mishra G, Crawford D. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2002 April; 26(4): 559-65. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12075584&dopt=Abstract
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Which method should be used to determine the obesity, in patients with coronary artery disease? (body mass index, waist circumference or waist-hip ratio). Author(s): Sonmez K, Akcakoyun M, Akcay A, Demir D, Duran NE, Gencbay M, Degertekin M, Turan F. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 March; 27(3): 341-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12629561&dopt=Abstract
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Why do we need an obesity review journal year 2000? Author(s): Astrup A. Source: Obesity Reviews : an Official Journal of the International Association for the Study of Obesity. 2000 May; 1(1): 1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12119639&dopt=Abstract
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Why should gastroenterologists be interested in nutrition and obesity? Author(s): Klein S. Source: Gastroenterology. 2002 October; 123(4): 967. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12360454&dopt=Abstract
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Work-related physical activity is not associated with body mass index and obesity. Author(s): Gutierrez-Fisac JL, Guallar-Castillon P, Diez-Ganan L, Lopez Garcia E, Banegas Banegas JR, Rodriguez Artalejo F. Source: Obesity Research. 2002 April; 10(4): 270-6. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11943836&dopt=Abstract
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World pandemic of obesity--any hope of its being controlled? Author(s): Walker AR. Source: South African Medical Journal. Suid-Afrikaanse Tydskrif Vir Geneeskunde. 2003 August; 93(8): 598-600. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=14531118&dopt=Abstract
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Years of life lost due to obesity. Author(s): Fontaine KR, Redden DT, Wang C, Westfall AO, Allison DB. Source: Jama : the Journal of the American Medical Association. 2003 January 8; 289(2): 187-93. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12517229&dopt=Abstract
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CHAPTER 2. NUTRITION AND OBESITY Overview In this chapter, we will show you how to find studies dedicated specifically to nutrition and obesity.
Finding Nutrition Studies on Obesity The National Institutes of Health’s Office of Dietary Supplements (ODS) offers a searchable bibliographic database called the IBIDS (International Bibliographic Information on Dietary Supplements; National Institutes of Health, Building 31, Room 1B29, 31 Center Drive, MSC 2086, Bethesda, Maryland 20892-2086, Tel: 301-435-2920, Fax: 301-480-1845, E-mail:
[email protected]). The IBIDS contains over 460,000 scientific citations and summaries about dietary supplements and nutrition as well as references to published international, scientific literature on dietary supplements such as vitamins, minerals, and botanicals.7 The IBIDS includes references and citations to both human and animal research studies. As a service of the ODS, access to the IBIDS database is available free of charge at the following Web address: http://ods.od.nih.gov/databases/ibids.html. After entering the search area, you have three choices: (1) IBIDS Consumer Database, (2) Full IBIDS Database, or (3) Peer Reviewed Citations Only. Now that you have selected a database, click on the “Advanced” tab. An advanced search allows you to retrieve up to 100 fully explained references in a comprehensive format. Type “obesity” (or synonyms) into the search box, and click “Go.” To narrow the search, you can also select the “Title” field.
7
Adapted from http://ods.od.nih.gov. IBIDS is produced by the Office of Dietary Supplements (ODS) at the National Institutes of Health to assist the public, healthcare providers, educators, and researchers in locating credible, scientific information on dietary supplements. IBIDS was developed and will be maintained through an interagency partnership with the Food and Nutrition Information Center of the National Agricultural Library, U.S. Department of Agriculture.
168 Obesity
The following is a typical result when searching for recently indexed consumer information on obesity: •
Fatty acid composition of skeletal muscle membrane phospholipids, insulin resistance and obesity. Author(s): The Center for Genetics, Nutrition and Health, Washington, DC. Source: Simopoulos, A.P. Nutrition-today (USA). (February 1994). volume 29(1) page 1216. fats overweight insulin glucose metabolic disorders muscles membranes phospholipids fatty acids physiological functions genotypes diet polyunsaturated fatty acids lipid content risk disease control physical activity weight 0029-666X Summary: corps gras surpoids insuline glucose trouble du metabolisme muscle membrane phosphatide acide gras fonction physiologique genotype regime alimentaire acide gras polyinsature teneur en lipides risque controle de maladies activite physique poids
Additional consumer oriented references include: •
A 'cure' for obesity? Source: Tufts-University-diet-and-nutrition-letter (USA). (March 1995). volume 13(1) page 1-2. new york overweight pathogenesis genes medical sciences research 0747-4105
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Are there long term protective effects of breast feeding against later obesity? Author(s): Department of Pediatrics, Dr. von Haunersches Kinderspital, LudwigMaximilians-University of Munich, Germany. Source: Koletzko, B von Kries, R Nutr-Health. 2001; 15(3-4): 225-36 0260-1060
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Dehydroepiandrosterone (DHEA): useful or useless as an antiobesity agent? Source: Berdanier, C.D. Nutrition-today (USA). (December 1993). volume 28(6) page 3438. androgens overweight drug therapy appetite drugs metabolism 0029-666X
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Diabetes contributes to cholesterol metabolism regardless of obesity. Author(s): Department of Medicine, Division of Internal Medicine, University of Helsinki, Finland.
[email protected] Source: Simonen, P P Gylling, H K Miettinen, T A Diabetes-Care. 2002 September; 25(9): 1511-5 0149-5992
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Dieting-induced obesity: a hidden hazard of weight cycling. Source: Environ-Nutr. New York : Environmental Nutrition, Inc. February 1987. volume 10 (2) page 1, 6. 0195-4024
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Do calories from alcohol contribute to obesity. Source: Kurtzweil, P. BNF-nutr-bull. London : The Foundation,. January 1996. volume 21 (77) page 45-53. 0141-9684
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EN speaks with obesity expert. Source: Milner, I. Environ-Nutr. New York, N.Y. : Environmental Nutrition, Inc. January 1990. volume 13 (1) page 1, 3. 0893-4452
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Factors associated with overweight and obesity among Kuwaiti college women. Author(s): Department of Community Medicine & Behavioural Sciences, Faculty of Medicine, University of Kuwait, Safat. Source: al Isa, A N Nutr-Health. 1998; 12(4): 227-33 0260-1060
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High red-meat intake, obesity linked to cancer. Source: Anonymous Health-News. 2002 February; 8(2): 9 1081-5880
Nutrition 169
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Leptin--the 'new' player in energy balance and obesity. Source: Porter, D.V. BNF-nutr-bull. London : The British Nutrition Foundation. Spring 1997. volume 22 (80) page 7-14. 0141-9684
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Natural hazards. Tonic or toxic? Americans are gobbling up nature's remedies for everything from obesity to depression. Source: Spake, A US-News-World-Repage 2001 February 12; 130(6): 42-9 0041-5537
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Obesity among Kuwaiti pre-school children aged 0-5 years: prevalence and comparison with the NCHS/CDC reference population. Author(s): Department of Community Medicine & Behavioural Sciences, Faculty of Medicine, University of Kuwait, Safat. Source: al Isa, A N Moussa, M A Nutr-Health. 1998; 12(4): 235-46 0260-1060
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Obesity, weight-reducing programmes and constipation. Source: Anderson, E. Davies, J. Nutr-food-sci. Bradford, West Yorkshire, England : MCB University Press. Nov/December 1999. (6) page 303-306. 0034-6659
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Overweight, obesity threaten U.S. health gains. Source: FDA-consum. Rockville, Md. : Food and Drug Administration, Department of Health & Human Services. Mar/April 2002. volume 36 (2) page 8. 0362-1332
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Professional singers with obesity or eating-related problems. Author(s): Frances Stern Nutrition Center. Source: Slover, A.N. Dwyer, J.T. Nutrition-today (USA). (June 1995). volume 30(3) page 123-127. overeating digestive disorders overweight occupational hazards music 0029666X
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Sugar gets a bad rap: not the villain in obesity or diabetes. Source: Ward, E.M. Environmental-nutrition (USA). (August 1993). volume 16(8) page 1, 6. sugar human nutrition 0893-4452
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Summary of the National Obesity and Weight Control Symposium. Source: VanItallie, T.B. Simopoulos, A.P. Nutrition-today (USA). (August 1993). volume 28(4) page 33-35. fats overweight weight diet weight gain aetiology 0029-666X
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Teen obesity: a heavy burden even in adulthood. Source: Tufts-University-diet-and-nutrition-letter (USA). (January 1993). volume 10(11) page 1-2. overweight youth diet physical activity disease control 0747-4105
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The effect of education and obesity on attitudes towards fads related to weight reduction among Arab women in Qatar. Source: Musaiger, A.O. Shahbeek, N.E. Nutr-food-sci. Bradford, West Yorkshire, England : MCB University Press. July/August 2001. volume 31 (4/5) page 201-204. 00346659
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The emerging epidemic of obesity in developing societies. Source: Schenker, S. BNF-nutr-bull. London : The British Nutrition Foundation. Spring 1999. volume 24 (86) page 8-13. 0141-9684
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The fruit bowl approach to the treatment of obesity. Source: Ashwell, M. BNF-nutr-bull. London : The Foundation,. Sept 1994. volume 19 (72) page 170-177. 0141-9684
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The news about overweight teens. Source: Weight-Watchers. New York, N.Y. : W/W Twentyfirst Corporation. March 1989. volume 22 (2) page 14, 16. 0043-2180
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The nutrient balance approach to obesity. Source: Bray, G.A. Nutrition-today (USA). (June 1993). volume 28(3) page 13-18. overweight nutrition physiology models nervous system nutrients hormones 0029-666X
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The other side of obesity: a bibliography of recent literature. Author(s): Illinois State University, Normal, IL. Source: Duran, N. Nutrition-today (USA). (April 1996). volume 31(2) page 80-81. overweight diet health hazards risk sociology 0029-666X
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Treatment with dietary trans10cis12 conjugated linoleic acid causes isomer-specific insulin resistance in obese men with the metabolic syndrome. Author(s): Department of Public Health and Caring Sciences/Geriatrics, Uppsala University, Uppsala, Sweden.
[email protected] Source: Riserus, U Arner, P BrisMarch, K Vessby, B Diabetes-Care. 2002 September; 25(9): 1516-21 0149-5992
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Understanding and treating human obesity: what's new. Source: Hill, J.O. Food-and-nutrition-news (USA). (Nov-December 1993). volume 65(5) page 29-31. overweight research energy balance men women 0015-6310
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Weight and overweight. Source: Youngs, Andrew. Nutr-Food-Sci. London, Eng. : Forbes Publications. May/June 1984. volume (88) page 16. 0034-6659
The following information is typical of that found when using the “Full IBIDS Database” to search for “obesity” (or a synonym): •
Acarbose improves indirectly both insulin resistance and secretion in obese type 2 diabetic patients. Author(s): Division of Therapeutic Education for Chronic Diseases, University Hospital Geneva, Switzerland. Source: Delgado, H Lehmann, T Bobbioni Harsch, E Ybarra, J Golay, A Diabetes-Metab. 2002 June; 28(3): 195-200 1262-3636
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Acute effects of valsartan on insulin sensitivity in obese, non-hypertensive subjects with and without type 2 diabetes. Author(s): Diabetes Research Unit, Llandough Hospital, Penlan Road, Penarth, S. Glam. CF64 2XX, Wales, UK.
[email protected] Source: Luzio, S D Dunseath, G Owens, D R Horm-Metab-Res. 2002 May; 34(5): 271-4 0018-5043
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Characterisation of the mouse diabetes susceptibilty locus Nidd/SJL: islet cell destruction, interaction with the obesity QTL Nob1, and effect of dietary fat. Author(s): Institute of Pharmacology and Toxicology, Medical Faculty, Technical University of Aachen, Aachen, Germany. Source: Plum, L Giesen, K Kluge, R Junger, E Linnartz, K Schurmann, A Becker, W Joost, H G Diabetologia. 2002 Jun; 45(6): 823-30 0012-186X
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Defective amplification of the late phase insulin response to glucose by GIP in obese Type II diabetic patients. Author(s): Department of Internal Medicine F, Gentofte Hospital, University of Copenhagen, Niels Andersens Vej 65, 2900 Hellerup, Denmark.
[email protected] Source: Vilsboll, T Krarup, T Madsbad, S Holst, J J Diabetologia. 2002 August; 45(8): 1111-9 0012-186X
Nutrition 171
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Diabetes mellitus and obesity. Author(s): Department of Family Practice, Mount Sinai School of Medicine, Jamaica Hospital Medical Center, 8900 Van Wyck Expressway, Jamaica, NY 11418, USA.
[email protected] Source: Roth, A Prim-Care. 2002 June; 29(2): 279-95 0095-4543
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Differential effect of polyherbal, antiobesity preparation, OB-200G in male and female mice and monosodium glutamate-treated rats. Author(s): Pharmacology Division, University Institute of Pharmaceutical Sciences, Panjab University, Chandigarh, 160 014, India. Source: Kaur, G Kulkarni, S K Indian-J-Exp-Biol. 2001 June; 39(6): 551-7 0019-5189
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Effect of obesity and starvation on thyroid hormone, growth hormone, and cortisol secretion. Author(s): Division of Endocrinology and Metabolism, Department of Internal Medicine, University of Michigan Medical School, 1150 West Medical Center Dr., Ann Arbor, MI 48109, USA. Source: Douyon, L Schteingart, D E Endocrinol-Metab-Clin-North-Am. 2002 March; 31(1): 173-89 0889-8529
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Effect of weight loss on QT dispersion in obesity. Author(s): Thoracic and Cardiovascular Institute and Sparrow Hospital Weight Management Center, Michigan State University, USA.
[email protected] Source: Gupta, A K Xie, B Thakur, R K Maheshwari, A Lokhandwala, Y Carella, M J Indian-Heart-J. 2002 Jul-August; 54(4): 399-403 0019-4832
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Effects of the beta3 adrenergic receptor agonist on developmental obesity in oophorectomized rats. Author(s): Department of Obstetrics and Gynecology, Niigata University, Faculty of Medicine, Niigata, Japan.
[email protected] Source: Tomita, M Kurabayashi, T Matsushita, H Honda, A Tanaka, K Horm-Metab-Res. 2002 July; 34(7): 389-93 0018-5043
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Evaluation and treatment of obesity. Author(s): Department of Internal Medicine, Division of Endocrinology, American University of Beirut Medical Center, Lebanon.
[email protected] Source: Azar, S T Zantout, M S J-Med-Liban. 2000 Sep-October; 48(5): 310-4 0023-9852
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Free fatty acids-the link between obesity and insulin resistance. Author(s): Division of Endocrinology/Diabetes/Metabolism and the General Clinical Research Center, Temple University School of Medicine, Philadelphia, Pennsylvania 19140, USA. Source: Boden, G Endocr-Pract. 2001 Jan-February; 7(1): 44-51 1530-891X
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Insulin signal transduction and glucose transport in human adipocytes: effects of obesity and low calorie diet. Author(s): Section of Integrative Physiology, Karolinska Institutet, Stockholm, Sweden. Source: Bjornholm, M Al Khalili, L Dicker, A Naslund, E Rossner, S Zierath, J R Arner, P Diabetologia. 2002 August; 45(8): 1128-35 0012-186X
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Is obesity associated with poor sleep quality in adolescents? Author(s): School of Public Health, University of Texas Health Science Center at Houston, Houston, Texas 77225, USA. Source: Gupta, N K Mueller, W H Chan, W Meininger, J C Am-J-Human-Biol. 2002 NovDecember; 14(6): 762-8 1042-0533
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Levels of hypothalamic neurotransmitters in lean and obese Zucker rats. Author(s): Obesity Research Program Department of Medicine, Louisiana State University Health Sciences Center, New Orleans 70112, USA.
[email protected] Source: Svec, F Thompson, H Corll, C Porter, J Nutr-Neurosci. 2002 October; 5(5): 321-6 1028-415X
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Lifestyle factors are associated with osteoporosis in lean women but not in normal and overweight women: a population-based cohort study of 1222 women. Author(s): Department of Sports Medicine, Deaconess Institute of Oulu, Isokatu 43, 90100 Oulu, Finland.
[email protected] Source: Korpelainen, R Korpelainen, J Heikkinen, J Vaananen, K Keinanen Kiukaanniemi, S Osteoporos-Int. 2003 January; 14(1): 34-43 0937-941X
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Metallothionein gene expression in human adipose tissue from lean and obese subjects. Author(s): School of Bioscience and Food Technology, Handong University, Pohang, Kyungbuk, Korea. Source: Do, M S Nam, S Y Hong, S E Kim, K W Duncan, J S Beattie, J H Trayhurn, P Horm-Metab-Res. 2002 June; 34(6): 348-51 0018-5043
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Neonatal nutrition: metabolic programming of pancreatic islets and obesity. Author(s): Department of Biochemistry, School of Medicine and Biomedical Sciences, State University of New York, Buffalo, NY 14214, USA. Source: Srinivasan, M Laychock, S G Hill, D J Patel, M S Exp-Biol-Med-(Maywood). 2003 January; 228(1): 15-23 1535-3702
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Nutritional regulation of hypothalamic leptin receptor gene expression is defective in diet-induced obesity. Author(s): Department of Cell Biology and Physiology, University of Pittsburgh School of Medicine, PA 15261, USA.
[email protected] Source: Sahu, A Nguyen, L O'Doherty, R M J-Neuroendocrinol. 2002 November; 14(11): 887-93 0953-8194
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Obese, older adults with knee osteoarthritis: weight loss, exercise, and quality of life. Author(s): Department of Health and Exercise Science, Wake Forest University, Winston-Salem, North Carolina 27109, USA.
[email protected] Source: Rejeski, W J Focht, B C Messier, S P Morgan, T Pahor, M Penninx, B HealthPsychol. 2002 September; 21(5): 419-26 0278-6133
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Obesity and central adiposity in Japanese immigrants: role of the Western dietary pattern. Author(s): Preventive Medicine Department, the Federal University of Sao Paulo, SP, Brazil. Source: Ferreira, S R Lerario, D D Gimeno, S G Sanudo, A Franco, L J J-Epidemiol. 2002 November; 12(6): 431-8 0917-5040
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Obesity and medicinal plants. Author(s): Department of Pharmaceutical and Toxicological Chemistry, Study University of Naples Federico II, via D. Montesano 49, 80131, Naples, Italy. Source: Moro, C O Basile, G Fitoterapia. 2000 August; 71 Suppl 1: S73-82 0367-326X
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Obesity clinical trials in youth: concepts and challenges. Author(s): Department of Pediatrics, Medical College of Georgia, Augusta, Georgia 30912-3770, USA.
[email protected] Source: Moore, D B Ethn-Dis. 2002 Fall; 12(4): S3-40-3 1049-510X
Nutrition 173
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Obesity correlates with increased blood pressures in urban Native American youth. Author(s): Department of Food Science and Nutrition, University of Minnesota, St Paul, Minnesota 55108, USA.
[email protected] Source: Smith, C Rinderknecht, K Am-J-Human-Biol. 2003 Jan-February; 15(1): 78-90 1042-0533
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Obesity exacerbates chemically induced neurodegeneration. Author(s): HELD/TMBB, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, Mailstop L-3014, 1095 Willowdale Road, Morgantown, WV 26505, USA. Source: Sriram, K Benkovic, S A Miller, D B O'Callaghan, J P Neuroscience. 2002; 115(4): 1335-46 0306-4522
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Obesity in Malaysia. Author(s): Department of Nutrition and Dietetics, University Kebangsaan Malaysia, Kuala, Lumpur.
[email protected] Source: Ismail, M N Chee, S S Nawawi, H Yusoff, K Lim, T O James, W P ObesRevolume 2002 August; 3(3): 203-8 1467-7881
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Observation on the therapeutic effects of acupuncture for 60 cases of simple obesity. Author(s): Tianjin Municipal Hospital of TCM, Tianjin 300140. Source: Wang, H J-Tradit-Chin-Med. 2002 September; 22(3): 187-9 0254-6272
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Overweight is an independent risk factor for cardiovascular disease in Chinese populations. Author(s): Cardiovascular Institute, Fu Wai Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing.
[email protected] Source: Zhou, B Wu, Y Yang, J Li, Y Zhang, H Zhao, L Obes-Revolume 2002 August; 3(3): 147-56 1467-7881
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Part III. Obesity. Author(s): Department of Surgery, University of Chicago Pritzker School of Medicine, Illinois, USA. Source: Boogerd, A Alverdy, J KuMarch, S Olson, D L Schwenk, W F Dis-Mon. 2002 November; 48(11): 725-42 0011-5029
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Pattern of dietary behaviour and obesity in Ahwaz, Islamic Republic of Iran. Author(s): Department of Community Medicine, School of Medicine, Ahwaz University of Medical Sciences, Ahwaz, Islamic Republic of Iran. Source: Soori, H East-Mediterr-Health-J. 2001 Jan-March; 7(1-2): 163-70 1020-3397
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Permanent prostate brachytherapy-induced morbidity in patients with grade II and III obesity. Author(s): Schiffler Cancer Center, Wheeling Hospital, Wheeling, West Virginia 260036300, USA. Source: Merrick, G S Butler, W M Wallner, K Galbreath, R W Anderson, R L Kurko, B S Lief, J H Urology. 2002 July; 60(1): 104-8 1527-9995
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Project Grow-2-Gether: a study of the genetic and environmental influences on child eating and obesity. Author(s): Weight and Eating Disorders Program, University of Pennsylvania School of Medicine, Philadelphia 19104, USA.
[email protected] Source: Faith, M S Keller, K L Matz, P Johnson, S L Lewis, R Jorge, M A Ridley, C Han, H Must, S Heo, M Pietrobelli, A Heymsfield, S B Allison, D B Twin-Res. 2002 October; 5(5): 472-5 1369-0523
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Recent developments in the treatment of obesity-related hypertension. Author(s): Franz Volhard Clinic - HELIOS-Klinikum Berlin Buch, Charite, Medical Faculty of the Humboldt University Berlin, Max Delbruck Center for Molecular Medicine, Germany. Source: Pischon, T Sharma, A M Curr-Opin-Nephrol-Hypertens. 2002 September; 11(5): 497-502 1062-4821
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Resumption of fertility with diet in overweight women. Author(s): First Department of Obstetrics and Gynaecology, University of Milan, Via della Commenda 12, 20122 Milan, Italy. piergiorgio.crosignani.it Source: Crosignani, P G Vegetti, W Colombo, M Ragni, G Reprod-Biomed-Online. 2002 Jul-August; 5(1): 60-4 1472-6483
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School-based obesity prevention: a blueprint for taming the epidemic. Author(s): Children's Nutrition Research Center, Baylor College of Medicine, Houston, TX 77030-2600, USA.
[email protected] Source: Baranowski, T Cullen, K W Nicklas, T Thompson, D Baranowski, J Am-J-HealthBehavolume 2002 Nov-December; 26(6): 486-93 1087-3244
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Synergic effect of overweight and cold on uncoupling proteins expression, a role of alpha(2)/beta(3) adrenergic receptor balance? Author(s): Departament de Biologia Fonamental i Ciencies de la Salut, Laboratori de Biologia Molecular, Nutricio i Biotecnologia, Universitat de les Illes Balears, Palma de Mallorca, 07071, Spain. Source: Rodriguez, A M Roca, P Palou, A Pflugers-Arch. 2002 July; 444(4): 484-90 00316768
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The effect of adrenalectomy on leptin levels and some metabolic parameters in rats with diet-induced obesity. Author(s): Department of Biochemistry, Faculty of Medicine, University of Ataturk, Erzurum, Turkey. Source: Yilmaz, A Suleyman, H Umudum, Z Sahin, Y N Biol-Pharm-Bull. 2002 May; 25(5): 580-3 0918-6158
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The effect of opioid antagonism on food intake behavior and body weight in a biobehavioral model of obese binge eating. Author(s): College of Nursing at Wayne State University, Detroit, Michigan 48202, USA.
[email protected] Source: Jarosz, P A Metzger, B L Biol-Res-Nurs. 2002 April; 3(4): 198-209 1099-8004
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The effects of miglitol on glucagon-like peptide-1 secretion and appetite sensations in obese type 2 diabetics. Author(s): Department of Medicine, St Louis University Medical Center, and GRECC, St Louis VA Medical Center, St Louis, MO, USA. Source: Lee, A Patrick, P Wishart, J Horowitz, M Morley, J E Diabetes-Obes-Metab. 2002 September; 4(5): 329-35 1462-8902
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The effects of orlistat on body weight and glycaemic control in overweight patients with type 2 diabetes: a randomized, placebo-controlled trial. Author(s): Zentrum fur Klinische Studien, GWT-Technische Universitat Dresden, Dresden, Germany.
[email protected] Source: Hanefeld, M Sachse, G Diabetes-Obes-Metab. 2002 November; 4(6): 415-23 14628902
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The elephant in the room: evolution, behavioralism, and counteradvertising in the coming war against obesity. Source: Anonymous Harv-Law-Revolume 2003 February; 116(4): 1161-84 0017-811X
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The epidemic of childhood obesity. Source: du Toit, G van der Merwe, M T S-Afr-Med-J. 2003 January; 93(1): 49-50 00382469
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The impact of a modified and supplemented diet on obesity syndrome in Kuwaiti citizens. Author(s): Dar Al-Shifa Hospital Kuwait Source: Rabie, M.M.A. Barlow, ,P.J. Taylor, K.D.A. Mansoura-University-Journal-ofAgricultural-Sciences (Egypt). (May 2001). volume 26 (5) page 2939-2957. Received 2002. foods food additives food hygiene overweight symptoms kuwait 1110-0346
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The lifecycle effects of nutrition and body size on adult adiposity, diabetes and cardiovascular disease. Author(s): Diabetes Unit, KEM Hospital Research Centre, Rasta Peth, Pune, India.
[email protected] Source: Yajnik, C S Obes-Revolume 2002 August; 3(3): 217-24 1467-7881
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The obesity pandemic--implications for Pakistan. Author(s): Department of Community Health Sciences, Aga Khan University, Karachi. Source: Nanan, D J J-Pak-Med-Assoc. 2002 August; 52(8): 342-6 0030-9982
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Treatment of morbid obesity with intragastric balloon in association with diet. Author(s): Cattedra di Chirurgia Generale dell'Universita degli Studi di Milano, Unita Operativa di Chirurgia Generale, Istituto Clinico Sant'Ambrogio di Milano, Italy.
[email protected] Source: Doldi, S B Micheletto, G Perrini, M N Librenti, M C Rella, S Obes-Surg. 2002 August; 12(4): 583-7 0960-8923
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Twenty-year changes in the prevalence of overweight in Japanese adults: the National Nutrition Survey 1976-95. Author(s): National Institute of Health and Nutrition, Tokyo, Japan.
[email protected] Source: Yoshiike, N Seino, F Tajima, S Arai, Y Kawano, M Furuhata, T Inoue, S ObesRevolume 2002 August; 3(3): 183-90 1467-7881
Federal Resources on Nutrition In addition to the IBIDS, the United States Department of Health and Human Services (HHS) and the United States Department of Agriculture (USDA) provide many sources of information on general nutrition and health. Recommended resources include: •
healthfinder®, HHS’s gateway to health information, including diet and nutrition: http://www.healthfinder.gov/scripts/SearchContext.asp?topic=238&page=0
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The United States Department of Agriculture’s Web site dedicated to nutrition information: www.nutrition.gov
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The Food and Drug Administration’s Web site for federal food safety information: www.foodsafety.gov
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The National Action Plan on Overweight and Obesity sponsored by the United States Surgeon General: http://www.surgeongeneral.gov/topics/obesity/
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The Center for Food Safety and Applied Nutrition has an Internet site sponsored by the Food and Drug Administration and the Department of Health and Human Services: http://vm.cfsan.fda.gov/
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Center for Nutrition Policy and Promotion sponsored by the United States Department of Agriculture: http://www.usda.gov/cnpp/
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Food and Nutrition Information Center, National Agricultural Library sponsored by the United States Department of Agriculture: http://www.nal.usda.gov/fnic/
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Food and Nutrition Service sponsored by the United States Department of Agriculture: http://www.fns.usda.gov/fns/
Additional Web Resources A number of additional Web sites offer encyclopedic information covering food and nutrition. The following is a representative sample: •
AOL: http://search.aol.com/cat.adp?id=174&layer=&from=subcats
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Family Village: http://www.familyvillage.wisc.edu/med_nutrition.html
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Google: http://directory.google.com/Top/Health/Nutrition/
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Healthnotes: http://www.healthnotes.com/
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Open Directory Project: http://dmoz.org/Health/Nutrition/
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Yahoo.com: http://dir.yahoo.com/Health/Nutrition/
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WebMDHealth: http://my.webmd.com/nutrition
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WholeHealthMD.com: http://www.wholehealthmd.com/reflib/0,1529,,00.html
The following is a specific Web list relating to obesity; please note that any particular subject below may indicate either a therapeutic use, or a contraindication (potential danger), and does not reflect an official recommendation (some Web sites are subscription based): •
Vitamins Vitamin D Alternative names: Calciferol, Calcitrol, Cholecalciferol, Erocalciferol Source: Integrative Medicine Communications; www.drkoop.com Vitamin E Source: Healthnotes, Inc. www.healthnotes.com
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Minerals Chromium Source: Integrative Medicine Communications; www.drkoop.com Chromium Source: Prima Communications, Inc.www.personalhealthzone.com
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Chromium Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10018,00.html Potassium Source: Prima Communications, Inc.www.personalhealthzone.com Vanadium Source: Prima Communications, Inc.www.personalhealthzone.com •
Food and Diet Atkins Diet Source: Healthnotes, Inc. www.healthnotes.com Beef Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/foods_view/0,1523,85,00.html Complex carbohydrates Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,993,00.html Fasting Diet Source: Healthnotes, Inc. www.healthnotes.com Guaraná Source: Healthnotes, Inc. www.healthnotes.com High-Fiber Diet Source: Healthnotes, Inc. www.healthnotes.com Hypertension Source: Healthnotes, Inc. www.healthnotes.com Low-Fat Diet Source: Healthnotes, Inc. www.healthnotes.com Low-Purine Diet Source: Healthnotes, Inc. www.healthnotes.com Low-Salt Diet Source: Healthnotes, Inc. www.healthnotes.com Omega-3 Fatty Acids Source: Integrative Medicine Communications; www.drkoop.com
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Vegetarian Diet Source: Healthnotes, Inc. www.healthnotes.com Weight Loss and Obesity Source: Healthnotes, Inc. www.healthnotes.com Weight Management Index Source: Healthnotes, Inc. www.healthnotes.com
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CHAPTER 3. ALTERNATIVE MEDICINE AND OBESITY Overview In this chapter, we will begin by introducing you to official information sources on complementary and alternative medicine (CAM) relating to obesity. At the conclusion of this chapter, we will provide additional sources.
The Combined Health Information Database The Combined Health Information Database (CHID) is a bibliographic database produced by health-related agencies of the U.S. federal government (mostly from the National Institutes of Health) that can offer concise information for a targeted search. The CHID database is updated four times a year at the end of January, April, July, and October. Check the titles, summaries, and availability of CAM-related information by using the “Simple Search” option at the following Web site: http://chid.nih.gov/simple/simple.html. In the drop box at the top, select “Complementary and Alternative Medicine.” Then type “obesity” (or synonyms) in the second search box. We recommend that you select 100 “documents per page” and to check the “whole records” options. The following was extracted using this technique: •
Complementary Therapies and Health Promotion Source: British Journal of Community Nursing. 7(2): 102-7. February 2002. Summary: This journal article reviews evidence that supports the role of complementary therapies as adjunctive treatments to enable nurses to talk about their use with clients as part of their health options. It discusses the rational for complementary and alternative medicine (CAM) and the two definitions of CAM offered by the British Medical Association. Information on study results related to addictive behaviors, obesity, and stress (including anxiety and depression) is given, because these are three lifestyle behaviors that may respond to health promotion interventions in which CAM can play a part. Numerous references. 6 pages.
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Using the Body To Heal the Body: Exercise and Disease Intervention Source: Alternative and Complementary Therapies. 4(3): 169-172. June 1998.
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Summary: This journal article discusses the multiple health benefits of exercise, highlighting the work in this area by Dr. L. Goldberg and D. L. Elliot at the Human Performance Laboratory, Division of Health Promotion and Sports Medicine, Oregon Health Sciences University in Portland. Drs. Goldberg and Elliot have focused their work on the effects of exercise in hypertension, neuromuscular diseases, certain metabolic conditions, and obesity. Clinicians at the Human Performance Laboratory offer patients a choice of testing options, and develop individualized exercise plans specifying exercise mode, intensity, duration, frequency, and progression. They also help patients develop strategies to overcome potential barriers to plan compliance. Exercise, along with diet, stress reduction, and social support, also is an integral component of the Opening Your Heart Program developed by Dr. D. Ornish at the Preventive Medicine Research Center in Sausalito, California. Dr. Ornish emphasizes that exercise does not have to be vigorous to be beneficial, noting that consistency is more important than intensity. In addition to its benefits in heart disease, recent research suggests a role for exercise in reducing cancer risk and improving function in older age. The article includes a list of recommended readings and 14 references.
National Center for Complementary and Alternative Medicine The National Center for Complementary and Alternative Medicine (NCCAM) of the National Institutes of Health (http://nccam.nih.gov/) has created a link to the National Library of Medicine’s databases to facilitate research for articles that specifically relate to obesity and complementary medicine. To search the database, go to the following Web site: http://www.nlm.nih.gov/nccam/camonpubmed.html. Select “CAM on PubMed.” Enter “obesity” (or synonyms) into the search box. Click “Go.” The following references provide information on particular aspects of complementary and alternative medicine that are related to obesity: •
A cost-analysis of adopting a healthful diet in a family-based obesity treatment program. Author(s): Raynor HA, Kilanowski CK, Esterlis I, Epstein LH. Source: Journal of the American Dietetic Association. 2002 May; 102(5): 645-56. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12008989&dopt=Abstract
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A cross-cultural analysis of 'motivation for eating' as a potential factor in the emergence of global obesity: Japan and the United States. Author(s): Hawks SR, Madanat HN, Merrill RM, Goudy MB, Miyagawa T. Source: Health Promotion International. 2003 June; 18(2): 153-62. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12746387&dopt=Abstract
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A perspective on obesity. Author(s): Johnson RW, Broadnax PA. Source: The Abnf Journal : Official Journal of the Association of Black Nursing Faculty in Higher Education, Inc. 2003 May-June; 14(3): 69-70. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12856445&dopt=Abstract
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A randomized trial of a low-carbohydrate diet for obesity. Author(s): Foster GD, Wyatt HR, Hill JO, McGuckin BG, Brill C, Mohammed BS, Szapary PO, Rader DJ, Edman JS, Klein S. Source: The New England Journal of Medicine. 2003 May 22; 348(21): 2082-90. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12761365&dopt=Abstract
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A succulent cure to end obesity. Author(s): Habeck M. Source: Drug Discovery Today. 2002 March 1; 7(5): 280-1. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11854044&dopt=Abstract
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Acupuncture for the treatment of obesity: a review of the evidence. Author(s): Lacey JM, Tershakovec AM, Foster GD. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2003 April; 27(4): 419-27. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12664074&dopt=Abstract
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Alternative therapies for obesity: benefit or rip-off. Author(s): Klein S. Source: Critical Reviews in Food Science and Nutrition. 2001 January; 41(1): 33-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11152043&dopt=Abstract
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Alternative therapies: Part I. Depression, diabetes, obesity. Author(s): Morelli V, Zoorob RJ. Source: American Family Physician. 2000 September 1; 62(5): 1051-60. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10997530&dopt=Abstract
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Beneficial effects of tea catechins on diet-induced obesity: stimulation of lipid catabolism in the liver. Author(s): Murase T, Nagasawa A, Suzuki J, Hase T, Tokimitsu I. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2002 November; 26(11): 1459-64. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12439647&dopt=Abstract
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Beneficial role of dietary phytoestrogens in obesity and diabetes. Author(s): Bhathena SJ, Velasquez MT. Source: The American Journal of Clinical Nutrition. 2002 December; 76(6): 1191-201. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12450882&dopt=Abstract
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Biocultural aspects of obesity in young Mexican schoolchildren. Author(s): Brewis A.
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Source: American Journal of Human Biology : the Official Journal of the Human Biology Council. 2003 May-June; 15(3): 446-60. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12704721&dopt=Abstract •
Biomarkers and functional foods for obesity and diabetes. Author(s): Hill JO, Peters JC. Source: The British Journal of Nutrition. 2002 November; 88 Suppl 2: S213-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12495462&dopt=Abstract
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Body image disturbance in obese outpatients before and after weight loss in relation to race, gender, binge eating, and age of onset of obesity. Author(s): Sorbara M, Geliebter A. Source: The International Journal of Eating Disorders. 2002 May; 31(4): 416-23. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11948646&dopt=Abstract
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Breast cancer and obesity. Author(s): La Guardia M, Giammanco M. Source: Panminerva Medica. 2001 June; 43(2): 123-33. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11449184&dopt=Abstract
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Calorie use and obesity among diabetic and non-diabetic Mvskoke Indians. Author(s): Edwards KA, Pryor S, Campbell J, Jacobsen S, Booton-Hiser D. Source: J Cult Divers. 2000 Summer; 7(2): 36-40. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11249259&dopt=Abstract
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Chemical toxins: a hypothesis to explain the global obesity epidemic. Author(s): Baillie-Hamilton PF. Source: Journal of Alternative and Complementary Medicine (New York, N.Y.). 2002 April; 8(2): 185-92. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12006126&dopt=Abstract
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Childhood obesity in Europe: a growing concern. Author(s): Livingstone MB. Source: Public Health Nutrition. 2001 February; 4(1A): 109-16. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11255500&dopt=Abstract
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Childhood obesity reduction by school based programs. Author(s): Davis SP, Davis M, Northington L, Moll G, Kolar K. Source: The Abnf Journal : Official Journal of the Association of Black Nursing Faculty in Higher Education, Inc. 2002 November-December; 13(6): 145-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12592832&dopt=Abstract
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Childhood obesity: the genetic-environmental interface. Author(s): Maffeis C. Source: Bailliere's Best Practice & Research. Clinical Endocrinology & Metabolism. 1999 April; 13(1): 31-46. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10932675&dopt=Abstract
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Childhood obesity: the health issue. Author(s): Deckelbaum RJ, Williams CL. Source: Obesity Research. 2001 November; 9 Suppl 4: 239S-243S. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11707548&dopt=Abstract
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Cholesterol absorption efficiency and sterol metabolism in obesity. Author(s): Miettinen TA, Gylling H. Source: Atherosclerosis. 2000 November; 153(1): 241-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11058720&dopt=Abstract
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Coagulation and fibrinolysis abnormalities in obesity. Author(s): De Pergola G, Pannacciulli N. Source: J Endocrinol Invest. 2002 November; 25(10): 899-904. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12508953&dopt=Abstract
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Cultural considerations for treatment of childhood obesity. Author(s): Davis SP, Northington L, Kolar K. Source: J Cult Divers. 2000 Winter; 7(4): 128-32. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11855259&dopt=Abstract
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Current concepts in the management of obesity. An evidence based review. Author(s): Al-Quaiz AJ. Source: Saudi Med J. 2001 March; 22(3): 205-10. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11307103&dopt=Abstract
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Current status of medical and surgical therapy for obesity. Author(s): Mun EC, Blackburn GL, Matthews JB. Source: Gastroenterology. 2001 February; 120(3): 669-81. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11179243&dopt=Abstract
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Developing health messages: qualitative studies with children, parents, and teachers help identify communications opportunities for healthful lifestyles and the prevention of obesity. Author(s): Borra ST, Kelly L, Shirreffs MB, Neville K, Geiger CJ.
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Source: Journal of the American Dietetic Association. 2003 June; 103(6): 721-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12778044&dopt=Abstract •
Diabetes mellitus and obesity. Author(s): Roth A. Source: Primary Care. 2002 June; 29(2): 279-95. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12391712&dopt=Abstract
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Diet culture and obesity in northern Africa. Author(s): Mokhtar N, Elati J, Chabir R, Bour A, Elkari K, Schlossman NP, Caballero B, Aguenaou H. Source: The Journal of Nutrition. 2001 March; 131(3): 887S-892S. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11238780&dopt=Abstract
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Dietary cyanidin 3-O-beta-D-glucoside-rich purple corn color prevents obesity and ameliorates hyperglycemia in mice. Author(s): Tsuda T, Horio F, Uchida K, Aoki H, Osawa T. Source: The Journal of Nutrition. 2003 July; 133(7): 2125-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12840166&dopt=Abstract
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Dietary fat subtypes and obesity. Author(s): Storlien LH, Huang XF, Lin S, Xin X, Wang HQ, Else PL. Source: World Review of Nutrition and Dietetics. 2001; 88: 148-54. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11935947&dopt=Abstract
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Epidemiology of childhood obesity in Europe. Author(s): Livingstone B. Source: European Journal of Pediatrics. 2000 September; 159 Suppl 1: S14-34. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11011953&dopt=Abstract
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Ethnic issues in the epidemiology of childhood obesity. Author(s): Crawford PB, Story M, Wang MC, Ritchie LD, Sabry ZI. Source: Pediatric Clinics of North America. 2001 August; 48(4): 855-78. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11494640&dopt=Abstract
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Evidence based paediatrics: Evidence based management of childhood obesity. Author(s): Edmunds L, Waters E, Elliott EJ. Source: Bmj (Clinical Research Ed.). 2001 October 20; 323(7318): 916-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11668139&dopt=Abstract
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For the patient. Are vegetarians at less risk for obesity, diabetes, and hypertension? Obesity, diabetes, hypertension, and vegetarian status among Seventh-Day
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Adventists in Barbados: preliminary results. Author(s): Brathwaite N, Fraser HS, Modeste N, Broome H, King R. Source: Ethn Dis. 2003 Winter; 13(1): 148. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12723025&dopt=Abstract •
Gourmand savants and environmental determinants of obesity. Author(s): Myslobodsky M. Source: Obesity Reviews : an Official Journal of the International Association for the Study of Obesity. 2003 May; 4(2): 121-8. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12760447&dopt=Abstract
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Hepatothermic therapy of obesity: rationale and an inventory of resources. Author(s): McCarty MF. Source: Medical Hypotheses. 2001 September; 57(3): 324-36. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11516225&dopt=Abstract
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Herbal simulation of ephedrine and caffeine in treatment of obesity. Author(s): Dulloo AG. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2002 May; 26(5): 590-2. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12032740&dopt=Abstract
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Herbal therapy for management of obesity: observations from a clinical endocrinology practice. Author(s): Sindler BH. Source: Endocrine Practice : Official Journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists. 2001 November-December; 7(6): 443-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11747280&dopt=Abstract
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Hunter-gatherers win profit-sharing deal for obesity drug. Author(s): Wise J. Source: Bulletin of the World Health Organization. 2003; 81(5): 382. Epub 2003 July 07. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12856057&dopt=Abstract
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Integrating the prevention of eating disorders and obesity: feasible or futile? Author(s): Irving LM, Neumark-Sztainer D. Source: Preventive Medicine. 2002 March; 34(3): 299-309. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11902846&dopt=Abstract
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Integrative medicine approach to obesity and diabetes. Author(s): Shintani TT.
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Source: Hawaii Med J. 2001 October; 60(10): 262-3. Review. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11732378&dopt=Abstract •
Laser acupuncture and low-calorie diet during visceral obesity therapy after menopause. Author(s): Wozniak P, Stachowiak G, Pieta-Dolinska A, Oszukowski P. Source: Acta Obstetricia Et Gynecologica Scandinavica. 2003 January; 82(1): 69-73. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12580844&dopt=Abstract
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Managing obesity like any other chronic condition. Long-term therapy may reduce comorbidity as well. Author(s): Agrawal M, Worzniak M, Diamond L. Source: Postgraduate Medicine. 2000 July; 108(1): 75-6, 79-82. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10914120&dopt=Abstract
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Modulation of adipocyte lipoprotein lipase expression as a strategy for preventing or treating visceral obesity. Author(s): McCarty MF. Source: Medical Hypotheses. 2001 August; 57(2): 192-200. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11461172&dopt=Abstract
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Modulation of obesity by a green tea catechin. Author(s): Kao YH, Hiipakka RA, Liao S. Source: The American Journal of Clinical Nutrition. 2000 November; 72(5): 1232-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11063454&dopt=Abstract
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Morbidity of severe obesity. Author(s): Kral JG. Source: The Surgical Clinics of North America. 2001 October; 81(5): 1039-61. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11589244&dopt=Abstract
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Natural hazards. Tonic or toxic? Americans are gobbling up nature's remedies for everything from obesity to depression. Author(s): Spake A. Source: U.S. News & World Report. 2001 February 12; 130(6): 42-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11216231&dopt=Abstract
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Nutrition for health promotion: phytochemicals, functional foods, and alternative approaches to combat obesity. Author(s): Bloch AS.
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Source: Dent Clin North Am. 2003 April; 47(2): 411-23, Viii-Ix. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12699239&dopt=Abstract •
Nutritional and other influences in childhood as predictors of adult obesity. Author(s): Power C, Parsons T. Source: The Proceedings of the Nutrition Society. 2000 May; 59(2): 267-72. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10946795&dopt=Abstract
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Obesity and associated modifiable environmental factors in Iranian adolescents: Isfahan Healthy Heart Program - Heart Health Promotion from Childhood. Author(s): Kelishadi R, Hashemi Pour M, Sarraf-Zadegan N, Sadry Gh G, Ansari R, Alikhassy H, Bashardoust N. Source: Pediatrics International : Official Journal of the Japan Pediatric Society. 2003 August; 45(4): 435-442. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12911481&dopt=Abstract
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Obesity and cortisol. Author(s): Bjorntorp P, Rosmond R. Source: Nutrition (Burbank, Los Angeles County, Calif.). 2000 October; 16(10): 924-36. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11054598&dopt=Abstract
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Obesity and medicinal plants. Author(s): Moro CO, Basile G. Source: Fitoterapia. 2000 August; 71 Suppl 1: S73-82. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10930716&dopt=Abstract
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Obesity intervention among African-American children and adolescents. Author(s): Baskin ML, Ahluwalia HK, Resnicow K. Source: Pediatric Clinics of North America. 2001 August; 48(4): 1027-39. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11494636&dopt=Abstract
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Obesity, diabetes, hypertension, and vegetarian status among Seventh-Day Adventists in Barbados: preliminary results. Author(s): Brathwaite N, Fraser HS, Modeste N, Broome H, King R. Source: Ethn Dis. 2003 Winter; 13(1): 34-9. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12723010&dopt=Abstract
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Obesity. Author(s): Yanovski SZ, Yanovski JA.
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Source: The New England Journal of Medicine. 2002 February 21; 346(8): 591-602. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11856799&dopt=Abstract •
Observation on the therapeutic effects of acupuncture for 60 cases of simple obesity. Author(s): Wang H. Source: J Tradit Chin Med. 2002 September; 22(3): 187-9. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12400423&dopt=Abstract
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Overweight and obesity in women: health risks and consequences. Author(s): Hu FB. Source: Journal of Women's Health (2002). 2003 March; 12(2): 163-72. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12737715&dopt=Abstract
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Platycodi radix affects lipid metabolism in mice with high fat diet-induced obesity. Author(s): Han LK, Xu BJ, Kimura Y, Zheng Y, Okuda H. Source: The Journal of Nutrition. 2000 November; 130(11): 2760-4. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11053518&dopt=Abstract
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Popular diets: correlation to health, nutrition, and obesity. Author(s): Kennedy ET, Bowman SA, Spence JT, Freedman M, King J. Source: Journal of the American Dietetic Association. 2001 April; 101(4): 411-20. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11320946&dopt=Abstract
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Possible lessons from the tobacco experience for obesity control. Author(s): Mercer SL, Green LW, Rosenthal AC, Husten CG, Khan LK, Dietz WH. Source: The American Journal of Clinical Nutrition. 2003 April; 77(4 Suppl): 1073S1082S. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12663321&dopt=Abstract
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Prevention of childhood obesity: sociocultural and familial factors. Author(s): Bruss MB, Morris J, Dannison L. Source: Journal of the American Dietetic Association. 2003 August; 103(8): 1042-5. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12891156&dopt=Abstract
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Preventive strategies against weight gain and obesity. Author(s): Swinburn B, Egger G. Source: Obesity Reviews : an Official Journal of the International Association for the Study of Obesity. 2002 November; 3(4): 289-301. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12458974&dopt=Abstract
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Principles and practices in the management of obesity. Author(s): Foster GD. Source: American Journal of Respiratory and Critical Care Medicine. 2003 August 1; 168(3): 274-80. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12888610&dopt=Abstract
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Protective effects of a soy diet in preventing obesity-linked renal disease. Author(s): Maddox DA, Alavi FK, Silbernick EM, Zawada ET. Source: Kidney International. 2002 January; 61(1): 96-104. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11786089&dopt=Abstract
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Randomized controlled trial of the effect of n-3 fatty acid supplementation on the metabolism of apolipoprotein B-100 and chylomicron remnants in men with visceral obesity. Author(s): Chan DC, Watts GF, Mori TA, Barrett PH, Redgrave TG, Beilin LJ. Source: The American Journal of Clinical Nutrition. 2003 February; 77(2): 300-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12540386&dopt=Abstract
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Recent findings of green tea extract AR25 (Exolise) and its activity for the treatment of obesity. Author(s): Chantre P, Lairon D. Source: Phytomedicine : International Journal of Phytotherapy and Phytopharmacology. 2002 January; 9(1): 3-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11924761&dopt=Abstract
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Reduction of abdominal obesity in lipodystrophy associated with human immunodeficiency virus infection by means of diet and exercise: case report and proof of principle. Author(s): Roubenoff R, Schmitz H, Bairos L, Layne J, Potts E, Cloutier GJ, Denry F. Source: Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America. 2002 February 1; 34(3): 390-3. Epub 2001 December 17. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11774087&dopt=Abstract
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Ripe for study: complementary and alternative treatments for obesity. Author(s): Evans M, Straus S. Source: Critical Reviews in Food Science and Nutrition. 2001 January; 41(1): 35-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11152044&dopt=Abstract
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Safety and efficacy of ephedra and ephedrine for enhancement of athletic performance, thermogenesis and the treatment of obesity. Author(s): Shekelle P, Hardy M.
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Source: Phytomedicine : International Journal of Phytotherapy and Phytopharmacology. 2002 January; 9(1): 78. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11924769&dopt=Abstract •
Salacia reticulata and its polyphenolic constituents with lipase inhibitory and lipolytic activities have mild antiobesity effects in rats. Author(s): Yoshikawa M, Shimoda H, Nishida N, Takada M, Matsuda H. Source: The Journal of Nutrition. 2002 July; 132(7): 1819-24. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12097653&dopt=Abstract
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Self-help and long-term behavior therapy for obesity. Author(s): Latner JD, Wilson GT, Stunkard AJ, Jackson ML. Source: Behaviour Research and Therapy. 2002 July; 40(7): 805-12. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12074374&dopt=Abstract
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Self-help in the long-term treatment of obesity. Author(s): Latner JD. Source: Obesity Reviews : an Official Journal of the International Association for the Study of Obesity. 2001 May; 2(2): 87-97. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12119666&dopt=Abstract
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Single nucleotide polymorphism identification in candidate gene systems of obesity. Author(s): Irizarry K, Hu G, Wong ML, Licinio J, Lee CJ. Source: The Pharmacogenomics Journal. 2001; 1(3): 193-203. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11908756&dopt=Abstract
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Site-specific differences in the fatty acid composition of abdominal adipose tissue in an obese population from a Mediterranean area: relation with dietary fatty acids, plasma lipid profile, serum insulin, and central obesity. Author(s): Garaulet M, Perez-Llamas F, Perez-Ayala M, Martinez P, de Medina FS, Tebar FJ, Zamora S. Source: The American Journal of Clinical Nutrition. 2001 November; 74(5): 585-91. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11684525&dopt=Abstract
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The associations of a marine diet with plasma lipids, blood glucose, blood pressure and obesity among the inuit in Greenland. Author(s): Bjerregaard P, Pedersen HS, Mulvad G. Source: European Journal of Clinical Nutrition. 2000 September; 54(9): 732-7. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11002386&dopt=Abstract
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The cross cultural context of obesity: an INCLEN multicentre collaborative study. Author(s): Treloar C, Porteous J, Hassan F, Kasniyah N, Lakshmanudu M, Sama M, Sja'bani M, Heller RF.
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Source: Health & Place. 1999 December; 5(4): 279-86. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10984582&dopt=Abstract •
The Hawaii Diet: ad libitum high carbohydrate, low fat multi-cultural diet for the reduction of chronic disease risk factors: obesity, hypertension, hypercholesterolemia, and hyperglycemia. Author(s): Shintani TT, Beckham S, Brown AC, O'Connor HK. Source: Hawaii Med J. 2001 March; 60(3): 69-73. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11320614&dopt=Abstract
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The Influence of Obesity on the Self-Reported Health Status of Chamorros and other Residents of Guam. Author(s): Pinhey TK, Heathcote GM, Rarick J. Source: Asian Am Pac Isl J Health. 1994 Summer; 2(3): 195-211. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11567272&dopt=Abstract
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The pathogenesis of obesity. Author(s): Campfield LA, Smith FJ. Source: Bailliere's Best Practice & Research. Clinical Endocrinology & Metabolism. 1999 April; 13(1): 13-30. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=10932674&dopt=Abstract
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The process of restructuring and the treatment of obesity in women. Author(s): Hayward LM, Nixon C, Jasper MP, Murphy KM, Harlan V, Swirda L, Hayward K. Source: Health Care for Women International. 2000 October-November; 21(7): 615-30. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11813769&dopt=Abstract
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The skinny on obesity and cancer. Obesity increases the risk of death from cancer, but being overweight isn't inescapable. Author(s): Blackburn GL. Source: Health News. 2003 June; 9(6): 3. No Abstract Available. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12793396&dopt=Abstract
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The treatment of obesity. Author(s): Mina WC, Burns RW, Terry BE. Source: Mo Med. 2003 May-June; 100(3): 248-55. Review. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12847866&dopt=Abstract
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Three-month tolerability of orlistat in adolescents with obesity-related comorbid conditions. Author(s): McDuffie JR, Calis KA, Uwaifo GI, Sebring NG, Fallon EM, Hubbard VS, Yanovski JA.
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Source: Obesity Research. 2002 July; 10(7): 642-50. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12105286&dopt=Abstract •
Treatment of child and adolescent obesity: reports from pediatricians, pediatric nurse practitioners, and registered dietitians. Author(s): Barlow SE, Trowbridge FL, Klish WJ, Dietz WH. Source: Pediatrics. 2002 July; 110(1 Pt 2): 229-35. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12094000&dopt=Abstract
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Triiodothyronine supplementation for hypothalamic obesity. Author(s): Fernandes JK, Klein MJ, Ater JL, Kuttesch JF, Vassilopoulou-Sellin R. Source: Metabolism: Clinical and Experimental. 2002 November; 51(11): 1381-3. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=12404183&dopt=Abstract
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Use of quality control indices in moderately hypocaloric Mediterranean diet for treatment of obesity. Author(s): De Lorenzo A, Petroni ML, De Luca PP, Andreoli A, Morini P, Iacopino L, Innocente I, Perriello G. Source: Diabetes Nutr Metab. 2001 August; 14(4): 181-8. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11716286&dopt=Abstract
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What is an optimal diet? Relationship of macronutrient intake to obesity, glucose tolerance, lipoprotein cholesterol levels and the metabolic syndrome in the Whitehall II study. Author(s): Brunner EJ, Wunsch H, Marmot MG. Source: International Journal of Obesity and Related Metabolic Disorders : Journal of the International Association for the Study of Obesity. 2001 January; 25(1): 45-53. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11244457&dopt=Abstract
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World pandemic of obesity: the situation in Southern African populations. Author(s): Walker AR, Adam F, Walker BF. Source: Public Health. 2001 November; 115(6): 368-72. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ uids=11781845&dopt=Abstract
Additional Web Resources A number of additional Web sites offer encyclopedic information covering CAM and related topics. The following is a representative sample: •
Alternative Medicine Foundation, Inc.: http://www.herbmed.org/
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AOL: http://search.aol.com/cat.adp?id=169&layer=&from=subcats
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Chinese Medicine: http://www.newcenturynutrition.com/
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drkoop.com: http://www.drkoop.com/InteractiveMedicine/IndexC.html
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Family Village: http://www.familyvillage.wisc.edu/med_altn.htm
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Google: http://directory.google.com/Top/Health/Alternative/
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Healthnotes: http://www.healthnotes.com/
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MedWebPlus: http://medwebplus.com/subject/Alternative_and_Complementary_Medicine
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Open Directory Project: http://dmoz.org/Health/Alternative/
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HealthGate: http://www.tnp.com/
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WebMDHealth: http://my.webmd.com/drugs_and_herbs
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WholeHealthMD.com: http://www.wholehealthmd.com/reflib/0,1529,,00.html
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Yahoo.com: http://dir.yahoo.com/Health/Alternative_Medicine/
The following is a specific Web list relating to obesity; please note that any particular subject below may indicate either a therapeutic use, or a contraindication (potential danger), and does not reflect an official recommendation (some Web sites are subscription based): •
General Overview Allergies and Sensitivities Source: Healthnotes, Inc. www.healthnotes.com Amenorrhea Source: Integrative Medicine Communications; www.drkoop.com Angina Source: Healthnotes, Inc. www.healthnotes.com Angina Source: Integrative Medicine Communications; www.drkoop.com Anorexia Nervosa Source: Integrative Medicine Communications; www.drkoop.com Asthma Source: Healthnotes, Inc. www.healthnotes.com Atherosclerosis Source: Healthnotes, Inc. www.healthnotes.com Birth Defects Prevention Source: Healthnotes, Inc. www.healthnotes.com Breast Cancer Source: Healthnotes, Inc. www.healthnotes.com
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Breast Cancer Source: Integrative Medicine Communications; www.drkoop.com Cancer, Breast Source: Integrative Medicine Communications; www.drkoop.com Cancer, Colorectal Source: Integrative Medicine Communications; www.drkoop.com Cancer, Skin Source: Integrative Medicine Communications; www.drkoop.com Candidiasis Source: Integrative Medicine Communications; www.drkoop.com Cardiovascular Disease Overview Source: Healthnotes, Inc. www.healthnotes.com Cataracts Source: Healthnotes, Inc. www.healthnotes.com Cholesterol, High Source: Integrative Medicine Communications; www.drkoop.com Cirrhosis Source: Integrative Medicine Communications; www.drkoop.com Colon Cancer Source: Healthnotes, Inc. www.healthnotes.com Colorectal Cancer Source: Integrative Medicine Communications; www.drkoop.com Depression Source: Integrative Medicine Communications; www.drkoop.com Diabetes Source: Healthnotes, Inc. www.healthnotes.com Diabetes Mellitus Source: Integrative Medicine Communications; www.drkoop.com Diverticular Disease Source: Healthnotes, Inc. www.healthnotes.com Diverticular Disease Source: Integrative Medicine Communications; www.drkoop.com Eating Disorders Source: Healthnotes, Inc. www.healthnotes.com
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Eating Disorders, Anorexia Source: Integrative Medicine Communications; www.drkoop.com Female Infertility Source: Healthnotes, Inc. www.healthnotes.com Gallstones Source: Healthnotes, Inc. www.healthnotes.com Gastroesophageal Reflux Disease Source: Healthnotes, Inc. www.healthnotes.com Gastroesophageal Reflux Disease Source: Integrative Medicine Communications; www.drkoop.com Gestational Hypertension Source: Healthnotes, Inc. www.healthnotes.com Gout Source: Healthnotes, Inc. www.healthnotes.com Hair Growth, Excessive Source: Integrative Medicine Communications; www.drkoop.com Heart Attack Source: Healthnotes, Inc. www.healthnotes.com Heartburn Source: Integrative Medicine Communications; www.drkoop.com Heat Exhaustion Source: Integrative Medicine Communications; www.drkoop.com High Blood Pressure Source: Integrative Medicine Communications; www.drkoop.com High Cholesterol Source: Healthnotes, Inc. www.healthnotes.com High Cholesterol Source: Integrative Medicine Communications; www.drkoop.com High Triglycerides Source: Healthnotes, Inc. www.healthnotes.com Hirsuitism Source: Integrative Medicine Communications; www.drkoop.com Hypercholesterolemia Source: Integrative Medicine Communications; www.drkoop.com
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Hypertension Source: Integrative Medicine Communications; www.drkoop.com Immune Function Source: Healthnotes, Inc. www.healthnotes.com Insulin Resistance Syndrome Source: Healthnotes, Inc. www.healthnotes.com Liver Disease Source: Integrative Medicine Communications; www.drkoop.com Low Back Pain Source: Healthnotes, Inc. www.healthnotes.com Ménière's Disease Source: Healthnotes, Inc. www.healthnotes.com Menstruation, Absence of Source: Integrative Medicine Communications; www.drkoop.com Obesity Source: Integrative Medicine Communications; www.drkoop.com Obesity Source: Integrative Medicine Communications; www.drkoop.com Osteoarthritis Source: Healthnotes, Inc. www.healthnotes.com Osteoarthritis Source: Integrative Medicine Communications; www.drkoop.com Pain Source: Healthnotes, Inc. www.healthnotes.com Preeclampsia Source: Healthnotes, Inc. www.healthnotes.com Pregnancy and Postpartum Support Source: Healthnotes, Inc. www.healthnotes.com Psoriasis Source: Integrative Medicine Communications; www.drkoop.com Pulmonary Edema Source: Integrative Medicine Communications; www.drkoop.com Pulmonary Hypertension Source: Integrative Medicine Communications; www.drkoop.com
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Skin Cancer Source: Integrative Medicine Communications; www.drkoop.com Sleep Apnea Source: Integrative Medicine Communications; www.drkoop.com Stroke Source: Healthnotes, Inc. www.healthnotes.com Vaginal Inflammation Source: Integrative Medicine Communications; www.drkoop.com Vaginitis Source: Integrative Medicine Communications; www.drkoop.com Varicose Veins Source: Healthnotes, Inc. www.healthnotes.com Varicose Veins Source: Integrative Medicine Communications; www.drkoop.com Varicose Veins Source: Prima Communications, Inc.www.personalhealthzone.com Wounds Source: Integrative Medicine Communications; www.drkoop.com Yeast Infection Source: Integrative Medicine Communications; www.drkoop.com •
Alternative Therapy Ayurveda Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,672,00.html Detoxification Therapy Source: Healthnotes, Inc. www.healthnotes.com Fasting Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,694,00.html Macrobiotics Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,714,00.html
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Nutrition Source: Integrative Medicine Communications; www.drkoop.com The Weigh Down Diet Alternative names: Weigh Down approach Weigh Down method Source: The Canoe version of A Dictionary of Alternative-Medicine Methods, by Priorities for Health editor Jack Raso, M.S., R.D. Hyperlink: http://www.canoe.ca/AltmedDictionary/w.html Traditional Chinese Medicine Source: Integrative Medicine Communications; www.drkoop.com •
Herbs and Supplements 5-HTP Source: Integrative Medicine Communications; www.drkoop.com 5-HTP (5-Hydroxytryptophan) Source: Prima Communications, Inc.www.personalhealthzone.com 5-Hydroxytryptophan Source: Healthnotes, Inc. www.healthnotes.com 5-Hydroxytryptophan (5-HTP) Source: Integrative Medicine Communications; www.drkoop.com 7-KETO Source: Healthnotes, Inc. www.healthnotes.com ALA Source: Integrative Medicine Communications; www.drkoop.com Alpha-Linolenic Acid (ALA) Source: Integrative Medicine Communications; www.drkoop.com Alpha-Lipoic Acid Source: Integrative Medicine Communications; www.drkoop.com Amino Acids Overview Source: Healthnotes, Inc. www.healthnotes.com Amlodipine Source: Healthnotes, Inc. www.healthnotes.com Antidepressants Source: Healthnotes, Inc. www.healthnotes.com Bladderwrack Source: The Canadian Internet Directory for Holistic Help, WellNet, Health and Wellness Network; www.wellnet.ca
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Blue-Green Algae Source: Healthnotes, Inc. www.healthnotes.com Calciferol Source: Integrative Medicine Communications; www.drkoop.com Calcitrol Source: Integrative Medicine Communications; www.drkoop.com Cayenne Alternative names: Capsicum annuum, Capsicum frutescens Source: Healthnotes, Inc. www.healthnotes.com Chickweed Source: The Canadian Internet Directory for Holistic Help, WellNet, Health and Wellness Network; www.wellnet.ca Chitosan Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10016,00.html Cholecalciferol Source: Integrative Medicine Communications; www.drkoop.com Coenzyme Q10 Source: Healthnotes, Inc. www.healthnotes.com Coenzyme Q10 (CoQ10) Source: Prima Communications, Inc.www.personalhealthzone.com Coleus Alternative names: Coleus forskohlii Source: Healthnotes, Inc. www.healthnotes.com Conjugated linoleic acid Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10102,00.html Dehydroepiandrosterone (DHEA) Source: Healthnotes, Inc. www.healthnotes.com Dehydroepiandrosterone (DHEA) Source: Integrative Medicine Communications; www.drkoop.com DHA Source: Integrative Medicine Communications; www.drkoop.com DHEA Source: Integrative Medicine Communications; www.drkoop.com
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Diltiazem Source: Healthnotes, Inc. www.healthnotes.com Docosahexaenoic Acid (DHA) Source: Integrative Medicine Communications; www.drkoop.com Eicosapentaenoic Acid (EPA) Source: Integrative Medicine Communications; www.drkoop.com Enalapril Source: Healthnotes, Inc. www.healthnotes.com EPA Source: Integrative Medicine Communications; www.drkoop.com Ephedra Alternative names: Ephedra sinensis, Ma huang Source: Integrative Medicine Communications; www.drkoop.com Ephedra (Ma huang) Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,777,00.html Ephedra sinensis Source: Integrative Medicine Communications; www.drkoop.com Erocalciferol Source: Integrative Medicine Communications; www.drkoop.com Fiber Source: Integrative Medicine Communications; www.drkoop.com Garcinia cambogia Alternative names: Citrin, Gambooge Source: Alternative Medicine Foundation, Inc. www.amfoundation.org GLA (Gamma-Linolenic Acid) Source: Prima Communications, Inc.www.personalhealthzone.com Glucomannan Source: Healthnotes, Inc. www.healthnotes.com Green tea Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10032,00.html Guggul Alternative names: Commiphora mukul Source: Healthnotes, Inc. www.healthnotes.com
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Guggul Source: Prima Communications, Inc.www.personalhealthzone.com Gugulipid Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,10033,00.html Hydroxycitric Acid Source: Healthnotes, Inc. www.healthnotes.com Hydroxycitric Acid Source: Prima Communications, Inc.www.personalhealthzone.com Indole-3-Carbinol Source: Healthnotes, Inc. www.healthnotes.com Insulin Alternative names: Humalog, Humulin, Iletin, Novolin, Velosulin Source: Prima Communications, Inc.www.personalhealthzone.com Ispaghula Source: Integrative Medicine Communications; www.drkoop.com Lipase Source: Integrative Medicine Communications; www.drkoop.com Lipase Source: Integrative Medicine Communications; www.drkoop.com Lipotropic combination Source: WholeHealthMD.com, LLC. www.wholehealthmd.com Hyperlink: http://www.wholehealthmd.com/refshelf/substances_view/0,1525,861,00.html Ma huang Source: Integrative Medicine Communications; www.drkoop.com Medium Chain Triglycerides Source: Healthnotes, Inc. www.healthnotes.com Metformin Source: Healthnotes, Inc. www.healthnotes.com Nadolol Source: Healthnotes, Inc. www.healthnotes.com Oral Hypoglycemics Source: Prima Communications, Inc.www.personalhealthzone.com
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Orlistat Source: Healthnotes, Inc. www.healthnotes.com Plantago isphagula Source: Integrative Medicine Communications; www.drkoop.com Plantago psyllium Alternative names: Psyllium, Ispaghula; Plantago psyllium/ovata Source: Alternative Medicine Foundation, Inc. www.amfoundation.org Psyllium Alternative names: Plantago ovata, Plantago ispaghula Source: Healthnotes, Inc. www.healthnotes.com Psyllium Alternative names: Ispaghula,Plantago isphagula Source: Integrative Medicine Communications; www.drkoop.com Pyruvate Source: Healthnotes, Inc. www.healthnotes.com Pyruvate Source: Prima Communications, Inc.www.personalhealthzone.com Ribes Alternative names: Black Currant; Ribes nigrum L. Source: Alternative Medicine Foundation, Inc. www.amfoundation.org Sibutramine Source: Healthnotes, Inc. www.healthnotes.com Thyroid Hormones Source: Healthnotes, Inc. www.healthnotes.com
General References A good place to find general background information on CAM is the National Library of Medicine. It has prepared within the MEDLINEplus system an information topic page dedicated to complementary and alternative medicine. To access this page, go to the MEDLINEplus site at http://www.nlm.nih.gov/medlineplus/alternativemedicine.html. This Web site provides a general overview of various topics and can lead to a number of general sources.
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CHAPTER 4. DISSERTATIONS ON OBESITY Overview In this chapter, we will give you a bibliography on recent dissertations relating to obesity. We will also provide you with information on how to use the Internet to stay current on dissertations. IMPORTANT NOTE: When following the search strategy described below, you may discover non-medical dissertations that use the generic term “obesity” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on obesity, we have not necessarily excluded non-medical dissertations in this bibliography.
Dissertations on Obesity ProQuest Digital Dissertations, the largest archive of academic dissertations available, is located at the following Web address: http://wwwlib.umi.com/dissertations. From this archive, we have compiled the following list covering dissertations devoted to obesity. You will see that the information provided includes the dissertation’s title, its author, and the institution with which the author is associated. The following covers recent dissertations found when using this search procedure: •
A Comparative Analysis of Absentee Rates and Health Care Costs for Obese and Nonobese Employees by Meesig Jondle, Mary Ann, Phd from The University of Toledo, 1989, 92 pages http://wwwlib.umi.com/dissertations/fullcit/8926339
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A Comparison of Body Composition, Body Cathexis, and Attitude toward Obesity in Women with Different Levels of Physical Activity by Lai, Shu-mei Mary, Phd from Oregon State University, 1984, 145 pages http://wwwlib.umi.com/dissertations/fullcit/8407284
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A Comparison of Different Exercise Prescriptions Combined with a Low-fat Ad Libitum Diet: Effects on Weight Loss, Health-related Variables and Psychological Well-being in Premenopausal Overweight Women by Brill, Janet Bond; Phd from University of Miami, 2001, 164 pages http://wwwlib.umi.com/dissertations/fullcit/3008195
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A Comparison of Hypnosis and Behavioral Treatments for Obesity with One Year Followup by Haynes, Judith A., Phd from The University of North Dakota, 1986, 137 pages http://wwwlib.umi.com/dissertations/fullcit/8702466
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A Comparison of Intensity of Educational Intervention on Knowledge, Attitude, Weight and Metabolic Control in Obese Individuals with Type Ii Non-insulin Dependent Diabetes Mellitus by D'eramo, Gail Ann, Edd from Columbia University Teachers College, 1987, 157 pages http://wwwlib.umi.com/dissertations/fullcit/8804209
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A Comparison of Physicians' Attitudes toward Obesity with Patients' Perceptions of Physicians' Attitudes toward Obesity by Siebring, Linda Lee, Phd from University of Arkansas, 1995, 97 pages http://wwwlib.umi.com/dissertations/fullcit/9536054
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A Consideration of the Ventral Noradrenergic Bundle As a Discrete System Modulating Feeding Implications for Ventromedial Hypothalamic Obesity and Lateral Hypothalamic Hunger by Zacharko, Robert Michael; Phd from The University of Saskatchewan (canada), 1980 http://wwwlib.umi.com/dissertations/fullcit/NK49191
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A Contextual Analysis of Obesity and Smoking among Women in Oklahoma City by Thompson, Virginia Marie, Phd from The University of Oklahoma, 1995, 128 pages http://wwwlib.umi.com/dissertations/fullcit/9538060
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A Genetic Dissection of Obesity and Type 2 Diabetes Mellitus in the Mouse by Stoehr, Jonathan Paul; Phd from The University of Wisconsin - Madison, 2002, 235 pages http://wwwlib.umi.com/dissertations/fullcit/3060449
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A Naturalistic Exploration of Weight Tolerance and Primary Socialization Sources in Overweight African American Women by Gordon, Leslene Elaine; Phd from University of South Florida, 2003, 163 pages http://wwwlib.umi.com/dissertations/fullcit/3079983
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A Proposed Psychosocial Consequences Model of Childhood Obesity by Haydenwade, Helen Anne; Phd from University of California, San Diego, 2002, 93 pages http://wwwlib.umi.com/dissertations/fullcit/3044785
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A Prospective Cohort Study of Maternal Factors in Childhood Asthma: Parity, Obesity, Fetal Growth, and Social Stressors by Held, Kathryn B. Phd from The University of Oklahoma, 2000, 312 pages http://wwwlib.umi.com/dissertations/fullcit/9985574
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A Reanalysis of Schachter's Externality Theory the Relationship between Externality and Obesity by Buser, Mary M; Phd from The University of Manitoba (canada), 1980 http://wwwlib.umi.com/dissertations/fullcit/NK47190
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A Study of Self-concept and Obesity in Adult Females by Grzegorek Hagene, Lorraine Marie, Phd from Southern Illinois University at Carbondale, 1990, 126 pages http://wwwlib.umi.com/dissertations/fullcit/9129826
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Adolescent Attitudes toward Obesity in Women: a Study of Sociodemographic Variables by Rubin, Marcia Ann, Phd from University of Illinois at Urbana-champaign, 1988, 235 pages http://wwwlib.umi.com/dissertations/fullcit/8908819
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An Empirical Validation of the Relationship between Contextual Correlates of Obesity and Enduring Self Variables by Haden, Tony Lynn, Phd from The University of Texas at Austin, 1987, 93 pages http://wwwlib.umi.com/dissertations/fullcit/8717425
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An Ethnographic Analysis of the Family Dynamics of the Obese Adolescent by Mcvoy, Joseph Henry, Jr., Phd from Virginia Polytechnic Institute and State University, 1986, 91 pages http://wwwlib.umi.com/dissertations/fullcit/8624344
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An Exploratory Study of an Obesity Reduction Education Program by Turner, Freda Walker, Phd from Walden University, 1996, 122 pages http://wwwlib.umi.com/dissertations/fullcit/9804463
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An Investigation of the Relationship between Obesity and Demographic, Eating Habit, Nutrient Intake, and Health Status Factors among Adults by Boasi, Claire Bernadette, Edd from Temple University, 1986, 172 pages http://wwwlib.umi.com/dissertations/fullcit/8611814
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Application of Exner's Rorschach System in the Study of Overweight, Restrained Eater and Normal Weight Comparison Subjects by Bunkis, Ruta Sternbergs, Edd from Boston University, 1987, 130 pages http://wwwlib.umi.com/dissertations/fullcit/8721314
•
Attributions towards Anorexic, Bulimic and Obese Others by Gousse, Alexandra; Ma from University of Guelph (canada), 2002, 72 pages http://wwwlib.umi.com/dissertations/fullcit/MQ65934
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Beauty and the Beast: a Social Psychological Study of Weight Satisfaction and Dieting Behavior (gender, Obesity) by Huff-corzine, Linda Kathrine, Phd from Washington University, 1986, 142 pages http://wwwlib.umi.com/dissertations/fullcit/8708374
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Binge Eating Disorder and Its Relationship to Bulimia Nervosa and Obesity by Lacaille, Lara Schultz; Phd from Utah State University, 2002, 173 pages http://wwwlib.umi.com/dissertations/fullcit/3042740
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Biological and Cultural Effects of Obesity on Women during Menopause by Smith, Linda Kay, Phd from Wayne State University, 1987, 160 pages http://wwwlib.umi.com/dissertations/fullcit/8714563
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Body Composition of Kuwaiti Youth: Prevalence of Obesity and Developmental Trends by Almarzouq, Hana Abdullah; Edd from University of Houston, 2001, 70 pages http://wwwlib.umi.com/dissertations/fullcit/3027881
•
Cardiovascular Consequences of Genetic and Diet-induced Obesity in Mice by Williams, Todd Dennis; Phd from The Florida State University, 2002, 90 pages http://wwwlib.umi.com/dissertations/fullcit/3055775
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Central Obesity and Diet in Relation to Gallstone Disease by Tsai, Chung-jyi; Sd from Harvard University, 2002 http://wwwlib.umi.com/dissertations/fullcit/f241745
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Central Obesity: Predisposing Factors and Consequences in Children Age 8 Through Young Adulthood by Appel, Susan J. Phd from The University of North Carolina at Chapel Hill, 2002, 132 pages http://wwwlib.umi.com/dissertations/fullcit/3046956
206 Obesity
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Childhood Obesity: Determinants, Treatment, and Risk Factors for Chronic Disease by Ball, Geoffery Denis Charles; Phd from University of Alberta (canada), 2002, 210 pages http://wwwlib.umi.com/dissertations/fullcit/NQ68540
•
Comparison of Weight Control Treatment Programs (obesity) by Krieshok, Susan Mary, Phd from University of Kansas, 1990, 182 pages http://wwwlib.umi.com/dissertations/fullcit/9119090
•
Control of Brown Adipose Tissue Growth and Function in Rats and Hamsters Normalities in Genetic Models of Human Disease (obesity Muscular Dystrophy) by Triandafillou, Joan; Phd from University of Ottawa (canada), 1985 http://wwwlib.umi.com/dissertations/fullcit/NK65634
•
Correlates of Obesity in Three Species of Captive Macaques by Klepper-kilgore, Nancy, Phd from Tulane University, 1986, 296 pages http://wwwlib.umi.com/dissertations/fullcit/8715185
•
Determining Rate of Subjective Time According to Subject Sex, Weight, and Locus of Control Orientation (obesity, Time Perception) by Faulkner, Kim Knox, Phd from The University of Southern Mississippi, 1985, 168 pages http://wwwlib.umi.com/dissertations/fullcit/8611219
•
Development and Evaluation of a Computer-based Resource Unit on Obesity and Weight Control for College Students by Hill, Charles Edward, Edd from State University of New York at Buffalo, 1972, 151 pages http://wwwlib.umi.com/dissertations/fullcit/7223526
•
Development and Evaluation of a Nutrition Curriculum to Prevent Obesity in Innercity Teens by Taitano, Rachael Tatiana, Phd from Colorado State University, 1998, 272 pages http://wwwlib.umi.com/dissertations/fullcit/9835036
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Diet, Activity and Cardiovascular Disease Risk Factors in Western Samoan Men (cholesterol, Blood Pressure, Obesity) by Pelletier, David Louis, Phd from The Pennsylvania State University, 1984, 390 pages http://wwwlib.umi.com/dissertations/fullcit/8429123
•
Differences in Attitudes toward Obesity, Knowledge of Cvd, and Self-efficacy in Catch and Non-catch Physical Educators by Thompson, James Frederick; Ms from University of Houston, 2002, 66 pages http://wwwlib.umi.com/dissertations/fullcit/1409800
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Differences in Physical Activity, Fitness Knowledge, and Obesity in Secondary Physical Education and Substitute Physical Education Students in Texas by Soukup, Gregory Jason, Sr. Edd from University of Houston, 2002, 75 pages http://wwwlib.umi.com/dissertations/fullcit/3056479
•
Differential Thermogenic Response in Juvenile-onset Type Obesity and Maturityonset Type Obesity (metabolism) by Oddou, William Eugene, Phd from Oregon State University, 1986, 233 pages http://wwwlib.umi.com/dissertations/fullcit/8527793
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Discriminant Analysis of Variables Affecting Childhood Obesity by Rose, Frank Vincent, Phd from The University of Mississippi, 1988, 111 pages http://wwwlib.umi.com/dissertations/fullcit/8826327
Dissertations 207
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Early and On-time Puberty and the Relationship to Anorexia, Bulimia, and Obesity (menarche, Eating Disorders) by Davis, Emily Clifton, Edd from The University of Memphis, 1994, 172 pages http://wwwlib.umi.com/dissertations/fullcit/9506753
•
Eating Disordered Pathology in Obese Pre-adolescent Children by Tanofsky-kraff, Marian; Phd from The Catholic University of America, 2003, 107 pages http://wwwlib.umi.com/dissertations/fullcit/3067499
•
Ecology of Obesity in West Philadelphia Adolescents by Gordon-larsen, Penny, Phd from University of Pennsylvania, 1997, 370 pages http://wwwlib.umi.com/dissertations/fullcit/9814876
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Education and Self-efficacy As Predictors of Weight Loss among Older Obese Females (older Women) by Vaiani, Livia Lee, Edd from Rutgers the State University of New Jersey - New Brunswick, 1991, 174 pages http://wwwlib.umi.com/dissertations/fullcit/9130059
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Effectiveness and Cost-effectiveness of Behavioral Self-help Manuals for the Treatment of Obesity a Study of Degree of Therapist Contact and Group Versus Individual Format by Pezzot-pearce, Terry Dianne; Phd from The University of Manitoba (canada), 1980 http://wwwlib.umi.com/dissertations/fullcit/NK47236
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Effectiveness of a Self-administered Assertiveness Training Manual As a Component of a Counselor-directed Weight Loss Program (obesity, Bibliotherapy) by Mishou, Lucretia Virginia, Edd from University of Maine, 1985, 156 pages http://wwwlib.umi.com/dissertations/fullcit/8614146
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Effects of Obesity on the Clinical Judgments by Christian and Non-christian Mental Health Professionals by Duncan Hassel, Tricia Lynn; Psyd from Fuller Theological Seminary, School of Psychology, 2002, 65 pages http://wwwlib.umi.com/dissertations/fullcit/3046364
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Energy Balance, Obesity and Acculturation among Hualapai Indian Women of Arizona (indian Women) by Teufel, Nicolette Irene, Phd from University of Colorado at Boulder, 1989, 247 pages http://wwwlib.umi.com/dissertations/fullcit/8923537
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Essential Hypertension in Urban Adolescents: the Epidemiology of Obesity and Physical Fitness by Wilson, Susan Louise, Phd from Southern Methodist University, 1982, 253 pages http://wwwlib.umi.com/dissertations/fullcit/8216732
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Evaluation of a Supervised Exercise Component in the Behavioral Control of Obesity by Blum, Miriam Deborah, Phd from The Pennsylvania State University, 1981, 233 pages http://wwwlib.umi.com/dissertations/fullcit/8205882
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Examination of a Self Concept Construct in Overweight and Non-overweight Elementary School-age Children (obesity) by Fisher, M. Lynette, Phd from Oklahoma State University, 1985, 100 pages http://wwwlib.umi.com/dissertations/fullcit/8611525
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Exercise Adherence in Obese Women: Evaluation of Two Intervention Strategies by Naylor, Patti-jean, Phd from University of Victoria (canada), 1992, 189 pages http://wwwlib.umi.com/dissertations/fullcit/NN79943
208 Obesity
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Factors Related to Visceral Obesity in Black and White Women during Mid-life by Rexroad, Annette Reif; Phd from University of Pittsburgh, 2002, 270 pages http://wwwlib.umi.com/dissertations/fullcit/3054331
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Family of Origin and Support System Factors Affecting Body Weight Management in Gastroplasty Patients (obesity) by Brower, Penny Lynn, Phd from The University of Iowa, 1991, 171 pages http://wwwlib.umi.com/dissertations/fullcit/9212857
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Family Patterns of Obesity: the Use of Weight As a Predictor of Family Type by Barker, Brenda Crabtree, Phd from Texas Woman's University, 1989, 77 pages http://wwwlib.umi.com/dissertations/fullcit/9008481
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Food Behaviors and Obesity among Urban American Indian Women (health, Diet, Disease, Diabetes, New World Syndrome) by Kay, Nina W., Phd from Southern Methodist University, 1986, 235 pages http://wwwlib.umi.com/dissertations/fullcit/8616217
•
Household Characteristics Affecting Childhood Obesity by Colison, Charlene V. Ms from D'youville College, 2002, 84 pages http://wwwlib.umi.com/dissertations/fullcit/1410116
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Human Leptin in Obesity and Diabetes: Anthropometric, Metabolic and Genetic Determinants by Wauters, Machteld; Phd from Universitaire Instelling Antwerpen (belgium), 2002, 268 pages http://wwwlib.umi.com/dissertations/fullcit/3042003
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Hypnotherapy and Client Suitability for the Treatment of Obesity by Cochrane, Gordon John, Edd from The University of British Columbia (canada), 1984 http://wwwlib.umi.com/dissertations/fullcit/f2118229
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Hypnotherapy and Client Suitability for the Treatment of Obesity by Cochrane, Gordon; Edd from The University of British Columbia (canada), 1984 http://wwwlib.umi.com/dissertations/fullcit/NK66878
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Independent Associations among Abdominal Obesity, Cardiorespiratory Fitness, Liver Fat and Lipid Variables in Men by Nguyen-duy, Thanh-binh; Msc from Queen's University at Kingston (canada), 2002, 64 pages http://wwwlib.umi.com/dissertations/fullcit/MQ73069
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Insulin and Cyclical Obesity in the Dormouse, Glis Glis by Melnyk, Roman Bohdan; Phd from University of Toronto (canada), 1981 http://wwwlib.umi.com/dissertations/fullcit/NK50313
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Is There a Relationship between Bmi, Dietary Intake, and Parent's Report of Food Preferences of Obese Hispanic Toddlers? by Popejoy, April Pauline; Ms from Texas Woman's University, 2003, 90 pages http://wwwlib.umi.com/dissertations/fullcit/1413513
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Lipid Metabolism during Exercise in Beta-2 Adrenoceptor Gln27glu Polymorphism Homozygous Obese Women by Macho Azcarate, Tatiana; Dr from Universidad De Navarra (spain), 2002, 200 pages http://wwwlib.umi.com/dissertations/fullcit/f674689
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Logoanalysis As a Group Treatment for Existential Vacuum and Weight Loss in Obese Women by Horton, Robert Craig, Phd from University of Southern California, 1983 http://wwwlib.umi.com/dissertations/fullcit/f2688741
Dissertations 209
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Mapping Genes for Complex Traits: Obesity, Diabetes, Hypertension, and Dyslipidemia on the Pacific Island of Kosrae by Shmulewitz, Dvora; Phd from The Rockefeller University, 2002, 165 pages http://wwwlib.umi.com/dissertations/fullcit/3053194
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Measures of Therapeutics in the Treatment of Obesity by Kennedy, Christine Joy; Phd from University of Louisiana at Monroe, 2002, 124 pages http://wwwlib.umi.com/dissertations/fullcit/3062279
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Mitochondrial Proton Leak and Uncoupling Protein Expression in Transgenic Mice and Human Obesity by Monemdjou, Shadi; Phd from University of Ottawa (canada), 2002, 143 pages http://wwwlib.umi.com/dissertations/fullcit/NQ67976
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Mortality, Survivorship and Longevity in American Samoa, 1950 to 1981 (cardiovascular, Hypertension, Diabetes, Obesity, Cancer) by Crews, Douglas Earl, Phd from The Pennsylvania State University, 1985, 176 pages http://wwwlib.umi.com/dissertations/fullcit/8516013
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Motivational Characteristics Associated with Attrition in Worksite Obesity Treatment by Leshine, Paula L., Phd from University of Pennsylvania, 1986, 342 pages http://wwwlib.umi.com/dissertations/fullcit/8703234
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No Laughing Matter: Experiencing Obesity by Howard, Dorothy E., Phd from Boston University, 1987, 663 pages http://wwwlib.umi.com/dissertations/fullcit/8709640
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Obese-child-families: a Psychological Study by Fieman, Lawrence S., Edd from Boston University School of Education, 1983, 137 pages http://wwwlib.umi.com/dissertations/fullcit/8319890
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Obesity and Health Care Utilization by Zizza, Claire Ann; Phd from The University of North Carolina at Chapel Hill, 2002, 145 pages http://wwwlib.umi.com/dissertations/fullcit/3061745
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Obesity and Social Marketing: a Life Style Approach to Product Design and Market Segmentation. by Lewis, David Leroy, Phd from Georgia State University, 1978, 171 pages http://wwwlib.umi.com/dissertations/fullcit/7815559
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Obesity and Weight Loss in Weight Watchers: a Study of Deviance and Resocialization by Wernick, Sarah, Phd from Columbia University, 1973, 212 pages http://wwwlib.umi.com/dissertations/fullcit/7329875
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Obesity As a Factor in Self-concept and Attitude toward Physical Fitness and Exercise by Brown, Venie Edward, Edd from The University of Mississippi, 1971, 113 pages http://wwwlib.umi.com/dissertations/fullcit/7125680
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Obesity in Persons with Diabetes: a Sociological Analysis by Braitman, Leonard Edward, Phd from The University of Chicago, 1980 http://wwwlib.umi.com/dissertations/fullcit/T-27562
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Obesity in the United States: Stratifying Factors. by Benbrook, Sandra Leigh, Phd from University of Southern California, 1976 http://wwwlib.umi.com/dissertations/fullcit/f3611494
210 Obesity
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Obesity: an Investigation of Personality Characteristics of Patients Participating in a Behaviorally-oriented Supplemented Fasting Program by Spiegelberg, Jane Slater, Phd from Kent State University, 1988, 176 pages http://wwwlib.umi.com/dissertations/fullcit/9332877
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On the Role of the Enteroinsular Axis in Obesity by Chan, Catherine Barbara; Phd from The University of British Columbia (canada), 1986 http://wwwlib.umi.com/dissertations/fullcit/NL35053
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Organismic Characteristics and Psychosocial Functioning: Is Obesity a Risk Factor in Adolescents' Psychosocial Adjustment? by Sukariyah, Muhamad Bassam, Phd from Indiana University, 1992, 227 pages http://wwwlib.umi.com/dissertations/fullcit/9310361
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Patient Responsibility and Obesity in Determining Helping Behavior of Students in the Health Professions (patient Education, Nursing Students, Medical Students) by Kahan, Miriam Rhea, Phd from University of California, Los Angeles, 1992, 212 pages http://wwwlib.umi.com/dissertations/fullcit/9317422
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Patterns of Influence of Some Known Correlates of Obesity in Middle-class Black Women by Scott, Mildred Ware, Phd from University of Maryland College Park, 1980, 210 pages http://wwwlib.umi.com/dissertations/fullcit/8105137
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Perceptual/conceptual Disturbances in Anorexia Nervosa and Obesity by Garner, David M; Phd from York University (canada), 1975 http://wwwlib.umi.com/dissertations/fullcit/NK25712
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Personality Correlates and Psychosocial Dimensions of Obesity in Women: a Profile Analysis of Optifast Participants by Kayloe, Judith C., Phd from Kent State University, 1989, 186 pages http://wwwlib.umi.com/dissertations/fullcit/8919780
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Physical, Psychological, Behavioral and Family Factors Predicting Weight Loss and Weight Loss Maintenance in Morbidly Obese Children and Adolescents (obesity, Childhood Obesity) by Miller, Lisa Alison, Phd from Depaul University, 1991, 325 pages http://wwwlib.umi.com/dissertations/fullcit/9136823
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Physician Self-efficacy in the Treatment of Obesity by Stoffelmayr, Amy Stern, Phd from Michigan State University, 1994, 140 pages http://wwwlib.umi.com/dissertations/fullcit/9512148
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Predicting Attrition and Adherence in a Very Low Calorie Diet Behaviorally-based Treatment Program for Obesity by Kitto, Gary C., Phd from Kansas State University, 1992, 255 pages http://wwwlib.umi.com/dissertations/fullcit/9221988
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Primary Prevention of Atherosclerosis and Obesity in Young Adults Using Dietary and Educational Interventions by Matvienko, Oksana Alexandrovna; Phd from Iowa State University, 2002, 138 pages http://wwwlib.umi.com/dissertations/fullcit/3061845
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Psychological Methods of Obesity Reduction in Adolescent Girls by Carmichael, John Alexander; Phd from University of Victoria (canada), 1975 http://wwwlib.umi.com/dissertations/fullcit/NK25522
Dissertations 211
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Psychological Type and Obesity by Harris, Clifton Tumlin Bud, Jr., Phd from Georgia State University, 1985, 200 pages http://wwwlib.umi.com/dissertations/fullcit/8521695
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Racial Differences in Obesity between Black and White Women in the United States, 1986--1994 by Rucker, Toni Denise; Phd from University of Michigan, 2000, 202 pages http://wwwlib.umi.com/dissertations/fullcit/9977252
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Relationship between Habitual Physical Activity and Direct/indirect Costs among Overweight and Obese Adults by Wang, Feifei; Phd from University of Michigan, 2002, 104 pages http://wwwlib.umi.com/dissertations/fullcit/3068988
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Relationship between Weight Loss and Body Image in Obese Individuals Seeking Weight Loss Treatment by Reas, Deborah Lynn; Phd from Louisiana State University and Agricultural & Mechanical College, 2002, 85 pages http://wwwlib.umi.com/dissertations/fullcit/3069730
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Resistance Training and Therapist Contact in a Maintenance Program for Mild to Moderate Obesity by Binks, Martin; Phd from Fairleigh Dickinson University, 2002, 205 pages http://wwwlib.umi.com/dissertations/fullcit/3034808
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Resting Metabolic Rates in Child-onset and Adult-onset Obese Women by Summerfield, Liane M., Phd from University of Maryland College Park, 1989, 198 pages http://wwwlib.umi.com/dissertations/fullcit/8924238
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School-based Obesity Intervention by Wolf, Marlin Christian, Jr., Phd from Temple University, 1986, 274 pages http://wwwlib.umi.com/dissertations/fullcit/8627536
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Second-order Change Through Brief Therapy among Obese Clients of a Universitybased Weight Management Program by Munro, Janice Fay; Edd from University of Missouri - Saint Louis, 2002, 151 pages http://wwwlib.umi.com/dissertations/fullcit/3049604
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Sensitivity to Reward: a Factor in Overeating and Overweight by Strachan, Shaelyn Margaret; Ma from York University (canada), 2002, 101 pages http://wwwlib.umi.com/dissertations/fullcit/MQ71625
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Shedding the Obese Role: a Three-year Study of Twenty Obese Females, Ages 13-53, Who Had Surgery for Weight Loss (gastric Bypass, Intestinal Bypass) by Wrobel, Sylvia Burroughs, Phd from University of Kentucky, 1989, 221 pages http://wwwlib.umi.com/dissertations/fullcit/9014238
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Social Work Practitioners' Comparative Evaluations of Obese and Lean Clients by Lehmann, Barbara A. Phd from Case Western Reserve University, 2001, 133 pages http://wwwlib.umi.com/dissertations/fullcit/3036345
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Sociocultural Aspects of Body Image: Explorations of Body Size and Weight Problem Perceptions in a Southern Rural Community (obesity, Overweight) by Wright, Erma J., Phd from The University of North Carolina at Chapel Hill, 1986, 194 pages http://wwwlib.umi.com/dissertations/fullcit/8628275
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Socio-demographic Factors As Predictors of Obesity among Women by Hall, Claudia A., Phd from Mississippi State University, 1989, 113 pages http://wwwlib.umi.com/dissertations/fullcit/8917062
212 Obesity
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Strength Training, Exercise and Diet in the Management of Obesity in Children by Yu, Chung Wah; Phd from Chinese University of Hong Kong (people's Republic of China), 2002, 351 pages http://wwwlib.umi.com/dissertations/fullcit/3066613
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Stress, Self-efficacy, Problem-solving Skills, and Levels of Obesity in Women: a Test of Group Differences by Kuntz, Carol B., Psyd from Central Michigan University, 1993, 95 pages http://wwwlib.umi.com/dissertations/fullcit/9334902
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Studies on Insulin Secretion and Glucose Tolerance in Experimental Obesity and Diabetes by Dalpé-scott, Marthe; Phd from University of Ottawa (canada), 1983 http://wwwlib.umi.com/dissertations/fullcit/NK65707
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The Addition of a Cognitive Intervention Based on Individualized Assessment to a Behavioral Intervention for Obesity by Delucia, Janice Lynn, Phd from The Pennsylvania State University, 1987, 243 pages http://wwwlib.umi.com/dissertations/fullcit/8727994
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The Association between Television Viewing and Related Video Activities, Physical Activity Level, and Weight in Obese and Nonobese Adolescents: a Multicultural Analysis by Albi, Kathleen Marie, Phd from University of Denver, 1997, 250 pages http://wwwlib.umi.com/dissertations/fullcit/9804090
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The Association between Television Viewing and Related Video Activities, Physical Activity Level, and Weight, in Obese and Nonobese Fourth-grade Children by Hammerberg, Diane Dehnert, Phd from University of Denver, 1992, 170 pages http://wwwlib.umi.com/dissertations/fullcit/9237590
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The Association of Obesity and Disability in Middle-aged Americans by Harrison, David Jeffrey; Phd from The University of North Carolina at Chapel Hill, 2002 http://wwwlib.umi.com/dissertations/fullcit/f653089
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The Association of Obesity and Physical Fitness with Inflammatory Markers in Children by Isasi, Carmen Rosa; Phd from Columbia University, 2002, 102 pages http://wwwlib.umi.com/dissertations/fullcit/3037721
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The Caloric Content, Macronutrient Composition, and Portion Size of Children's Meals in Restaurants: a Risk Factor for Childhood Obesity? by Hyder, Melissa L. Phd from University of Missouri - Kansas City, 2003, 69 pages http://wwwlib.umi.com/dissertations/fullcit/3085593
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The Child's Concept of Obesity by Wolfle, Jane Allen, Phd from Virginia Polytechnic Institute and State University, 1981, 174 pages http://wwwlib.umi.com/dissertations/fullcit/8121508
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The Cultural Beliefs and Values That Influence Perceptions of African American Mothers Regarding Obesity in Their Daughters by Senatore, Pamela Nichelle; Mph from California State University, Fresno, 2002, 97 pages http://wwwlib.umi.com/dissertations/fullcit/1412229
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The Development of an Instrument for the Assessment of Obesity-related Cognitions (obesity Cognition Inventory, Cognition Testing, Health Knowledge) by Christian, David Earl, Phd from Utah State University, 1992, 108 pages http://wwwlib.umi.com/dissertations/fullcit/9301633
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The Eating Disorder Inventory and Other Predictors of Successful Symptom Management in Bulimic and Obese Women Following an Inpatient Treatment
Dissertations 213
Program Employing an Addictions Paradigm by Carroll, Mary Theodora, Phd from University of South Florida, 1993, 271 pages http://wwwlib.umi.com/dissertations/fullcit/9323672 •
The Effect of a Split Exercise Session on Excess Postexercise Oxygen Consumption in Young Obese Women (women) by Bronstein, Maridy Mcneff, Edd from The University of Alabama, 1992, 95 pages http://wwwlib.umi.com/dissertations/fullcit/9225803
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The Effect of a Token Reinforcement on Physical Activity, Body Weight, and Selfconcept of Overweight and Obese Adolescents with Serious Emotional Disturbances/behavioral Disorders (emotional Disturbances, Behavioral Disorders) by Hall, Darlene York, Phd from University of Idaho, 1992, 172 pages http://wwwlib.umi.com/dissertations/fullcit/9312472
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The Effect of Client Obesity on Counselor Clinical Judgments by Young, Laura Mim, Phd from The Catholic University of America, 1983, 121 pages http://wwwlib.umi.com/dissertations/fullcit/8313957
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The Effect of Pre-exercise Caffeine Ingestion on Free Fatty Acid Mobilization and Metabolism at Rest, During, and Following Prolonged Submaximal Exercise in Lean and Obese Volunteers by Kamimori, Gary H., Phd from Southern Illinois University at Carbondale, 1985, 203 pages http://wwwlib.umi.com/dissertations/fullcit/8610570
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The Effects of a Moderate Progressive Aerobic Exercise Program on the Severely and Morbidly Obese by Zelasko, Chester John, Phd from Michigan State University, 1987, 74 pages http://wwwlib.umi.com/dissertations/fullcit/8801890
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The Effects of Aerobic Exercise and Slow-speed Strength Training on Body Composition and Weight Loss in Obese Women by Silver, Francine J. Phd from Fairleigh Dickinson University, 2002, 176 pages http://wwwlib.umi.com/dissertations/fullcit/3036299
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The Effects of Assertion Training and Husband Involvement in the Behavioral Treatment of Obesity by Elterman, Michael Frank; Phd from Queen's University at Kingston (canada), 1981 http://wwwlib.umi.com/dissertations/fullcit/NK55934
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The Effects of Obesity on Skill Attainment in Twelve Year-old Children As Measured by Performance on Three Novel Manipulative Skills by Andrews, Stanley Cooper, Edd from The University of Mississippi, 1987, 99 pages http://wwwlib.umi.com/dissertations/fullcit/8724391
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The Effects of Some Sociological and Social Psychological Factors on the Outcome of Obesity Treatment Programs by Barker, Matilda Inez Nowell, Phd from University of California, Riverside, 1985, 216 pages http://wwwlib.umi.com/dissertations/fullcit/8520622
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The Efficacy of Geometric Versus Cluster Analysis on Assessing Psychosocial Adjustment Related to Obesity by Wong, Shu-yeng, Phd from Indiana University, 1980, 154 pages http://wwwlib.umi.com/dissertations/fullcit/8029264
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The Genetics of Obesity and Obesity-related Factors among Samoans by Choh, Audrey C. Phd from State University of New York at Albany, 2002, 167 pages http://wwwlib.umi.com/dissertations/fullcit/3072613
214 Obesity
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The Impact of Kin, Friend and Neighbor Networks on Infantile Obesity. by Bryant, Carol Anne, Phd from University of Kentucky, 1978, 139 pages http://wwwlib.umi.com/dissertations/fullcit/7824381
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The Influence of Hyperandrogenism, Obesity and Infertility on the Psychosocial Health and Well-being of Women with Polycystic Ovary Syndrome by Mccook, Judy Griffin; Phd from University of Michigan, 2002, 150 pages http://wwwlib.umi.com/dissertations/fullcit/3042131
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The Management of Obesity in Everyday Life. by Hoover, Michael Coleman, Phd from The University of Tennessee, 1976, 319 pages http://wwwlib.umi.com/dissertations/fullcit/7710773
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The Medicalization Vs. the Politicization of Obesity in Women by Spencer, Barbara Duffy, Phd from St. John's University (new York), 1987, 567 pages http://wwwlib.umi.com/dissertations/fullcit/8914737
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The Ppar Pathway to Obesity and Type-2 Diabetes: a Multi-locus Approach to Understanding Complex Disease by Moffett, Susan Patricia; Phd from University of Pittsburgh, 2002, 176 pages http://wwwlib.umi.com/dissertations/fullcit/3068712
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The Prediction of Relapse from Obesity Treatment by Self-efficacy for Coping, Stress and Rationality of Beliefs by Macaulay, Mickle John, Edd from Northern Illinois University, 1998, 105 pages http://wwwlib.umi.com/dissertations/fullcit/9922468
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The Process of Overcoming Compulsive Overeating and Obesity by Spitalny, Gloria, Edd from Boston University School of Education, 1982, 142 pages http://wwwlib.umi.com/dissertations/fullcit/8300780
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The Relationship between Insulin Resistance Syndrome, Body Fat Distribution, Dietary Intake Variables and Subclinical Atherosclerosis in Obese Type 2 Diabetes by Hegazi, Refaat Mohamed; Phd from University of Pittsburgh, 2002, 179 pages http://wwwlib.umi.com/dissertations/fullcit/3054285
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The Relationship between Milk Consumption and Obesity among Low-income Hispanic Children Participating in the Special Supplemental Nutrition Wic Program by Grafton, Laura; Mph from Southern Connecticut State University, 2002, 57 pages http://wwwlib.umi.com/dissertations/fullcit/1410370
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The Relationship between the Age at Onset of Self-perceived Obesity and Personal Orientation by Creekmore, Carol Lynn, Edd from The University of Tulsa, 1984, 107 pages http://wwwlib.umi.com/dissertations/fullcit/8412635
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The Relationship of Obesity and Body Fat Distribution to Non-insulin Dependent Diabetes Mellitus in a Navajo Community by Hall, Teri-christine Ruan, Phd from The University of Wisconsin - Madison, 1990, 92 pages http://wwwlib.umi.com/dissertations/fullcit/9027499
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The Relationship of Obesity-related Metabolic Hormones and Prognosis in Young Women with Breast Cancer by Johnson, Lisa Godefroy; Phd from University of Washington, 2003, 89 pages http://wwwlib.umi.com/dissertations/fullcit/3079227
Dissertations 215
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The Relationship of Social Support Contracting to Worksite Weight Control (weight Loss, Obesity Treatment) by Wynne, Kathleen Louise, Edd from University of South Carolina, 1986, 188 pages http://wwwlib.umi.com/dissertations/fullcit/8704657
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The Relationship of Weight Loss in an Obesity Treatment Program to Expectancy of Success and to Selected Attribution Constructs by Niemeier, Dianne Frances, Phd from University of Southern California, 1982 http://wwwlib.umi.com/dissertations/fullcit/f91110
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The Relationships of Alexithymia, Body Image Distortion, and Body Image Dissatisfaction to Binge Eating in Obese Populations by Delaney, Letty Ward Lauffer; Phd from New York University, 2002, 221 pages http://wwwlib.umi.com/dissertations/fullcit/3045719
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The Relative Effects of Sociocultural Factors on Levels of Obesity among Africanamerican Women by Jordan, Audrey Denise; Phd from Virginia Commonwealth University, 1999, 192 pages http://wwwlib.umi.com/dissertations/fullcit/9938296
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The Role of Cognitive Thought Processes in the Maintenance of Weight Loss (obesity, Relapse) by Herb, Ellyn D., Phd from The Fielding Institute, 1985, 240 pages http://wwwlib.umi.com/dissertations/fullcit/8602957
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The Role of Obesity Screening and Health Risk in Canadians: Application of the National Cholesterol Education Program Adult Treatment Panel Iii Guidelines by Ardern, Christopher Ian; Msc from York University (canada), 2002, 108 pages http://wwwlib.umi.com/dissertations/fullcit/MQ77131
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The Social Stratification of Obesity: Bodily Assets and the Stylization of Health by Chang, Virginia Wei-wen; Phd from The University of Chicago, 2003, 280 pages http://wwwlib.umi.com/dissertations/fullcit/3077046
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The Symbolic World of Obesity: a Study of the Rhetorical Visions of Obese Women by Madden, Mary Jane, Phd from University of Minnesota, 1982, 174 pages http://wwwlib.umi.com/dissertations/fullcit/8301964
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The Validity of Convenient Obesity Indicators by Marshall, J. Dru; Phd from University of Alberta (canada), 1989 http://wwwlib.umi.com/dissertations/fullcit/NL55544
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The Validity of Convenient Obesity Indicators by Marshall, June Dru, Phd from University of Alberta (canada), 1989 http://wwwlib.umi.com/dissertations/fullcit/f3162852
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Treatment Acceptability for the Prevention of Obesity and Type 2 Diabetes Mellitus: the Effects of Ethnicity, Weight, and Genetic Predisposition by Thaw, Jean Marie; Phd from Louisiana State University and Agricultural & Mechanical College, 2002, 97 pages http://wwwlib.umi.com/dissertations/fullcit/3069735
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Use of Behavioral Stage-of-change and Preference for Weight Loss Interventions As a System for Client-matching Treatment of Obesity by Ostendorf, Wendy R., Edd from University of Sarasota, 1999, 187 pages http://wwwlib.umi.com/dissertations/fullcit/9929538
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Utilization of the Health Belief Model in Predicting Dieting and Exercising Behavior of Obese and Non-obese Adolescents by O'connell, Janelle Kay, Phd from The University of Toledo, 1984, 202 pages http://wwwlib.umi.com/dissertations/fullcit/8429739
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Variables Impacting Obesity among African American Women in Omaha (nebraska) by Blanchard, Shirley Ann; Phd from The University of Nebraska - Lincoln, 2002, 201 pages http://wwwlib.umi.com/dissertations/fullcit/3074068
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Weight Loss Maintenance in a Multicomponent Behavioral Treatment of Obesity by Barger, Sharon Ann, Phd from The University of Wisconsin - Madison, 1987, 383 pages http://wwwlib.umi.com/dissertations/fullcit/8712405
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Weight-based Stigmatization and Ideological Beliefs: Relation to Psychological Distress in an Obese, Treatment-seeking Population by Friedman, Kelli E. Phd from Duke University, 2002, 114 pages http://wwwlib.umi.com/dissertations/fullcit/3041578
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Why Lose? a Study of the Motivational Variables Operative in the Decision of Obese Individuals to Instigate Weight Reduction Activity (health Behavior, Decisionmaking) by Cregheur, Lucille Annette, Dsw from University of California, Berkeley, 1986, 184 pages http://wwwlib.umi.com/dissertations/fullcit/8624691
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Women, Weight, and Embodiment: an Intuitive Inquiry into Women's Psychospiritual Process of Healing Obesity by Coleman, Becky; Phd from Institute of Transpersonal Psychology, 2000, 470 pages http://wwwlib.umi.com/dissertations/fullcit/9969177
Keeping Current Ask the medical librarian at your library if it has full and unlimited access to the ProQuest Digital Dissertations database. From the library, you should be able to do more complete searches via http://wwwlib.umi.com/dissertations.
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CHAPTER 5. CLINICAL TRIALS AND OBESITY Overview In this chapter, we will show you how to keep informed of the latest clinical trials concerning obesity.
Recent Trials on Obesity The following is a list of recent trials dedicated to obesity.8 Further information on a trial is available at the Web site indicated. •
Diet and Physical Activity Interactions in Obesity Condition(s): Obesity Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Purpose - Excerpt: The projects funded by this grant, primarily focus on environmental factors that promote weight-gain in the general human population, and how to modify these factors, to prevent further weight-gain in the future. In the coming years, the researchers at the University of Colorado-HSC hope to gain an understanding as to how small changes in diet and physical activity can be achieved and sustained to prevent weight-gain. Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00067964
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Effects of Leptin Treatment on Weight Loss Condition(s): Obesity Study Status: This study is currently recruiting patients. Sponsor(s): Rockefeller University
8
These are listed at www.ClinicalTrials.gov.
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Purpose - Excerpt: This is a double blind placebo controlled clinical study designed to determine the effects of leptin on the changes that occur in the body during weight loss achieved by a very low calorie diet. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00050791 •
Effects of Oral Glucosamine on Insulin and Blood Vessel Activity in Normal and Obese People Condition(s): Obesity; Insulin Resistance Study Status: This study is currently recruiting patients. Sponsor(s): National Center for Complementary and Alternative Medicine (NCCAM) Purpose - Excerpt: This study will examine whether glucosamine affects the way the body responds to insulin. Insulin is a hormone that causes the body to use glucose (sugar). Insulin does not work as well in overweight people, causing a condition called insulin resistance. Insulin also increases the flow of blood into muscle by opening inactive blood vessels. This study will test whether glucosamine, a nutritional supplement that many people take to treat arthritis, can cause or worsen insulin resistance or change how blood vessels react to insulin in normal weight and overweight people. Healthy normal weight and overweight volunteers between 21 and 65 years of age may be eligible for this study. Candidates will be screened with a brief physical examination, medical history, and blood and urine tests. After screening, participants will have three additional outpatient clinic visits for the following procedures: Visit 1 - Glucose clamp test to measure the body's response to insulin: For this procedure, a needle is placed in a vein of each arm, one for drawing blood samples, and one for infusing glucose and a potassium solution. The glucose is infused continuously during this 4-hour test and blood is drawn frequently to monitor glucose and insulin levels. After the test, blood glucose levels are monitored for another 2 hours to make sure they remain at an adequate level to prevent hypoglycemia (low blood sugar). - Blood flow measurement: Blood flow in the brachial artery of the arm is measured to assess how many capillaries (very small blood vessels) are being used to supply nutrients and oxygen to the muscle in the forearm. This test is done at the same time as the glucose clamp test. Blood flow is measured using a technique called contrast ultrasound. A small amount of contrast agent consisting of gas-filled bubbles the size of red blood cells is infused over 10 minutes through one of the catheters placed in the vein for the glucose clamp test. The contrast agent is infused twice, once at the beginning of the glucose clamp test and once at the end of the test. The contrast material creates a signal in response to ultrasound that provides information about the distribution of capillaries in the forearm. - Assignment to medication group: Participants are randomly assigned to take either glucosamine or placebo three times a day by mouth for 6 weeks. At the end of the 6 weeks, no study drug is taken for 1 week, and then participants "cross-over" medications, those who took glucosamine for the first 6 weeks take placebo for the next 6 weeks and vice versa. Visits 2 and 3 For these visits, the glucose clamp test and blood flow measurements are repeated. Visit 2 is scheduled at the end of the first 6week treatment period, and Visit 3 is scheduled at the end of the second 6-week treatment period. Phase(s): Phase I
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Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00065377 •
Exercise Training in Obesity-prone Black and White Women Condition(s): Obesity Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Purpose - Excerpt: Overweight premenopausal Black and White women are randomized to either diet-only, diet+aerobic or diet+resistance exercise training. Diet/behavior intervention, with or without the aerobic or resistance exercise training, will be provided throughout the 18 months of study. Major outcomes will include measures of perceived and physiologic difficulty of exercise (cardiac, ventilatory, electromyographic responses to standardized exercise tasks); aerobic fitness; strength fitness; and spontaneous freeliving energy expenditure (all derived from doubly labeled water). The results will provide insight into the effectiveness of, and the mechanisms by which, different types of exercise training can improve physical fitness, spontaneous engagement in physical activities of daily living and, in turn, weight-loss maintenance. Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00067873
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FFA Metabolism in Different Types of Human Obesity Condition(s): Obesity Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Purpose - Excerpt: We will give intravenous fat molecules to help us understand how the fat that is released from peoples fat cells is used. This will be done when people are eating, not eating and walking. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00068900
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Genetics, Metabolism and Weight Loss in Older, Obese Veterans Condition(s): Obesity Study Status: This study is currently recruiting patients. Sponsor(s): Department of Veterans Affairs Medical Research Service Purpose - Excerpt: This study is designed to determine whether sequence variation in the lipoprotein lipase (LPQ) gene affects the amount of weight loss and metabolic responses during a hypocaloric diet treatment for overweight and obese (BMI=25-35 kg/m2), older (50-65 yrs), sedentary veterans. Study Type: Interventional Contact(s): see Web site below
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Web Site: http://clinicaltrials.gov/ct/show/NCT00018330 •
Girls Health Enrichment Multi-Site Studies (GEMS) Condition(s): Cardiovascular Diseases; Heart Diseases; Obesity Study Status: This study is currently recruiting patients. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To develop and test interventions to prevent obesity by decreasing weight gain during the high-risk transitional period from pre-puberty to puberty in African-American girls who are at high risk for developing obesity. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00000615
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Heart Disease Risk Factors in African Americans Condition(s): Coronary Disease; Obesity Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Purpose - Excerpt: It is unknown if obesity contributes to the development of heart disease in African American men and women. This study was created to determine whether there is a relationship between sex and body size and the incidence of heart disease in African American men and women. Researchers will attempt to associate obesity with the presence of heart disease risk factors. Risk factors that will be studied include; total body fat, body fat distribution, fat content of the blood (triglyceride concentration, low density lipoproteins [LDL], and high density lipoproteins [HDL]), how fast fat is removed from the blood, and how well insulin works in the body. Scientific studies have shown that obesity and increased levels of fat content in the blood are important risk factors for heart disease in Caucasian women. However, similar studies in African American women have failed to show the same correlation. In fact, it appears that African American women in all three body weight groupings, nonobese, overweight, and obese experience high death rates due to heart disease. In addition, prior research has shown that obese African American men tend to have elevated levels of fat in the blood while African American women have normal blood fat levels. Therefore, if high levels of triglycerides (fat found in the blood) are not seen in non-diabetic obese African American women, it cannot be considered a risk factor in this population. This suggests that studies conducted on Caucasian women may not provide insight into heart disease risk factors in African American women. The study will take 120 healthy nondiabetic African American men and women (ages 18-50) grouped by sex (60 men and 60 women) and body mass index 3 subgroups; nonobese, overweight and obese). Diabetes undeniably increases the risk of heart disease. Therefore patients suffering from diabetes will not be included in the study. Candidates for the study will undergo a series of tests and examinations over 5 outpatient visits. Subjects will have body fat analyses, resting energy expenditure measurements, an EKG (electrocardiogram), and specific blood tests. Researchers believe this study will provide significant insight into the causes of obesity and heart disease in African Americans. Study Type: Observational
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Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00001853 •
Impact of Non-Commercialism Policy in Seattle Schools Condition(s): Obesity Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Purpose - Excerpt: This pilot study on the impact of a non-commercialism policy in Seattle schools will assess and evaluate obesity-related health outcomes of a real-life policy decision, recently voted on and adopted by the Seattle School Board. The policy reduces the exposure to advertising and other marketing pressures, including those from commercial food vendors. Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00063700
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Inhibition of Intestinal Glucose Absorption by the Bioflavonoid Quercetin in the Obese and in Obese Type 2 Diabetes Condition(s): Diabetes Mellitus; Obesity Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Purpose - Excerpt: Postprandial hyperglycemia and the resultant hyperinsulinemia contribute to the cardiovascular complications seen in obesity and in type 2 diabetes. Epidemiological studies suggest that slow absorption of carbohydrates dampens glucose and insulin peaks, and reduces cardiovascular morbidity. The polyphenol quercetin is the most abundant flavanoid in plant-derived foods, and is sold as a dietary supplement. In vitro, quercetin is a potent and reversible inhibitor of glucose transport by the intestinal glucose transporter GLUT2. In vivo quercetin inhibits post absorptive glucose peaks in obese, diabetic rats. We hypothesize that quercetin blunts intestinal glucose absorption in humans, and attenuates postprandial hyperglycemia. We propose to test, in a double blind placebo controlled study, whether coadministration of 1 or 2 grams of quercetin with 50 grams of glucose will reduce plasma glucose concentrations during a 6 hour 50g oral glucose tolerance test in non-diabetic obese subjects and in obese type 2 diabetic subjects. Study subjects will be 19-65 years with a body mass index greater than or equal to 30, without complications of diabetes, or on any medication other than oral hypoglycemic agents and aspirin. We will study 16 obese non diabetic subjects and 16 obese type 2 diabetic. Each subject will have 3 oral glucose tolerance tests, and will serve as his or her own control. We will compare the peak plasma glucose concentrations achieved during oral glucose tolerance tests and the area under the curve of plasma glucose to determine whether quercetin inhibits glucose absorption in humans. Such inhibition may partially explain the protective effects of plant derived foods on cardiovascular disease, and enable us to use quercetin or related compounds to dampen intestinal glucose absorption. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below
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Web Site: http://clinicaltrials.gov/ct/show/NCT00065676 •
Metabolic Differences of Overweight Children and Children of Overweight Parents Condition(s): Cardiovascular Disease; Hypertension; Non Insulin Dependent Diabetes Mellitus; Obesity Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Child Health and Human Development (NICHD) Purpose - Excerpt: This study focuses on the way weight is gained. Individuals who gain weight primarily in their midsection (visceral weight) are at an increased risk for developing diabetes and high blood pressure. Research has shown that African Americans suffer more often from high blood pressure, diabetes (non-insulin dependent), and heart disease than Caucasian Americans. These conditions lead to significant numbers of deaths and diseases associated with and made worse by obesity. African American women in particular suffer from obesity and the associated conditions of obesity more than any other race or gender. However, it is unknown if the conditions seen in African American women are a result of the obesity or differences in their insulin sensitivity, glucose disposal, or fat metabolism. This study will compare body composition, total and resting energy expenditure, and glucose disposal of obese African American and Caucasian children and of non-obese children of obese African American and Caucasian parents, to characterize the timing and nature of factors that may contribute to the prevalence of obesity and its complications. Patients participating in this study will be followed for 15 years and be evaluated every 5 years during the study. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00001522
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Metformin to Treat Obesity in Children with Insulin Resistance Condition(s): Hyperinsulinemia; Obesity Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Child Health and Human Development (NICHD) Purpose - Excerpt: This study will examine the safety and effectiveness of the medicine metformin to help overweight children control their food intake, weight, insulin, cholesterol, and triglyceride (blood fat) levels. Obesity and high insulin levels can lead to high blood pressure, diabetes, high cholesterol and triglyceride levels and heart disease. Metformin-approved by the Food and Drug Administration to treat adults with type 2 diabetes mellitus-helps lower insulin levels and may control weight gain in adults. Overweight children 6 to 11 years old who are in general good health may be eligible for this study. Children will be studied at the National Institutes of Health in Bethesda, Maryland, and at the Phoenix Indian Medical Center and the Gila River Reservation in the Phoenix, Arizona area. Candidates will have a medical history and physical examination and fasting blood test, and will provide a 7-day record of their food intake as part of the screening process. Those enrolled will be randomly assigned to receive either metformin or placebo (a look-alike tablet with no active medicine) twice a day for a six month period. After the 6 month study period, all children will be offered the opportunity to take metformin for another 6 months. Participants will be hospitalized for 2-3 days for the following procedures: history and physical
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examination; fasting blood test; several urine collections; X-ray studies to determine bone age and amount of body fat and muscle; magnetic resonance imaging (MRI) scan to measure body fat; "hyperglycemic clamp study" to evaluate insulin resistance; food intake testing; nutrition consultation; resting metabolic rate; and a "doubly labeled water" test. For the hyperglycemic clamp study, a catheter (thin flexible tube) is inserted into a vein in each arm. A sugar solution is given through one tube and blood samples are drawn every 5 minutes through the other to measure insulin. For the food intake testing, the child is asked about his or her hunger level, then given various foods he or she may choose to eat, then questioned again at various intervals both during and after finishing eating about his or her hunger level. The doubly labeled water study involves drinking "heavy water" (water which is enriched to have special kinds of hydrogen and oxygen). Urine specimens are collected 2, 3 and 4 hours after drinking the water. The child also drinks a special milk shake called a Scandishake and repeats the calorie intake and hunger study. (Two food intake studies are done on separate days.) One week after the heavy water test, additional urine samples are collected one week later. After completing the tests, the child will begin treatment with metformin or placebo, plus a daily vitamin tablet. Participants will be followed once a month with a brief history and physical examination, including a blood test. After 6 months, all of the tests described above will be repeated. All children who complete the second round of tests-both those who took metformin and those who took placebo-will be offered metformin for an additional 6 months and will be seen once a month for follow-up evaluations. Parents will not be told which children received metformin and which received placebo until all children in the study complete the first 6 months of the trial. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005669 •
Methods for Measuring Insulin Sensitivity Condition(s): Diabetes Mellitus; Healthy; Hypertension; Obesity Study Status: This study is currently recruiting patients. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: Patients with high blood pressure, diabetes, and who are overweight are known to have defects in the way their body responds to insulin. The purpose of this study is to develop better methods for measuring the way body tissue responds to insulin and sugar (glucose). Researchers are planning to study four groups of patients. 1. Normal volunteers 2. Patients who have mild to moderate high blood pressure 3. Patients who are overweight 4. Patients who have mild to moderate diabetes controlled with oral medication In this study patients and volunteers will undergo two separate tests designed to determine how well insulin is working in the body. The first test is called a glucose clamp test. Patients will have two needles placed in the veins of their arms. One needle will be used to take blood samples, the other needle will be used to inject doses of sugar (glucose) and insulin. The second test is called the frequently sample intravenous glucose tolerance test. In this test patients will have sugar (glucose) injected into their veins followed by a slow injected dose (infusion) of insulin. Researchers will periodically take blood samples during the test. Patients participating in the study will not directly benefit from it. However, the information gained from this
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study may be useful for improving the diagnosis and therapy of diseases such as diabetes, obesity, and high blood pressure (hypertension). Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00001625 •
Modifying the Home Television Watching Environment Condition(s): Obesity; Body Weight Changes Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Purpose - Excerpt: The purpose of this study is to determine if limiting television and computer time will result in a stabilization or smaller increase in BMI, lower energy intake, and increased physical activity in 4-7 year old obese (>85th BMI percentile) children over two years. Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00065052
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Nutritional Restriction and Activity Thermogenesis Condition(s): Obesity Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Purpose - Excerpt: These studies will provide us with enormous insight regarding how obese patients adapt energetically during negative energy balance. We will gain fundamental information regarding the metabolic implications of combining food restriction with a walking program compatible to that advocated by statutory agencies. These studies will lead to improved understanding of the energetic adaptation that occurs during negative energy balance and how best to treat patients with obesity. Phase(s): Phase I Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00065338
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Obesity Prevention in African American School Children Condition(s): Obesity Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Purpose - Excerpt: Obesity is the second leading preventable cause of disease and death in the United States. Low socioeconomic status (SES) and minorities are disproportionately affected. Obesity prevention among children and adolescents is a public health priority. Schools have been identified as key settings for obesity prevention; however, most health education interventions have had only a moderate effect on body weight. We propose a randomized intervention trial (pilot study) to test
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the feasibility and effectiveness of a school-based, environmental obesity prevention program in urban low-SES African American students. Schools, students and their families, and local communities will be involved to promote healthy eating and physical activity (HEPA) for prevention of childhood obesity. Six Chicago public schools will be randomly assigned as intervention (4 schools) and controls (2 schools). Focus group studies will assess needs and barriers for promotion of HEPA and guide the intervention. The intervention group will receive a School Environment Enrichment (SEE) program to modify the school physical and social environment, targeting food service, recess, physical education (PE) and school climate, and a Community Support & Environment Modification (CSEM) program, involving local corner and chain grocery stores to promote healthy eating among students and their families. Family involvement will be included for 5th and 6th graders, who will be followed for two years, to test ways to modify family environment. To assess the intervention effectiveness, multilevel data will be collected from schools (eg, food service, recess and PE), students (eg, body weight, eating and physical activity), parents (eg, family food purchasing practices) and communities (eg, available choices of snack foods in local stores). In addition, process evaluation data will be collected to assess the feasibility and acceptance (participation and satisfaction) of various intervention components by the target audience. The primary outcome variable is change in students' body weight status; secondary outcomes include changes in students' eating behavior and physical activity and changes in target environmental factors. In addition, cost-effectiveness of the intervention will be determined. If the intervention proves effective, a full-scale study will be developed. Findings from this study will provide insights into the prevention of obesity among low-SES and minority students. Study Type: Interventional Contact(s): Youfa Wang, PhD, MD 312 355 3382
[email protected]; Lisa Tussing, MS 312 996 0995
[email protected] Web Site: http://clinicaltrials.gov/ct/show/NCT00061165 •
Prevalence of carbohydrate intolerance in lean and obese children Condition(s): Obesity; Glucose Intolerance; Diabetes; Acanthosis Nigricans Study Status: This study is currently recruiting patients. Sponsor(s): National Center for Research Resources (NCRR) Purpose - Excerpt: The prevalence of obesity in children is reaching epidemic proportions. Excess adiposity is more than just a cosmetic problem, having substantial metabolic consequences. Insulin resistance, hyperinsulinemia, impaired glucose tolerance, and frank diabetes are often seen in obese children. In this study the prevalence of impaired glucose (carbohydrate) tolerance in lean children with a family history of diabetes and obese children with acanthosis nigricans with or without a family history of diabetes mellitus will be studied. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00000112
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Safety and Efficacy of Xenical in Children and Adolescents with Obesity-Related Diseases Condition(s): Diabetes Mellitus; Hypertension; Metabolic Disease; Obesity; Sleep Apnea Syndrome Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Child Health and Human Development (NICHD) Purpose - Excerpt: Obesity is a condition affecting one-third off the U.S. population and is a major risk actor for the development of Type 2 diabetes, hyperlipidemia (increased levels of fat in the blood), hypertension (high blood pressure), and other disorders of the heart and lungs. Individuals with the onset of obesity during childhood or adolescence are at an increased risk of obesity-related, diseases, both during adolescence and later in adult life. African American girls and women are at an increased risk for obesity, and have substantial rates of obesity-related diseases and causes of death. Further, many African American adult women fail to respond to many of the therapeutic approaches used to treat obesity. At present there are no medical therapies proven effective for the correction of severe obesity in children or adolescents. One medication that may have a favorable risk-benefit ratio in pediatric populations is Orlistat (Xenical, Hoffmann LaRoche). Orlistat works by preventing the action of enzymes in the digestive process, interfering with the absorption of approximately 1/3 of the fat eaten in the diet. Xenical appears to be effective for reducing weight and obesity-associated diseases in obese adults. Researchers propose to determine the safety, tolerability, and efficacy of Xenical in 12-17 year old severely obese African American and Caucasian children and adolescents who have one or more obesity-related disease (hypertension, hyperlipidemia, sleep apnea, hepatic steatosis, insulin resistance, impaired glucose tolerance, or Type 2 diabetes). Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00001723
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Strength Training Following Gastric Bypass for Obesity Condition(s): Obesity Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Purpose - Excerpt: We will assess whether undesirable loss of lean tissue following gastric bypass surgery for obesity can be minimized by protein supplementation and exercise training. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00065013
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Strength Training for Obesity Prevention Condition(s): Obesity Study Status: This study is currently recruiting patients.
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Sponsor(s): National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Purpose - Excerpt: Recent obesity prevalence increases have made obesity prevention a clear and pressing public health issue. The average US. woman gains about 0.5 kg per year. Overweight women aged 25 to 44 have a higher prevalence of significant weight gains (BMI increases of > 5 kg/m2) than men or older or thinner women. The difficulty in successfully losing weight and maintaining weight loss has resulted in recommendations from several expert panels to advise overweight and mildly obese individuals free of co-morbidities to avoid weight gains rather than to lose weight. Physical activity is observed to decline with age while caloric intake remains stable or declines slightly. There is strong observational evidence that physical activity could prevent or attenuate age associated fat gains. This randomized, controlled behavioral intervention trial will test the hypothesis that regular participation in a twice weekly strength training program over 2 years, can prevent age associated body fat increases (total and abdominal fat) in 80 overweight to mildly obese premenopausal women between the ages of 25 and 44 years, compared to a 'standard care' group (n=80). The overall aim of the study is to prevent body fat gains and to reduce health risks associated with obesity. Treatment effects will be assessed for insulin sensitivity, blood pressure, blood lipids, muscle strength, and psychosocial predictors of strength training adherence. The innovation of this approach rests in its simplicity and the minimal time requirement for full participation (2 exercise sessions weekly). A preliminary study of this innovative approach resulted in 88% exercise session attendance over 12 months and maintenance of treatment effects on total body fat percentage to the end of pilot study measurements (9 months). This supports the feasibility and potential for long term efficacy of the proposed intervention approach. The long-term implication of success in this efficacy trial would be that this modest behavior change could prevent the fat gains and associated co-morbidities commonly observed in midlife women. Phase(s): Phase II Study Type: Interventional Contact(s): Robyn A Abear, MS 612-625-8056
[email protected] Web Site: http://clinicaltrials.gov/ct/show/NCT00030160 •
Supplemental Calcium in Overweight People Condition(s): Obesity Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Child Health and Human Development (NICHD) Purpose - Excerpt: This study will examine the health effects of calcium supplements in overweight adults. overweight adults often eat a diet low in calcium. Some studies have found low calcium intake in people who have some of the medical problems often seen in overweight adults. This study will see if extra calcium improves the health of overweight adults. Volunteers in general good health 18 years of age or older who are overweight (body mass index equal to or greater than 25 kilograms per square meter of body surface) may be eligible for this study. Women who are pregnant or breastfeeding may not participate. The study includes four visits, described below. Visit 1 Volunteers will be screened for participation in the study with a medical history, physical examination, and blood and urine tests. At home, they will collect a 24-hour urine sample; fill out questionnaires to assess their average calcium intake; and record their food intake for 7 days. Those enrolled in the study will continue with the next 3 visits. Visit 2 Participants will complete a physical activity questionnaire, have their food diary
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reviewed, and meet with a dietitian for nutritional counseling. Triceps fold thickness and waist and hip circumferences will be measured three times. Body composition will be analyzed by a DEXA study. For this procedure, the subject lies on a flat table while a small dose of X-rays is passed through the body. Participants will be randomly assigned to take either calcium carbonate (1500 mg/day) or placebo capsules twice a day by mouth for 2 years. (The placebo looks like the calcium capsules but contains no calcium.) They will receive a 6-month supply of study capsules during visit 2 and return to NIH every 6 months for the next supply. They will also be sent questionnaires by mail every 3 months to complete information about health problems and how often the study capsules are being taken. Visits 3 and 4 Visit 3 is scheduled after participants have taken the study capsules for 1 year; visit 4 is scheduled after 2 years (the end of the study). At each of these visits, participants will have a DEXA scan, blood and urine tests, blood pressure measurements, and measurements of height, weight, waist and hip circumference. They will complete questionnaires about their medical history, side effects of the study medications, dietary calcium intake, and physical activity, and they will meet with one of the study investigators to talk about any concerns regarding the study. At the fourth visit, participants will answer some additional questions about their study participation and return the Diet History Questionnaire that was mailed to them before the visit. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00030238 •
Type 2 Diabetes Primary Prevention for At Risk Girls Condition(s): Obesity; Diabetes Mellitus; Prediabetic State Study Status: This study is currently recruiting patients. Sponsor(s): National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Purpose - Excerpt: Purpose: To evaluate two approaches to prevent obesity and type 2 diabetes in young girls. The Need: We are experiencing an epidemic of childhood obesity. Rates of obesity have doubled to tripled in the past two decades, with the highest rates among poor and ethnic minority girls. Type 2 diabetes (what used to be called adult-onset diabetes) is now showing up in overweight children, and more children are manifesting precursors of heart disease and stroke. Our Two Approaches: 1. A state-of-the-art nutrition education program with monthly newsletters mailed to girls and their parents and quarterly evening lectures/educational events at school sites, including cooking demonstrations and games to improve nutrition and increase physical activity. 2. After-school dance classes held five days per week all year long at school sites from the time school lets out until 6PM. Dance classes will include a 1-1.5 hour supervised homework study hall each day, and emphasize both traditional ethnic dances and popular dance. Participants: Second, third and fourth grade girls and their families will be eligible to participate. All activities are free of charge. To be able to perform a valid evaluation, to be able to accommodate all girls at their own school, and to be fair about which girls receive which program, families who wish to participate will be randomly selected to participate in either one program or the other (nutrition education or dance classes). Each family will participate for two years. Evaluation: Trained Stanford staff will perform all evaluation procedures with participating families
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in their own homes at the beginning and every six months. Families will be compensated for their participation. Phase(s): Phase II; Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00063674 •
APEX: Adiposity Prevention by Exercise in Black Girls Condition(s): Cardiovascular Diseases; Heart Diseases; Obesity Study Status: This study is no longer recruiting patients. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To determine whether a one year afternoon exercise program will reduce adiposity in African American girls, ages 8 to 10. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00006405
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Family Based Interventions: Preschool Children and Parent Condition(s): Cardiovascular Diseases; Heart Diseases; Obesity Study Status: This study is no longer recruiting patients. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To assess the efficacy of a 2-year family-based weight prevention program in a cohort of overweight preschool children and overweight parent pairs. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00024843
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Genetic Determinants:Low HDL, High Triglycerides, Obesity Condition(s): Cardiovascular Diseases; Atherosclerosis; Hypertriglyceridemia; Obesity; Heart Diseases Study Status: This study is no longer recruiting patients. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To conduct genetic studies of the metabolic syndrome which is characterized by very low levels of high density lipoprotein cholesterol (HDL-C), hypertriglyceridemia, and obesity. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00049881
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Heavy Metals, Obesity and Cardiovascular Risk - Ancillary to Look AHEAD Condition(s): Diabetes Mellitus, non-insulin dependent; Cardiovascular Diseases; Obesity; Myocardial Infarction; Heart Diseases; Diabetes Mellitus Study Status: This study is no longer recruiting patients. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To evaluate the relationship of baseline toenail chromium concentrations to weight loss, as well as the interaction between heavy metals and the beneficial effects of weight loss. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00031213
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Lifestyle, Adiposity and Cardiovascular Health in Youths Condition(s): Cardiovascular Diseases; Heart Diseases; Obesity Study Status: This study is no longer recruiting patients. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To determine the influences of diet and physical activity (PA) on total body fatness and regional fat distribution and the relationship of these to risk factors of cardiovascular disease during adolescence. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00006402
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Obesity Prevention after Smoking Cessation in Menopause Condition(s): Obesity; Menopause Study Status: This study is no longer recruiting patients. Sponsor(s): National Institute on Aging (NIA) Purpose - Excerpt: This study addresses the high risk of weight gain associated with smoking cessation in women. The obesity prevention pilot study is designed for the primary prevention of weight gain that can lead to overweight in normal-weight women, that can progress to obesity in women who are already overweight, and for the prevention of additional weight gain in obese women with BMI greater than or equal to 30.0. Fat and other macronutrient intake, specifically, sugar, complex carbohydrates, and protein, are analyzed as a target for individually tailored, weight control intervention following smoking cessation in Caucasian and African American women. Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00064961
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Obesity Treatment in a Managed Care Setting Condition(s): Obesity; Weight Loss Study Status: This study is no longer recruiting patients.
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Sponsor(s): National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Purpose - Excerpt: The aim of the present study is to evaluate the effectiveness of two different delivery formats for weight management in a managed care setting. Mailbased weight counseling and phone-based weight counseling will be compared to each other and a control condition. Primary outcomes are participation rates in programs, weight change, and cost. Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00062985 •
Physical Activity and Childhood Obesity Condition(s): Cardiovascular Diseases; Heart Diseases; Obesity Study Status: This study is no longer recruiting patients. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To measure associations between physical activity and obesity in a large, population-based cohort of children. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00063544
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The Assessment of a weight-gain agent for the Treatment of Olanzapine-Associated Anti-obesity Agent in Patients with Schizophrenia, Schizophreniform Disorder, Schizoaffective Disorder, and Bipolar I Disorder Condition(s): Schizophrenia; Psychotic Disorders; Bipolar Disorder Study Status: This study is no longer recruiting patients. Sponsor(s): Eli Lilly and Company Purpose - Excerpt: Olanzapine is currently marketed for the treatment of schizophrenia and acute manic episodes with bipolar 1 disorder. This Anti-obesity Agent is currently marketed for the management of obesity. In this study, the Anti-obesity Agent is being tested to see if it can treat weight gain that may be associated with taking olanzapine. The purposes of this study are to determine the safety of olanzapine when given in combination with the Anti-obesity Agent and any side effects that might be associated with it and whether weight-gain agent can help treat weight gain that may be associated with taking olanzapine. Phase(s): Phase IV Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00044187
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Theory-based Interventions for Smoking and Obesity (Challenge) Trial Condition(s): Smoking; Obesity Study Status: This study is no longer recruiting patients. Sponsor(s): National Institute of Neurological Disorders and Stroke (NINDS)
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Purpose - Excerpt: The purpose of this study is to examine a new theory for understanding the processes that govern behavior change by observing how people's beliefs and feelings about smoking cessation or weight loss change as they participate in smoking cessation or weight control programs. This study also seeks to improve the ability of treatment programs to help people maintain changes in their behavior. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00040287 •
Visceral Adiposity and CVD Risk in Women Condition(s): Cardiovascular Diseases; Heart Diseases; Obesity; Diabetes Mellitus Study Status: This study is no longer recruiting patients. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To investigate the influence of total body fat and visceral fat on risk factors of diabetes and cardiovascular disease (CVD) in black and white women. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00021879
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Adiposity and Fat Patterning in Black Americans Condition(s): Heart Diseases; Diabetes Mellitus; Obesity Study Status: This study is completed. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To examine the relationships of obesity and fat patterning with morbidity and mortality in Black Americans. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005248
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Biobehavioral Determinants of Obesity in Black Women Condition(s): Cardiovascular Diseases; Heart Diseases; Obesity; Telangiectasis Study Status: This study is completed. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To examine the biobehavioral determinants of obesity in Black as compared with white women. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005386
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Cardiovascular System in Obesity: Effect of Treatment Condition(s): Heart Diseases; Obesity; Vascular Diseases Study Status: This study is completed. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To determine the long-term efficacy of the combination therapy of phentermine and fenfluramine in conjunction with diet, exercise, and behavior modification in the treatment of simple, moderate obesity. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00000506
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Central Obesity and Disease Risk in Japanese Americans Condition(s): Cardiovascular Diseases; Heart Diseases; Atherosclerosis; Hypertension; Obesity; Diabetes Mellitus, non-insulin dependent; Hyperinsulinism; Insulin Resistance; Coronary Arteriosclerosis; Diabetes Mellitus Study Status: This study is completed. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To conduct a longitudinal study of central obesity and related risk factors found to be associated with hypertension and atherosclerotic cardiovascular disease (ASCVD) in a previously-examined cross-sectional cohort of second-generation Japanese Americans and in a newly-recruited cohort of third generation Japanese Americans. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005365
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Effectiveness of primary care physicians in delivering weight control counseling Condition(s): Obesity Study Status: This study is completed. Sponsor(s): National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Purpose - Excerpt: This randomized clinical trial will determine the efficacy of physicians providing weight control advice to their overweight and obese patients in primary care practice. Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00017706
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Genetic Epidemiology of Blood Lipids and Obesity - Ancillary to NGHS Condition(s): Cardiovascular Diseases; Heart Diseases; Coronary Disease; Obesity Study Status: This study is completed. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI)
234 Obesity
Purpose - Excerpt: To conduct a genetic epidemiologic study of the coronary heart disease (CHD) risk factors of blood lipids and obesity in Black and white girls who participated in the NHLBI-supported National Growth and Health Study (NGHS). The study was ancillary to NGHS. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005345 •
Genome Scan for Obesity in a Multi-Ethnic Sample Condition(s): Cardiovascular Diseases; Heart Diseases; Obesity Study Status: This study is completed. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To scan the genome for obesity in a multi-ethnic sample. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00037271
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Health Effects of Liposuction in Overweight Women with Elevated Insulin Levels, Impaired Glucose Tolerance and/or Type 2 Diabetes Condition(s): Glucose Intolerance; Hyperinsulinemia; Non Insulin Dependent Diabetes Mellitus; Obesity Study Status: This study is completed. Sponsor(s): National Institute of Child Health and Human Development (NICHD) Purpose - Excerpt: This study is for women who have already decided to undergo liposuction at Georgetown University Medical Center in Washington, D.C. To take part in this study, a woman must first meet with the plastic surgeons there, and be accepted by them to have liposuction. This study will investigate whether large volume liposuction improves risk factors for heart disease in overweight women with type 2 (adult onset) diabetes, impaired glucose tolerance, or elevated blood insulin levels. Large volume liposuction is the surgical removal of at least 10 pounds (4.5 kg) of body fat, usually from the abdomen, hips or chest. Risk factors for heart disease include high blood pressure and elevated levels of blood lipids (cholesterol and triglycerides), blood glucose (sugar), and blood insulin. Subjects who participate in all parts of this study will receive a total of $930.00. overweight women 18 years or older with high blood insulin levels, impaired glucose tolerance, or type 2 diabetes, who are planning to have large volume liposuction performed at Georgetown University Medical Center in Washington, D.C., may be eligible for this study. For a subject to be accepted into this study, she must first meet with the plastic surgeons at Georgetown University Medical Center, and they have to agree to perform large volume liposuction. The decision that someone is suitable for liposuction is not under the control of the NIH or of any NIH investigator. Those enrolled will undergo the following procedures at four separate times - before undergoing liposuction, 4 weeks after surgery, 4 months after surgery and 1 year after surgery: - Body measurements - taken with calipers to measure several skinfold thicknesses (the width of a fat fold) and with a tape measure to measure the circumference of parts of the body. - Urine sample and 6-hour urine collection - to test for pregnancy and to evaluate kidney function. - Glucose tolerance test - measures
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insulin sensitivity and how the body uses sugar, how well insulin works, and insulin sensitivity. The procedure involves placement of two catheters (thin, flexible tubes) through a needle into a vein in each arm. Sugar water is infused into one catheter and 20 minutes into the test a small amount of insulin is injected. Blood samples are drawn from the other catheter at frequent intervals for a total of 5 hours. - Electrocardiogram (ECG) and echocardiography - measure the heart's electrical activity and function. Abdominal computerized tomography (CT) scan - produces images for measuring body fat in the abdomen. (not done at the 4-week visit). Takes about half an hour to complete. - DXA X-ray - measures body fat, muscle and bone mineral content. Takes about half an hour to complete. - Bod Pod - capsule-like device used to determine the proportion of body weight composed of fat and non-fat tissue. Takes less than 10 minutes - Bioelectric impedance analysis device - measures the proportions of body fat based on electrical conduction of a small electric current. Takes 2-3 minutes. - 24-hour blood pressure monitoring - a device attached to a blood pressure cuff strapped to the arm measures blood pressure every 15 to 30 minutes continuously for 24 hours. - Vascular reactivity tests - a blood pressure cuff is inflated for about 4 minutes before deflating, providing information on the function of the small blood vessels in the skin, as well as an idea of the function level of small blood vessels elsewhere in the body. Takes half an hour. Blood samples - collected to evaluate kidney and liver function and to measure body lipids, such as cholesterol, minerals, and other substances. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005760 •
NEW DAY: Nutrition, Exercise, Weight loss, Diabetes And You Condition(s): Diabetes Mellitus, Type 2; Obesity Study Status: This study is completed. Sponsor(s): National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Purpose - Excerpt: This clinical trial examines whether the addition of individual sessions of a motivational intervention to a state-of-the art behavioral group weight loss intervention for overweight women with Type 2 diabetes improves the weight losses and glycemic control outcomes. Phase(s): Phase II Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00007800
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Obese Patients with or without Comorbidities Condition(s): Obesity; Weight Loss Study Status: This study is completed. Sponsor(s): Sanofi-Synthelabo Purpose - Excerpt: To assess the effects of weight loss and weight maintenance over a period of two years when prescribed with a hypocaloric diet in obese patients with or without comorbidities Phase(s): Phase III
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Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00029861 •
Obese Patients with Type 2 Diabetes Condition(s): Obesity; Diabetes Mellitus, Non-Insulin-Dependent; Obesity in Diabetes Study Status: This study is completed. Sponsor(s): Sanofi-Synthelabo Purpose - Excerpt: To assess the effect on weight loss and weight maintenance over a period of one year when prescribed with a hypocaloric diet in obese patients with Type 2 Diabetes Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00029848
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Obese Patients with Untreated Dyslipidemias Condition(s): Obesity; Dyslipidemia Study Status: This study is completed. Sponsor(s): Sanofi-Synthelabo Purpose - Excerpt: To assess the effect on weight loss and weight maintenance over a period of one year when prescribed with a hypocaloric diet in obese patients with untreated dyslipidemia Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00029835
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Overweight Adults--Ethnic, SES and Behavioral Influences Condition(s): Cardiovascular Diseases; Heart Diseases; Obesity Study Status: This study is completed. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To examine the effects of ethnicity, socioeconomic status (SES) and behavior in overweight adults. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005752
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Randomized Trial of Dietary Intervention Therapy in Obese Hypertensives (DITOH) Condition(s): Cardiovascular Diseases; Heart Diseases; Hypertension; Obesity Study Status: This study is completed.
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Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To determine the effects on blood pressure of dietary intervention, restricting caloric intake to 600 calories per day for 16 weeks compared to a control diet of 1200 calories per day in obese hypertensives. Secondary aims included a study of psychological characteristics at baseline and during the weight loss and maintenance phases of the study. Phase(s): Phase III Study Type: Interventional Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00000515 •
School and Family-Based Obesity Prevention for Children Condition(s): Cardiovascular Diseases; Heart Diseases; Obesity Study Status: This study is completed. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To conduct an integrated, multiple-component, school- and community-based intervention targeting both primary and secondary prevention of obesity among third-fourth-and fifth-graders ("School- and Family-Based Obesity Prevention for Children"). Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005750
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Sex Steroids, Obesity and Lipids in Adolescent Females Condition(s): Cardiovascular Diseases; Heart Diseases; Obesity; Hypercholesterolemia Study Status: This study is completed. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To prospectively explore the relationships of endogenous sex steroid hormones and obesity and their interactions with lipoprotein cholesterol and apolipoprotein levels in nine and ten year old Black and white adolescent girls for five years during puberty. Study Type: Observational Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005210
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Strong Heart Study Analyses Obesity and Lipoproteins Condition(s): Cardiovascular Diseases; Heart Diseases; Atherosclerosis; Obesity Study Status: This study is completed. Sponsor(s): National Heart, Lung, and Blood Institute (NHLBI) Purpose - Excerpt: To examine the relationship of obesity and body fat distribution to lipoprotein concentrations in members of the Strong Heart Study. Study Type: Observational
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Contact(s): see Web site below Web Site: http://clinicaltrials.gov/ct/show/NCT00005510
Keeping Current on Clinical Trials The U.S. National Institutes of Health, through the National Library of Medicine, has developed ClinicalTrials.gov to provide current information about clinical research across the broadest number of diseases and conditions. The site was launched in February 2000 and currently contains approximately 5,700 clinical studies in over 59,000 locations worldwide, with most studies being conducted in the United States. ClinicalTrials.gov receives about 2 million hits per month and hosts approximately 5,400 visitors daily. To access this database, simply go to the Web site at http://www.clinicaltrials.gov/ and search by “obesity” (or synonyms). While ClinicalTrials.gov is the most comprehensive listing of NIH-supported clinical trials available, not all trials are in the database. The database is updated regularly, so clinical trials are continually being added. The following is a list of specialty databases affiliated with the National Institutes of Health that offer additional information on trials: •
For clinical studies at the Warren Grant Magnuson Clinical Center located in Bethesda, Maryland, visit their Web site: http://clinicalstudies.info.nih.gov/
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For clinical studies conducted at the Bayview Campus in Baltimore, Maryland, visit their Web site: http://www.jhbmc.jhu.edu/studies/index.html
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For cancer trials, visit the National Cancer Institute: http://cancertrials.nci.nih.gov/
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For eye-related trials, visit and search the Web page of the National Eye Institute: http://www.nei.nih.gov/neitrials/index.htm
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For heart, lung and blood trials, visit the Web page of the National Heart, Lung and Blood Institute: http://www.nhlbi.nih.gov/studies/index.htm
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For trials on aging, visit and search the Web site of the National Institute on Aging: http://www.grc.nia.nih.gov/studies/index.htm
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For rare diseases, visit and search the Web site sponsored by the Office of Rare Diseases: http://ord.aspensys.com/asp/resources/rsch_trials.asp
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For alcoholism, visit the National Institute on Alcohol Abuse and Alcoholism: http://www.niaaa.nih.gov/intramural/Web_dicbr_hp/particip.htm
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For trials on infectious, immune, and allergic diseases, visit the site of the National Institute of Allergy and Infectious Diseases: http://www.niaid.nih.gov/clintrials/
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For trials on arthritis, musculoskeletal and skin diseases, visit newly revised site of the National Institute of Arthritis and Musculoskeletal and Skin Diseases of the National Institutes of Health: http://www.niams.nih.gov/hi/studies/index.htm
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For hearing-related trials, visit the National Institute on Deafness and Other Communication Disorders: http://www.nidcd.nih.gov/health/clinical/index.htm
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For trials on diseases of the digestive system and kidneys, and diabetes, visit the National Institute of Diabetes and Digestive and Kidney Diseases: http://www.niddk.nih.gov/patient/patient.htm
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For drug abuse trials, visit and search the Web site sponsored by the National Institute on Drug Abuse: http://www.nida.nih.gov/CTN/Index.htm
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For trials on mental disorders, visit and search the Web site of the National Institute of Mental Health: http://www.nimh.nih.gov/studies/index.cfm
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For trials on neurological disorders and stroke, visit and search the Web site sponsored by the National Institute of Neurological Disorders and Stroke of the NIH: http://www.ninds.nih.gov/funding/funding_opportunities.htm#Clinical_Trials
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CHAPTER 6. PATENTS ON OBESITY Overview Patents can be physical innovations (e.g. chemicals, pharmaceuticals, medical equipment) or processes (e.g. treatments or diagnostic procedures). The United States Patent and Trademark Office defines a patent as a grant of a property right to the inventor, issued by the Patent and Trademark Office.9 Patents, therefore, are intellectual property. For the United States, the term of a new patent is 20 years from the date when the patent application was filed. If the inventor wishes to receive economic benefits, it is likely that the invention will become commercially available within 20 years of the initial filing. It is important to understand, therefore, that an inventor’s patent does not indicate that a product or service is or will be commercially available. The patent implies only that the inventor has “the right to exclude others from making, using, offering for sale, or selling” the invention in the United States. While this relates to U.S. patents, similar rules govern foreign patents. In this chapter, we show you how to locate information on patents and their inventors. If you find a patent that is particularly interesting to you, contact the inventor or the assignee for further information. IMPORTANT NOTE: When following the search strategy described below, you may discover non-medical patents that use the generic term “obesity” (or a synonym) in their titles. To accurately reflect the results that you might find while conducting research on obesity, we have not necessarily excluded non-medical patents in this bibliography.
Patents on Obesity By performing a patent search focusing on obesity, you can obtain information such as the title of the invention, the names of the inventor(s), the assignee(s) or the company that owns or controls the patent, a short abstract that summarizes the patent, and a few excerpts from the description of the patent. The abstract of a patent tends to be more technical in nature, while the description is often written for the public. Full patent descriptions contain much more information than is presented here (e.g. claims, references, figures, diagrams, etc.). We
9Adapted
from the United States Patent and Trademark Office: http://www.uspto.gov/web/offices/pac/doc/general/whatis.htm.
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will tell you how to obtain this information later in the chapter. The following is an example of the type of information that you can expect to obtain from a patent search on obesity: •
.alpha.-Blocking agents in the treatment of obesity Inventor(s): Milavec; Maria (St. Louis, FR), Wagner; Heribert (Pfeffingen, CH) Assignee(s): Sandoz Ltd. (Basel, CH) Patent Number: 4,239,763 Date filed: June 22, 1979 Abstract: Alpha-blocking agents, especially 9,10-dihydroergot-peptide alkaloids, are anti-obesity agents. Excerpt(s): By way of example the following compositions may be used in the method of the invention.... If desired tablets may be made with 0.25 mg or 15 mg of dihydroergotoxin mesylate in analogous manner.... The above-mentioned tablets are useful in the treatment of obesity when administered 3 to 5 times a day. Web site: http://www.delphion.com/details?pn=US04239763__
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Acute and chronic electrical signal therapy for obesity Inventor(s): Flesler; Melina (Misgav, IL), Mika; Yuval (Zichron Yaakov, IL), Belsky; Ziv (Haifa, IL), Ben Arie; Yaakov (Haifa, IL), Darvish; Nissim (Tzrufa, IL), Ben-Haim; Shlomo (Cesarea, IL) Assignee(s): Impulse Dynamics N.V. (Curacao, NL) Patent Number: 6,600,953 Date filed: December 11, 2000 Abstract: Apparatus is provided for treating a condition such as obesity. The apparatus includes a set of one or more electrodes, which are adapted to be applied to one or more respective sites in a vicinity of a body of a stomach of a patient. A control unit is adapted to drive the electrode set to apply to the body of the stomach a signal, configured such that application thereof increases a level of contraction of muscle tissue of the body of the stomach, and decreases a cross-sectional area of a portion of the body of the stomach for a substantially continuous period greater than about 3 seconds. Excerpt(s): The present invention relates generally to treatment of obesity, and specifically to invasive techniques and apparatus for treating obesity.... Invasive treatments for obesity are often recommended for patients with a body mass index (mass/height.sup.2 [kg/m.sup.2 ]) which is greater than 35 or 40. For such patients, their weight is commonly associated with increased risk of heart disease, diabetes, and arthritis. Preferably, the invasive treatments are accompanied by changes in lifestyle, such as improved eating habits and an appropriate exercise regimen.... U.S. Pat. No. 6,067,991 to Forsell, U.S. Pat. No. 5,601,604 to Vincent, and U.S. Pat. No. 5,234,454 to Bangs, and U.S. Pat. Nos. 5,449,368, 5,226,429 and 5,074,868 to Kuzmak, which are incorporated herein by reference, describe mechanical instruments for implantation in or around the stomach of an obese patient. Web site: http://www.delphion.com/details?pn=US06600953__
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•
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anti-obesity
and
Inventor(s): Krsek; George (Culver, IN) Assignee(s): Progenics, Inc. (New York, NY) Patent Number: 4,602,008 Date filed: December 14, 1984 Abstract: 16-Alkylated and 16-alkylated-7-hydroxy 5.beta.-androstan-3-ol-17-one, and the esters and ethers thereof, are used as an anti-diabetic, anti-obesity and erythropoietic agent in mammals. Excerpt(s): The major function of the adrenal gland is to regulate metabolism in the body so that an intermittent intake of food can be regulated to maintain a constant metabolite supply to the cells. This is accomplished by producing steroid hormones which can control the conversion of incoming nutrients, such as aminoacids, glucose and fats into storage depots from which they can thereafter be released or interchanged, allowing a continuous flow of optimum energy and growth factors to the cells.... The steroid hormones are divided mainly into three classes. The first is glucocorticoids (cortisol), also known as gluconeogenic or diabetogenic steroids, which can convert aminoacids into glucose for direct use or store the glucose as glycogen for later use. Cortisol can therefore have an anti-anabolic effect through the depletion of aminoacids needed for protein synthesis and a diabetogenic effect through the direct release of glucose from the glycogen store.... A glucocorticoid excess, resulting from an excess of the pituitary hormone, adrenal cortico-trophic hormone (ACTH), which controls cortisol production, causes Cushing's Syndrome, an uncommon disease. Intake of an excess amount of cortisol from pharmacological use of steroids can also cause Cushing's Syndrome or Cushingoid-like disorders (hypercorticosteroidism, or more briefly hypercorticoidism) which are progeric in that they resemble the symptoms of the diseases of aging, e.g. obesity, hypertension, diabetes, renal stones, osteoporosis, mental disorder, menstrual disturbance, susceptibility to infection and poor wound healing. Web site: http://www.delphion.com/details?pn=US04602008__ •
Amino acid derivatives, pharmaceutical compositions containing these compounds and their use in the treatment of obesity Inventor(s): Rudolf; Klaus (Biberach, DE), Eberlein; Wolfgang (Biberach, DE), Engel; Wolfhard (Biberach, DE), Mihm; Gerhard (Biberach, DE), Doods; Henri (Warthausen, DE), Wieland; Heike A. (Biberach, DE), Willim; Klaus-Dieter (Schweinhausen/Hochdorf, DE), Krause; Jurgen (Ummendorf, DE), Dollinger; Horst (Ingelheim, DE), Esser; Franz (Ingelheim, DE), Schnorrenberg; Gerd (Gau-Algesheim, DE), Entzeroth; Michael (Warthausen, DE), Wienen; Wolfgang (Apfingen, DE) Assignee(s): Karl Thomae GmbH (Biberach an der Riss, DE) Patent Number: 5,616,620 Date filed: June 1, 1995 Abstract: Amino acid derivatives, suitable for the treatment of obesity. The following compound is exemplary of the class: (R)-N2-(diphenylacetyl)-N-[(4-hydroxyphenyl) methyl]-argininamide-acetate.
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Excerpt(s): the tautomers, diastereomers and enantiomers thereof, mixtures thereof and salts thereof, more particularly the physiologically acceptable salts thereof with inorganic or organic acids or bases, and processes for preparing them.... T.sup.1 to T.sup.3, which may be identical or different, denote phenyl groups or 6-membered heteroaryl groups bound via carbon atoms and which each contain one or two nitrogen atoms.... and unless otherwise specified the above-mentioned alkyl and alkoxy moieties may each contain 1 to 3 carbon atoms. Web site: http://www.delphion.com/details?pn=US05616620__ •
Anti-obesity agents Inventor(s): Suzuki; Kunio (Saitama, JP), Nakata; Tadashi (Saitama, JP), Shimizu; Takeshi (Saitama, JP), Enomoto; Kotaro (Saitama, JP) Assignee(s): Institute of Physical and Chemical Research (Saitama, JP) Patent Number: 5,710,143 Date filed: March 27, 1996 Abstract: Disclosed are anti-obesity agents comprising 3-ketosteroidal compounds as defined in the specification. The present invention also discloses pharmaceutical compositions and use of these compounds in the prevention and treatment of obesity. Excerpt(s): This application is a 371 of PCT/JP94/01631 filed Sep. 30, 1994.... The present invention relates to anti-obesity agents, more specifically to anti-obesity agents which comprise as an active ingredient 3-ketosteroid compounds having ketone groups at the C.sub.3 position of the cholestane skeletons.... Obesity is a condition under which the proliferation of tissues of body-composing lipids is increased abnormally. This abnormal condition is produced when energy intake is continuously greater than energy consumption, with the resulting excess energy being converted into neutral lipid which is accumulated in lipid tissues. Web site: http://www.delphion.com/details?pn=US05710143__
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Anti-obesity agents Inventor(s): Suzuki; Kunio (Saitama, JP), Nakata; Tadashi (Saitama, JP), Shimizu; Takeshi (Saitama, JP), Enomoto; Kotaro (Saitama, JP) Assignee(s): The Institute of Physical and Chemical Research (Saitama, JP) Patent Number: 5,846,962 Date filed: July 21, 1997 Abstract: Anti-obesity agents which comprise 3-ketosteroid compounds as an active ingredient are provided. The anti-obesity agents of the present invention have a high anti-obesity effect with little or no side effects and toxicity. Food products which contain anti-obesity agents comprising 3-ketosteroid compounds as an active ingredient, pharmaceutical compositions which comprise 3-ketosteroid compounds as an active ingredient and pharmaceutically acceptable carriers, and methods for preventing and treating obesity which comprise administering an effective amount of a 3-ketosteroid compound to a human are also provided.
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Excerpt(s): The present invention relates to anti-obesity agents, more specifically to antiobesity agents which comprise as an active ingredient 3-ketosteroid compounds having ketone groups at the C.sub.3 position of the cholestane skeletons.... Obesity is a condition under which the proliferation of tissues of body-composing lipids is increased abnormally. This abnormal condition is produced when energy intake is continuously greater than energy consumption, with the resulting excess energy being converted into neutral lipid which is accumulated in lipid tissues.... Obesity is important as a risk factor of the onset of diseases represented by geriatric diseases from hygienic and cosmetic viewpoints. Harmful influences of obesity have been recognized for a long time in advanced nations. Agents for preventing and/or treating obesity which have been developed until now have side effects or produce unsatisfactory effects. Web site: http://www.delphion.com/details?pn=US05846962__ •
Anti-obesity balloon placement system Inventor(s): Kullas; Karen E. (Taunton, MA), Giusto; Joseph (Warren, RI) Assignee(s): C. R. Bard, Inc. (Murray Hill, NJ) Patent Number: 4,723,547 Date filed: May 7, 1985 Abstract: An anti-obesity balloon and a placement system for the balloon includes a balloon with a needle-pierceable, self-sealing plug and an insertion catheter having a needle at its distal end. The needle is movable between an extended position in which it protrudes distally of the insertion catheter and a retracted position in which it is withdrawn interiorly of the insertion catheter. A handle arrangement is provided at the proximal end of the insertion catheter to control the position of the needle. Means are provided for aspirating and inflating the balloon. The balloon structure and insertion catheter structure protect and enclosed the sharp tip of the needle at all times during insertion and withdrawal of the insertion catheter. The insertion catheter is detachable from the balloon, after the balloon has been inflated in the patient's stomach, in a manner which imposes no force or load on the balloon. Excerpt(s): This invention relates to techniques for treating obesity by placement of a balloon in the patient's stomach to reduce the patient's appetite and control the patient's food intake.... Various techniques and devices have been proposed and used to treat obese patients so as to reduce their weight and to maintain their weight at a reduced, more acceptable level. The techniques have included surgical as well as non-surgical approaches. By way of example, one such surgical procedure involves an abdominal surgical procedure in which the stomach is surgically exposed and then is stapled in a manner to reduce the available volume of the stomach. In another surgical technique the stomach is wrapped in a non-expandable fabric or mesh so that it cannot expand beyond the volume defined by the wrap. Other surgical procedures for the treatment of obesity include shortening or placing shunts in the intestinal tract so as to reduce the time during which food is exposed to the patient's digestive process.... Also among the techniques which have been proposed has been to place a balloon within a patient's stomach so as to occupy a substantial volume of the stomach thereby to limit the available unfilled volume within the stomach and to provide the patient with an early sensation of satiety. The balloon systems which have been proposed have suffered from various difficulties and none is believed to have achieved any practical lasting use. Among the difficulties have been in the valving arrangement for inflating the balloon and for maintaining the balloon in an inflated condition over an extended period of
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time. Additionally, the balloon structures and placement techniques which have been proposed generally have been cumbersome and awkward. It is among the general objects of the present invention to provide an improved anti-obesity balloon and placement system which avoids the difficulties presented by the prior proposed devices. Web site: http://www.delphion.com/details?pn=US04723547__ •
Anti-obesity drugs Inventor(s): Shinitzky; Meir (Kfar Shmaryahu, IL), Shenfeld; Avner (Rehovot, IL) Assignee(s): Senyorina Ltd. (Kfar Shmaryahu, IL) Patent Number: 5,602,164 Date filed: March 18, 1996 Abstract: Obesity is treated by the administration to a subject of a compound having the general formula (I): R.sub.4 --(CH.sub.2).sub.n --CO--N(R.sub.1)--CH(R.sub.2)--CO(-R.sub.3), wherein R.sub.1 represents H or CH.sub.3; R.sub.2 represents a side chain of a naturally occurring amino acid; R.sub.3 represents OH, OCH.sub.2 CH.sub.3 and NH.sub.2; n is 6-18; and R.sub.4 represents CH.sub.3 or a group having the general formula (II): R.sub.3 --CO--CH(R.sub.2)--N(R.sub.1)--CO--, wherein R.sub.1, R.sub.2 and R.sub.3 have the above meanings. The compounds of formula (I) wherein R.sub.4 is a group of formula (II), are novel compounds. Excerpt(s): The present invention is in the field of treatment and prevention of obesity. The present invention provides compositions and methods for the treatment or prevention of such disorders utilizing, as active ingredient, lypophilic derivatives of natural amine acids. Furthermore, the present invention provides certain such novel compounds.... 1. Bar-Tana et al., J. Biol. Chem., 1985, 260, 8404-8410.... 2. Rose-Kakn et al., J. Biol. Chem., 1985, 260, 8411-8415. Web site: http://www.delphion.com/details?pn=US05602164__
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Anti-obesity proteins Inventor(s): DiMarchi; Richard D. (Carmel, IN), Flora; David B. (Greenfield, IN), Heath, Jr. William F. (Fishers, IN), Hoffmann; James A. (Greenwood, IN), Shields; James E. (Noblesville, IN), Smiley; David L. (Greenfield, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,532,336 Date filed: January 31, 1995 Abstract: The present invention provides anti-obesity proteins, which when administered to a patient regulate fat tissue. Accordingly, such agents allow patients to overcome their obesity handicap and live normal lives with much reduced risk for type II diabetes, cardiovascular disease and cancer. Excerpt(s): The present invention is in the field of human medicine, particularly in the treatment of obesity and disorders associated with obesity. Most specifically the invention relates to anti-obesity proteins that when administered to a patient regulate fat tissue.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout the world. According to
Patents 247
recent statistics, more than 25% of the United States population and 27% of the Canadian population are over weight. Kuczmarski, Amer. J. of Clin. Nut. 55: 495S-502S (1992); Reeder et. al., Can. Med. Ass. J., 23:226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society.... Much of this obesity induced pathology can be attributed to the strong association with dyslipidemia, hypertension, and insulin resistance. Many studies have demonstrated that reduction in obesity by diet and exercise reduces these risk factors dramatically. Unfortunately these treatments are largely unsuccessful with a failure rate reaching 95%. This failure may be due to the fact that the condition is strongly associated with genetically inherited factors that contribute to increased appetite, preference for highly caloric foods, reduced physical activity, and increased lipogenic metabolism. This indicates that people inheriting these genetic traits are prone to becoming obese regardless of their efforts to combat the condition. Therefore, a new pharmacological agent that can correct this adiposity handicap and allow the physician to successfully treat obese patients in spite of their genetic inheritance is needed. Web site: http://www.delphion.com/details?pn=US05532336__ •
Anti-obesity proteins Inventor(s): DiMarchi; Richard D. (Carmel, IN), Flora; David B. (Greenfield, IN), Heath, Jr. William F. (Fishers, IN), Hoffmann; James A. (Greenwood, IN), Shields; James E. (Noblesville, IN), Smiley; David L. (Greenfield, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,552,522 Date filed: January 31, 1995 Abstract: The present invention provides anti-obesity proteins, which when administered to a patient regulate fat tissue. Accordingly, such agents allow patients to overcome their obesity handicap and live normal lives with much reduced risk for type II diabetes, cardiovascular disease and cancer. Excerpt(s): The present invention is in the field of human medicine, particularly in the treatment of obesity and disorders associated with obesity. Most specifically the invention relates to anti-obesity proteins that when administered to a patient regulate fat tissue.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout the world. According to recent statistics, more than 25% of the United States population and 27% of the Canadian population are over weight. Kuczmarski, Amer. J. of Clin. Nut. 55:495S-502S (1992); Reeder et. al., Can. Med. Ass. J., 23:226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society.... Much of this obesity induced pathology can be attributed to the strong association with dyslipidemia, hypertension, and insulin resistance. Many studies have demonstrated that reduction in obesity by diet and exercise reduces these risk factors dramatically. Unfortunately these treatments are
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largely unsuccessful with a failure rate reaching 95%. This failure may be due to the fact that the condition is strongly associated with genetically inherited factors that contribute to increased appetite, preference for highly caloric foods, reduced physical activity, and increased lipogenic metabolism. This indicates that people inheriting these genetic traits are prone to becoming obese regardless of their efforts to combat the condition. Therefore, a new pharmacological agent that can correct this adiposity handicap and allow the physician to successfully treat obese patients in spite of their genetic inheritance is needed. Web site: http://www.delphion.com/details?pn=US05552522__ •
Anti-obesity proteins Inventor(s): Basinski; Margret B. (Indianapolis, IN), DiMarchi; Richard D. (Carmel, IN), Heath, Jr. William F. (Fishers, IN), Schoner; Brigitte E. (Monrovia, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,552,523 Date filed: February 6, 1995 Abstract: The present invention provides anti-obesity proteins, which when administered to a patient regulate fat tissue. Accordingly, such agents allow patients to overcome their obesity handicap and live normal lives with much reduced risk for type II diabetes, cardiovascular disease and cancer. Excerpt(s): The present invention is in the field of human medicine, particularly in the treatment of obesity and disorders associated with obesity. Most specifically the invention relates to anti-obesity proteins that when administered to a patient regulate fat tissue.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout. the world. According to recent statistics, more than 25% of the United States population and 27% of the Canadian population are over weight. Kuczmarski, Amer. J, of Clin. Nut. 5: 495S-502S (1992); Reeder et. al., Can. Med. Ass. J., 23: 226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society.... Much of this obesity induced pathology can be attributed to the strong association with dyslipidemia, hypertension, and insulin resistance. Many studies have demonstrated that reduction in obesity by diet and exercise reduces these risk factors dramatically. Unfortunately these treatments are largely unsuccessful with a failure rate reaching 95%. This failure may be due no the fact that the condition is strongly associated with genetically inherited factors that contribute to increased appetite, preference for highly caloric foods, reduced physical activity, and increased lipogenic metabolism. This indicates that people inheriting these genetic traits are prone to becoming obese regardless of their efforts to combat the condition. Therefore, a new pharmacological agent that can correct this adiposity handicap and allow the physician to successfully treat obese patients in spite of their genetic inheritance is needed. Web site: http://www.delphion.com/details?pn=US05552523__
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Anti-obesity proteins Inventor(s): Basinski; Margret B. (Indianapolis, IN), DiMarchi; Richard D. (Carmel, IN), Heath, Jr. William F. (Fishers, IN), Schoner; Brigitte E. (Monrovia, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,552,524 Date filed: February 6, 1995 Abstract: The present invention provides anti-obesity proteins, which when administered to a patient regulate fat tissue. Accordingly, such agents allow patients to overcome their obesity handicap and live normal lives with much reduced risk for type II diabetes, cardiovascular disease and cancer. Excerpt(s): The present invention is in the field of human medicine, particularly in the treatment of obesity and disorders associated with obesity. Most specifically the invention relates to anti-obesity proteins that when administered to a patient regulate fat tissue.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout the world. According to recent statistics, more than 25% of the United States population and 27% of the Canadian population are over weight. Kuczmarski, Amer. J. of Clin. Nut. 52: 495S-502S (1992); Reeder et. al., Can. Med. Ass. J., 23:226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society.... Much of this obesity induced pathology can be attributed to the strong association with dyslipidemia, hypertension, and insulin resistance. Many studies have demonstrated that reduction in obesity by diet and exercise reduces these risk factors dramatically. Unfortunately these treatments are largely unsuccessful with a failure rate reaching 95%. This failure may be due to the fact that the condition is strongly associated with genetically inherited factors that contribute to increased appetite, preference for highly caloric foods, reduced physical activity, and increased lipogenic metabolism. This indicates that people inheriting these genetic traits are prone to becoming obese regardless of their efforts to combat the condition. Therefore, a new pharmacological agent that can correct this adiposity handicap and allow the physician to successfully treat obese patients in spite of their genetic inheritance is needed. Web site: http://www.delphion.com/details?pn=US05552524__
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Anti-obesity proteins Inventor(s): DiMarchi; Richard D. (Carmel, IN), Flora; David B. (Greenfield, IN), Heath, Jr. William F. (Fishers, IN), Hoffmann; James A. (Greenwood, IN), Shields; James E. (Noblesville, IN), Smiley; David L. (Greenfield, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,525,705 Date filed: January 31, 1995 Abstract: The present invention provides anti-obesity proteins, which when administered to a patient regulate fat tissue. Accordingly, such agents allow patients to
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overcome their obesity handicap and live normal lives with much reduced risk for type II diabetes, cardiovascular disease and cancer. Excerpt(s): The present invention is in the field of human medicine, particularly in the treatment of obesity and disorders associated with obesity. Most specifically the invention relates to anti-obesity proteins that when administered to a patient regulate fat tissue.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout the world. According to recent statistics, more than 25% of the United States population and 27% of the Canadian population are over weight. Kuczmarski, Amer, J. Of Clin, Nut. 55: 495S-502S (1992); Reeder et. al., Can. Med. Ass. J., 23: 226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society.... Huch of this obesity induced pathology can be attributed to the strong association with dyslipidemia, hypertension, and insulin resistance. Many studies have demonstrated that reduction in obesity by diet and exercise reduces these risk factors dramatically. Unfortunately these treatments are largely unsuccessful with a failure rate reaching 95%. This failure may be due to the fact that the condition is strongly associated with genetically inherited factors that contribute to increased appetite, preference for highly caloric foods, reduced physical activity, and increased lipogenic metabolism. This indicates that people inheriting these genetic traits are prone to becoming obese regardless of their efforts to combat the condition. Therefore, a new pharmacological agent that can correct this adiposity handicap and allow the physician to successfully treat obese patients in spite of their genetic inheritance is needed. Web site: http://www.delphion.com/details?pn=US05525705__ •
Anti-obesity proteins Inventor(s): Basinski; Margret B. (Indianapolis, IN), DiMarchi; Richard D. (Carmel, IN), Heath, Jr. William F. (Fishers, IN), Schoner; Brigitte E. (Monrovia, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,554,727 Date filed: February 6, 1995 Abstract: The present invention provides anti-obesity proteins, which when administered to a patient regulate fat tissue. Accordingly, such agents allow patients to overcome their obesity handicap and live normal lives with much reduced risk for type II diabetes, cardiovascular disease and cancer. Excerpt(s): The present invention is in the field of human medicine, particularly in the treatment of obesity and disorders associated with obesity. Most specifically the invention relates to anti-obesity proteins that when administered to a patient regulate fan tissue.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout the world. According to recent statistics, more than 25% of the United States population and 27% of the Canadian population are over weight. Kuczmarski, Amer. J of Clin. Nut. 55: 495S-502S (1992); Reeder et. al., Can. Med. Ass. J., 23: 226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for
Patents 251
cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society.... Much of this obesity induced pathology can be attributed to the strong association with dyslipidemia, hypertension, and insulin resistance. Many studies have demonstrated that reduction in obesity by diet and exercise reduces these risk factors dramatically. Unfortunately these treatments are largely unsuccessful with a failure rate reaching 95%. This failure may be due to the fact that the condition is strongly associated with genetically inherited factors that contribute to increased appetite, preference for highly caloric foods, reduced physical activity, and increased lipogenic metabolism. This indicates that people inheriting these genetic traits. are prone to becoming obese regardless of their efforts to combat the condition. Therefore, a new pharmacological agent that can correct this adiposity handicap and allow the physician to successfully treat obese patients in spite of their genetic inheritance is needed. Web site: http://www.delphion.com/details?pn=US05554727__ •
Anti-obesity proteins Inventor(s): Basinski; Margret B. (Indianapolis, IN), DiMarchi; Richard D. (Carmel, IN), Heath, Jr. William F. (Fishers, IN), Schoner; Brigitte E. (Monrovia, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,559,208 Date filed: February 6, 1995 Abstract: The present invention provides anti-obesity proteins, which when administered to a patient regulate fat tissue. Accordingly, such agents allow patients to overcome their obesity handicap and live normal lives with much reduced risk for type II diabetes, cardiovascular disease and cancer. Excerpt(s): The present invention is in the field of human medicine, particularly in the treatment of obesity and disorders associated with obesity. Most specifically the invention relates to anti-obesity proteins that when administered to a patient regulate fat tissue.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout the world. According to recent statistics, more than 25% of the United States population and 27% of the Canadian population are over weight. Kuczmarski, Amer. J. of Clin. Nut. 55: 495S-502S (1992); Reeder et. al., Can. Med. Ass. J., 23:226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society.... Much of this obesity induced pathology can be attributed to the strong association with dyslipidemia, hypertension, and insulin resistance. Many studies have demonstrated that reduction in obesity by diet and exercise reduces these risk factors dramatically. Unfortunately these treatments are largely unsuccessful with a failure rate reaching 95%. This failure may be due to the fact that the condition is strongly associated with genetically inherited factors that contribute to increased appetite, preference for highly caloric foods, reduced physical activity, and increased lipogenic metabolism. This indicates that people inheriting these genetic traits are prone to becoming obese regardless of their efforts to combat the condition.
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Therefore, a new pharmacological agent that can correct this adiposity handicap and allow the physician to successfully treat obese patients in spite of their genetic inheritance is needed. Web site: http://www.delphion.com/details?pn=US05559208__ •
Anti-obesity proteins Inventor(s): DiMarchi; Richard D. (Carmel, IN), Flora; David B. (Greenfield, IN), Heath, Jr. William F. (Fishers, IN), Hoffmann; James A. (Greenwood, IN), Shields; James E. (Noblesville, IN), Smiley; David L. (Greenfield, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,563,243 Date filed: January 31, 1995 Abstract: The present invention provides anti-obesity proteins, which when administered to a patient regulate fat tissue. Accordingly, such agents allow patients to overcome their obesity handicap and live normal lives with much reduced risk for type II diabetes, cardiovascular disease and cancer. Excerpt(s): The present invention is in the field of human medicine, particularly in the treatment of obesity and disorders associated with obesity. Most specifically the invention relates to anti-obesity proteins that when administered to a patient regulate fat tissue.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout the world. According to recent statistics, more than 25% of the United States population and 27% of the Canadian population are over weight. Kuczmarski, Amer. J. of Clin. Nut 55: 495S-502S (1992); Reeder et. al., Can. Med. Ass. J., 23: 226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society.... Much of this obesity induced pathology can be attributed to the strong association with dyslipidemia, hypertension, and insulin resistance. Many studies have demonstrated that reduction in obesity by diet and exercise reduces these risk factors dramatically. Unfortunately these treatments are largely unsuccessful with a failure rate reaching 95%. This failure may be due to the fact that the condition is strongly associated with genetically inherited factors that contribute to increased appetite, preference for highly caloric foods, reduced physical activity, and increased lipogenic metabolism. This indicates that people inheriting these genetic traits are prone to becoming obese regardless of their efforts to combat the condition. Therefore, a new pharmacological agent that can correct this adiposity handicap and allow the physician to successfully treat obese patients in spite of their genetic inheritance is needed. Web site: http://www.delphion.com/details?pn=US05563243__
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Anti-obesity proteins Inventor(s): DiMarchi; Richard D. (Carmel, IN), Flora; David B. (Greenfield, IN), Heath, Jr. William F. (Fishers, IN), Hoffmann; James A. (Greenwood, IN), Shields; James E. (Noblesville, IN), Smiley; David L. (Greenfield, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,563,244 Date filed: January 31, 1995 Abstract: The present invention provides anti-obesity proteins, which when administered to a patient regulate fat tissue. Accordingly, such agents allow patients to overcome their obesity handicap and live normal lives with much reduced risk for type II diabetes, cardiovascular disease and cancer. Excerpt(s): The present invention is in the field of human medicine, particularly in the treatment of obesity and disorders associated with obesity. Most specifically the invention relates to anti-obesity proteins that when administered to a patient regulate fat tissue.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout the world. According to recent statistics, more than 25% of the United States population and 27% of the Canadian population are over weight. Kuczmarski, Amer, J., of Clin. Nut. 55: 495-502S (1992); Reeder et. al., Can. Med. Ass. J., 23: 226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society.... Much of this obesity induced pathology can be attributed to the strong association with dyslipidemia, hypertension, and insulin resistance. Many studies have demonstrated that reduction in obesity by diet and exercise reduces these risk factors dramatically. Unfortunately these treatments are largely unsuccessful with a failure rate reaching 95%. This failure may be due to the fact that the condition is strongly associated with genetically inherited factors that contribute to increased appetite, preference for highly caloric foods, reduced physical activity, and increased lipogenic metabolism. This indicates that people inheriting these genetic traits are prone to becoming obese regardless of their efforts to combat the condition. Therefore, a new pharmacological agent that can correct this adiposity handicap and allow the physician to successfully treat obese patients in spite of their genetic inheritance is needed. Web site: http://www.delphion.com/details?pn=US05563244__
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Anti-obesity proteins Inventor(s): DiMarchi; Richard D. (Carmel, IN), Flora; David B. (Greenfield, IN), Heath, Jr. William F. (Fishers, IN), Hoffmann; James A. (Greenwood, IN), Shields; James E. (Noblesville, IN), Smiley; David L. (Greenfield, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,563,245 Date filed: January 31, 1995
254 Obesity
Abstract: The present invention provides anti-obesity proteins, which when administered to a patient regulate fat tissue. Accordingly, such agents allow patients to overcome their obesity handicap and live normal lives with much reduced risk for type II diabetes, cardiovascular disease and cancer. Excerpt(s): The present invention is in the field of human medicine, particularly in the treatment of obesity and disorders associated with obesity. Most specifically the invention relates to anti-obesity proteins that when administered to a patient regulate fat tissue.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout the world. According to recent statistics, more than 25% of the United States population and 27% of the Canadian population are over weight. Kuczmarski, Amer. J. of Clin. Nut. 55:495S-502S (1992); Reeder et. al., Can. Med. Ass. J., 23:226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society.... Much of this obesity induced pathology can be attributed to the strong association with dyslipidemia, hypertension, and insulin resistance. Many studies have demonstrated that reduction in obesity by diet and exercise reduces these risk factors dramatically. Unfortunately these treatments are largely unsuccessful with a failure rate reaching 95%. This failure may be due to the fact that the condition is strongly associated with genetically inherited factors that contribute to increased appetite, preference for highly caloric foods, reduced physical activity, and increased lipogenic metabolism. This indicates that people inheriting these genetic traits are prone to becoming obese regardless of their efforts to combat the condition. Therefore, a new pharmacological agent that can correct this adiposity handicap and allow the physician to successfully treat obese patients in spite of their genetic inheritance is needed. Web site: http://www.delphion.com/details?pn=US05563245__ •
Anti-obesity proteins Inventor(s): DiMarchi; Richard D. (Carmel, IN), Flora; David B. (Greenfield, IN), Heath, Jr. William F. (Fishers, IN), Hoffmann; James A. (Greenwood, IN), Shields; James E. (Noblesville, IN), Smiley; David L. (Greenfield, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,567,678 Date filed: January 31, 1995 Abstract: The present invention provides anti-obesity proteins, which when administered to a patient regulate fat tissue. Accordingly, such agents allow patients to overcome their obesity handicap and live normal lives with much reduced risk for type II diabetes, cardiovascular disease and cancer. Excerpt(s): The present invention is in the field of human medicine, particularly in the treatment of obesity and disorders associated with obesity. Most specifically the invention relates to anti-obesity proteins that when administered to a patient regulate fat tissue.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout the world. According to recent statistics, more than 25% of the United States population and 27% of the
Patents 255
Canadian population are over weight. Kuczmarski, Amer. J. of Clin. Nut. 55: 495S-502S (1992); Reeder et. al., Can. Med. Ass. J., 23: 226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society.... Much of this obesity induced pathology can be attributed to the strong association with dyslipidemia, hypertension, and insulin resistance. Many studies have demonstrated that reduction in obesity by diet and exercise reduces these risk factors dramatically. Unfortunately these treatments are largely unsuccessful with a failure rate reaching 95%. This failure may be due to the fact that the condition is strongly associated with genetically inherited factors that contribute to increased appetite, preference for highly caloric foods, reduced physical activity, and increased lipogenic metabolism. This indicates that people inheriting these genetic traits are prone to becoming obese regardless of their efforts to combat the condition. Therefore, a new pharmacological agent that can correct this adiposity handicap and allow the physician to successfully treat obese patients in spite of their genetic inheritance is needed. Web site: http://www.delphion.com/details?pn=US05567678__ •
Anti-obesity proteins Inventor(s): Basinski; Margret (Indianapolis, IN), DiMarchi; Richard D. (Carmel, IN), Flora; David B. (Greenfield, IN), Heath, Jr. William F. (Fishers, IN), Hoffmann; James A. (Greenwood, IN), Schoner; Brigitte E. (Monrovia, IN), Shields; James E. (Noblesville, IN), Smiley; David L. (Greenfield, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,567,803 Date filed: February 6, 1995 Abstract: The present invention provides anti-obesity proteins, which when administered to a patient regulate fat tissue. Accordingly, such agents allow patients to overcome their obesity handicap and live normal lives with much reduced risk for type II diabetes, cardiovascular disease and cancer. Excerpt(s): The present invention is in the field of human medicine, particularly in the treatment of obesity and disorders associated with obesity. Most specifically the invention relates to anti-obesity proteins that when administered to a patient regulate fat tissue.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout the world. According to recent statistics, more than 25% of the United States population and 27% of the Canadian population are over weight. Kuczmarski, Amer. J. of Clin. Nut. 55: 495S-502S (1992); Reeder et. al., Can. Med. Ass. J., 23:226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society.... Much of this obesity induced pathology can be attributed to the strong association with dyslipidemia, hypertension, and insulin resistance. Many studies have demonstrated that reduction in obesity by diet and exercise reduces these risk factors dramatically. Unfortunately these treatments are
256 Obesity
largely unsuccessful with a failure rate reaching 95%. This failure may be due to the fact that the condition is strongly associated with genetically inherited factors that contribute to increased appetite, preference for highly caloric foods, reduced physical activity, and increased lipogenic metabolism. This indicates that people inheriting these genetic traits are prone to becoming obese regardless of their efforts to combat the condition. Therefore, a new pharmacological agent that can correct this adiposity handicap and allow the physician to successfully treat obese patients in spite of their genetic inheritance is needed. Web site: http://www.delphion.com/details?pn=US05567803__ •
Anti-obesity proteins Inventor(s): DiMarchi; Richard D. (Carmel, IN), Flora; David B. (Greenfield, IN), Heath, Jr. William F. (Fishers, IN), Hoffman; James A. (Greenwood, IN), Shields; James E. (Noblesville, IN), Smiley; David L. (Greenfield, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,569,743 Date filed: January 31, 1995 Abstract: The present invention provides anti-obesity proteins, which when administered to a patient regulate fat tissue. Accordingly, such agents allow patients to overcome their obesity handicap and live normal lives with much reduced risk for type II diabetes, cardiovascular disease and cancer. Excerpt(s): The present invention is in the field of human medicine, particularly in the treatment of obesity and disorders associated with obesity. Most specifically the invention relates to anti-obesity proteins that when administered to a patient regulate fat tissue.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout the world. According to recent statistics, more than 25% of the United States population and 27% of the Canadian population are over weight. Kuczmarski, Amer. J. of Clin. Nut. 55: 495S-502S (1992); Reeder et. al., Can. Med. Ass. J., 23: 226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society.... Much of this obesity induced pathology can be attributed to the strong association with dyslipidemia, hypertension, and insulin resistance. Many studies have demonstrated that reduction in obesity by diet and exercise reduces these risk factors dramatically. Unfortunately these treatments are largely unsuccessful with a failure rate reaching 95%. This failure may be due to the fact that the condition is strongly associated with genetically inherited factors that contribute to increased appetite, preference for highly caloric foods, reduced physical activity, and increased lipogenic metabolism. This indicates that people inheriting these genetic traits are prone to becoming obese regardless of their efforts to combat the condition. Therefore, a new pharmacological agent that can correct this adiposity handicap and allow the physician to successfully treat obese patients in spite of their genetic inheritance is needed. Web site: http://www.delphion.com/details?pn=US05569743__
Patents 257
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Anti-obesity proteins Inventor(s): Basinski; Margret B. (Indianapolis, IN), DiMarchi; Richard D. (Carmel, IN), Flora; David B. (Greenfield, IN), Heath, Jr. William F. (Fishers, IN), Hoffmann; James A. (Greenwood, IN), Schoner; Brigitte E. (Monrovia, IN), Shields; James E. (Noblesville, IN), Smiley; David L. (Greenfield, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,569,744 Date filed: February 6, 1995 Abstract: The present invention provides anti-obesity proteins, which when administered to a patient regulate fat tissue. Accordingly, such agents allow patients to overcome their obesity handicap and live normal lives with much reduced risk for type II diabetes, cardiovascular disease and cancer. Excerpt(s): The present invention is in the field of human medicine, particularly in the treatment of obesity and disorders associated with obesity. Most specifically the invention relates to anti-obesity proteins that when administered to a patient regulate fat tissue.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout the world. According to recent statistics, more than 25% of the United States population and 27% of the Canadian population are over weight. Kuczmarski, Amer. J. of Clin. Nut. 55:495S-502S (1992); Reeder et. al., Can. Med. Ass. J., 23:226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society.... Much of this obesity induced pathology can be attributed to the strong association with dyslipidemia, hypertension, and insulin resistance. Many studies have demonstrated that reduction in obesity by diet and exercise reduces these risk factors dramatically. Unfortunately these treatments are largely unsuccessful with a failure rate reaching 95%. This failure may be due to the fact that the condition is strongly associated with genetically inherited factors that contribute to increased appetite, preference for highly caloric foods, reduced physical activity, and increased lipogenic metabolism. This indicates that people inheriting these genetic traits are prone to becoming obese regardless of their efforts to combat the condition. Therefore, a new pharmacological agent that can correct this adiposity handicap and allow the physician to successfully treat obese patients in spite of their genetic inheritance is needed. Web site: http://www.delphion.com/details?pn=US05569744__
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Anti-obesity proteins Inventor(s): DiMarchi; Richard D. (Carmel, IN), Flora; David B. (Greenfield, IN), Heath, Jr. William F. (Fishers, IN), Hoffmann; James A. (Greenwood, IN), Shields; James E. (Noblesville, IN), Smiley; David L. (Greenfield, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,574,133 Date filed: January 31, 1995
258 Obesity
Abstract: The present invention provides anti-obesity proteins, which when administered to a patient regulate fat tissue. Accordingly, such agents allow patients to overcome their obesity handicap and live normal lives with much reduced risk for type II diabetes, cardiovascular disease and cancer. Excerpt(s): The present invention is in the field of human medicine, particularly in the treatment of obesity and disorders associated with obesity. Moist specifically the invention relates to anti-obesity proteins that when administered to a patient regulate fat tissue.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout the world. According to recent statistics, more than 25% of the United States population and 27% of the Canadian population are over weight. Kuczmarski, Amer. J. of Clin. Nut. 55: 495S-502S (1992); Reeder et. al., Can. Med. Ass. J., 23: 226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society.... Much of this obesity inducted pathology can be attributed to the strong association with dyslipidemia, hypertension, and insulin resistance. Many studies have demonstrated that reduction in obesity by diet and exercise reduces these risk factors dramatically. Unfortunately these treatments are largely unsuccessful with a failure rate reaching 95%. This failure may be due to the fact that the condition is strongly associated with genetically inherited factors that contribute to increased appetite, preference for highly caloric foods, reduced physical activity, and increased lipogenic metabolism. This indicates that people inheriting these genetic traits are prone to becoming obese regardless of their efforts to combat the condition. Therefore, a new pharmacological agent that can correct this adiposity handicap and allow the physician to successfully treat obese patients in spite of their genetic inheritance is needed. Web site: http://www.delphion.com/details?pn=US05574133__ •
Anti-obesity proteins Inventor(s): DiMarchi; Richard D. (Carmel, IN), Flora; David B. (Greenfield, IN), Heath, Jr. William F. (Fishers, IN), Hoffmann; James A. (Greenwood, IN), Shields; James E. (Noblesville, IN), Smiley; David L. (Greenfield, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,580,954 Date filed: January 31, 1995 Abstract: The present invention provides anti-obesity proteins, which when administered to a patient regulate fat tissue. Accordingly, such agents allow patients to overcome their obesity handicap and live normal lives with much reduced risk for type II diabetes, cardiovascular disease and cancer. Excerpt(s): The present invention is in the field of human medicine, particularly in the treatment of obesity and disorders associated with obesity. Most specifically the invention relates to anti-obesity proteins that when administered to a patient regulate fat tissue.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout the world. According to recent statistics, more than 25% of the United States population and 27% of the
Patents 259
Canadian population are over weight. Kuczmarski, Amer. J. of Clin. Nut. 55: 495S-502S (1992); Reeder et. al., Can. Med. Ass. J., 23:226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society.... Much of this obesity induced pathology can be attributed to the strong association with dyslipidemia, hypertension, and insulin resistance. Many studies have demonstrated that reduction in obesity by diet and exercise reduces these risk factors dramatically. Unfortunately these treatments are largely unsuccessful with a failure rate reaching 95%. This failure may be due to the fact that the condition is strongly associated with genetically inherited factors that contribute to increased appetite, preference for highly caloric foods, reduced physical activity, and increased lipogenic metabolism. This indicates that people inheriting these genetic traits are prone to becoming obese regardless of their efforts to combat the condition. Therefore, a new pharmacological agent that can correct this adiposity handicap and allow the physician to successfully treat obese patients in spite of their genetic inheritance is needed. Web site: http://www.delphion.com/details?pn=US05580954__ •
Anti-obesity proteins Inventor(s): Becker; Gerald W. (Fishers, IN), Hale; John E. (Fishers, IN), MacKellar; Warren C. (Plainfield, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,594,101 Date filed: March 3, 1995 Abstract: The present invention provides anti-obesity proteins, which when administered to a patient regulate fat tissue. Accordingly, such agents allow patients to overcome their obesity handicap and live normal lives with much reduced risk for type II diabetes, cardiovascular disease and cancer. Excerpt(s): The present invention is in the field of human medicine, particularly in the treatment of obesity and disorders associated with obesity. Most specifically, the invention relates to anti-obesity proteins that, when administered to a patient, regulate fat tissue.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout the world. According to recent statistics, more than 25% of the United States population and 27% of the Canadian population are over weight. Kuczmarski, Amer. J. of Clin. Nut. 55: 495S-502S (1992); Reeder et. al., Can. Med,. Ass. J., 23:226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society.... Much of this obesity induced pathology can be attributed to the strong association with dyslipidemia, hypertension, and insulin resistance. Many studies have demonstrated that reduction in obesity by diet and exercise reduces these risk factors dramatically. Unfortunately these treatments are largely unsuccessful with a failure rate reaching 95%. This failure may be due to the fact that the condition is strongly associated with genetically inherited factors that contribute
260 Obesity
to increased appetite, preference for highly caloric foods, reduced physical activity, and increased lipogenic metabolism. This indicates that people inheriting these genetic traits are prone to becoming obese regardless of their efforts to combat the condition. Therefore, a new pharmacological agent that can correct this adiposity handicap and allow the physician to successfully treat obese patients in spite of their genetic inheritance is needed. Web site: http://www.delphion.com/details?pn=US05594101__ •
Anti-obesity proteins Inventor(s): Basinski; Margret B. (Indianapolis, IN), DiMarchi; Richard D. (Carmel, IN), Flora; David B. (Greenfield, IN), Heath, Jr. William F. (Fishers, IN), Hoffmann; James A. (Greenwood, IN), Schoner; Brigitte E. (Monrovia, IN), Shields; James E. (Noblesville, IN), Smiley; David L. (Greenfield, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,594,104 Date filed: February 6, 1995 Abstract: The present invention provides anti-obesity proteins, which when administered to a patient regulate fat tissue. Accordingly, such agents allow patients to overcome their obesity handicap and live normal lives with much reduced risk for type II diabetes, cardiovascular disease and cancer. Excerpt(s): The present invention is in the field of human medicine, particularly in the treatment of obesity and disorders associated with obesity. Most specifically the invention relates to anti-obesity proteins that when administered to a patient regulate fat tissue.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout the world. According to recent statistics, more than 25% of the United States population and 27% of the Canadian population are over weight. Kuczmarski, Amer. J. of Clin. Nut. 55:495S-502S (1992); Reeder et. al., Can. Med. Ass. J., 23:226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society.... Much of this obesity induced pathology can be attributed to the strong association with dyslipidemia, hypertension, and insulin resistance. Many studies have demonstrated that reduction in obesity by diet and exercise reduces these risk factors dramatically. Unfortunately these treatments are largely unsuccessful with a failure rate reaching 95%. This failure may be due to the fact that the condition is strongly associated with genetically inherited factors that contribute to increased appetite, preference for highly caloric foods, reduced physical activity, and increased lipogenic metabolism. This indicates that people inheriting these genetic traits are prone to becoming obese regardless of their efforts to combat the condition. Therefore, a new pharmacological agent that can correct this adiposity handicap and allow the physician to successfully treat obese patients in spite of their genetic inheritance is needed. Web site: http://www.delphion.com/details?pn=US05594104__
Patents 261
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Anti-obesity proteins Inventor(s): Basinski; Margret B. (Indianapolis, IN), DiMarchi; Richard D. (Carmel, IN), Flora; David B. (Greenfield, IN), Heath, Jr. William F. (Fishers, IN), Hoffmann; James A. (Greenwood, IN), Schoner; Brigitte E. (Monrovia, IN), Shields; James E. (Noblesville, IN), Smiley; David L. (Greenfield, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,605,886 Date filed: May 17, 1995 Abstract: The present invention provides anti-obesity proteins, which when administered to a patient regulate fat tissue. Accordingly, such agents allow patients to overcome their obesity handicap and live normal lives with much reduced risk for type II diabetes, cardiovascular disease and cancer. Excerpt(s): The present invention is in the field of human medicine, particularly in the treatment of obesity and disorders associated with obesity. Most specifically the invention relates to anti-obesity proteins that when administered to a patient regulate fat tissue.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout the world. According to recent statistics, more than 25% of the United States population and 27% of the Canadian population are over weight. Kuczmarski, Amer. J. of Clin. Nut. 55: 495S-502S (1992); Reeder et. al., Can. Med. Ass. J., 23: 226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society.... Much of this obesity induced pathology can be attributed to the strong association with dyslipidemia, hypertension, and insulin resistance. Many studies have demonstrated that reduction in obesity by diet and exercise reduces these risk factors dramatically. Unfortunately these treatments are largely unsuccessful with a failure rate reaching 95%. This failure may be due to the fact that the condition is strongly associated with genetically inherited factors that contribute to increased appetite, preference for highly caloric foods, reduced physical activity, and increased lipogenic metabolism. This indicates that people inheriting these genetic traits are prone to becoming obese regardless of their efforts to combat the condition. Therefore, a new pharmacological agent that can correct this adiposity handicap and allow the physician to successfully treat obese patients in spite of their genetic inheritance is needed. Web site: http://www.delphion.com/details?pn=US05605886__
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Anti-obesity proteins Inventor(s): Basinski; Margret B. (Indianapolis, IN), DiMarchi; Richard D. (Carmel, IN), Flora; David B. (Greenfield, IN), Heath, Jr. William F. (Fishers, IN), Hoffmann; James A. (Greenwood, IN), Schoner; Brigitte E. (Monrovia, IN), Shields; James E. (Noblesville, IN), Smiley; David L. (Greenfield, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,691,309 Date filed: February 6, 1995
262 Obesity
Abstract: The present invention provides anti-obesity proteins, which when administered to a patient regulate fat tissue. Accordingly, such agents allow patients to overcome their obesity handicap and live normal lives with much reduced risk for type II diabetes, cardiovascular disease and cancer. Excerpt(s): The present invention is in the field of human medicine, particularly in the treatment of obesity and disorders associated with obesity. Most specifically the invention relates to anti-obesity proteins that when administered to a patient regulate fat tissue.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout the world. According to recent statistics, more than 25% of the United States population and 27% of the Canadian population are over weight. Kuczmarski, Amer. J. of Clin. Nut. 55: 495S-502S (1992); Reeder et. al., Can. Med. Ass. J., 23: 226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society.... Much of this obesity induced pathology can be attributed to the strong association with dyslipidemia, hypertension, and insulin resistance. Many studies have demonstrated that reduction in obesity by diet and exercise reduces these risk factors dramatically. Unfortunately these treatments are largely unsuccessful with a failure rate reaching 95%. This failure may be due to the fact that the condition is strongly associated with genetically inherited factors that contribute to increased appetite, preference for highly caloric foods, reduced physical activity, and increased lipogenic metabolism. This indicates that people inheriting these genetic traits are prone to becoming obese regardless of their efforts to combat the condition. Therefore, a new pharmacological agent that can correct this adiposity handicap and allow the physician to successfully treat obese patients in spite of their genetic inheritance is needed. Web site: http://www.delphion.com/details?pn=US05691309__ •
Anti-obesity proteins Inventor(s): DiMarchi; Richard D. (Carmel, IN), Hermeling; Ronald N. (Indianapolis, IN), Hoffmann; James A. (Greenwood, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,719,266 Date filed: March 17, 1995 Abstract: The present invention provides anti-obesity proteins, which when administered to a patient regulate fat tissue. Accordingly, such agents allow patients to overcome their obesity handicap and live normal lives with much reduced risk for type II diabetes, cardiovascular disease and cancer. Excerpt(s): The present invention is in the field of human medicine, particularly in the treatment of obesity and disorders associated with obesity. Most specifically the invention relates to anti-obesity proteins that when administered to a patient regulate fat tissue.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout the world. According to recent statistics, more than 25% of the United States population and 27% of the Canadian population are overweight. Kuczmarski, Amer. J. of Clin. Nutr. 55: 495S-502S
Patents 263
(1992); Reeder et. al., Can. Med. Ass. J., 23: 226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society.... Much of this obesity induced pathology can be attributed to the strong association with dyslipidemia, hypertension, and insulin resistance. Many studies have demonstrated that reduction in obesity by diet and exercise reduces these risk factors dramatically. Unfortunately, these treatments are largely unsuccessful with a failure rate reaching 95%. This failure may be due to the fact that the condition is strongly associated with genetically inherited factors that contribute to increased appetite, preference for highly caloric foods, reduced physical activity, and increased lipogenic metabolism. This indicates that people inheriting these genetic traits are prone to becoming obese regardless of their efforts to combat the condition. Therefore, a pharmacological agent that can correct this adiposity handicap and allow the physician to successfully treat obese patients in spite of their genetic inheritance is needed. Web site: http://www.delphion.com/details?pn=US05719266__ •
Anti-obesity proteins Inventor(s): Basinski; Margret B. (Indianapolis, IN), DiMarchi; Richard D. (Carmel, IN), Flora; David B. (Greenfield, IN), Heath, Jr. William F. (Fishers, IN), Hoffmann; James A. (Greenwood, IN), Schoner; Brigitte E. (Monrovia, IN), Shields; James E. (Noblesville, IN), Smiley; David L. (Greenfield, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,851,995 Date filed: August 4, 1997 Abstract: The present invention provides anti-obesity proteins, which when administered to a patient regulate fat tissue. Accordingly, such agents allow patients to overcome their obesity handicap and live normal lives with much reduced risk for type II diabetes, cardiovascular disease and cancer. Excerpt(s): The present invention is in the field of human medicine, particularly in the treatment of obesity and disorders associated with obesity. Most specifically the invention relates to anti-obesity proteins that when administered to a patient regulate fat tissue.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout the world. According to recent statistics, more than 25% of the United States population and 27% of the Canadian population are over weight. Kuczmarski, Amer. J. of Clin. Nut. 55: 495S-502S (1992); Reeder et. al., Can, Med. Ass. J., 23: 226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society.... Much of this obesity induced pathology can be attributed to the strong association with dyslipidemia, hypertension, and insulin resistance. Many studies have demonstrated that reduction in obesity by diet and exercise reduces these risk factors dramatically. Unfortunately these treatments are largely unsuccessful with a failure rate reaching 95%. This failure may be due to the fact
264 Obesity
that the condition is strongly associated with genetically inherited factors that contribute to increased appetite, preference for highly caloric foods, reduced physical activity, and increased lipogenic metabolism. This indicates that people inheriting these genetic traits are prone to becoming obese regardless of their efforts to combat the condition. Therefore, a new pharmacological agent that can correct this adiposity handicap and allow the physician to successfully treat obese patients in spite of their genetic inheritance is needed. Web site: http://www.delphion.com/details?pn=US05851995__ •
Apparatus and method for neuromodulation therapy for obesity and compulsive eating disorders using an implantable lead-receiver and an external stimulator Inventor(s): Boveja; Birinder R. (P.O. Box 210095, Milwaukee, WI 53221) Assignee(s): none reported Patent Number: 6,611,715 Date filed: April 19, 2001 Abstract: A system and method of neuromodulation adjunct (add-on) therapy for obesity and compulsive eating disorders, comprises an implantable lead-receiver and an external stimulator. Neuromodulation is performed using pulsed electrical stimulation. The external stimulator contains a power source, controlling circuitry, a primary coil, and predetermined programs which control the different levels of therapy. The primary coil of the external stimulator inductively transfers electrical signals to the lead-receiver, which is also in electrical contact with the left vagus nerve. The external stimulator emits electrical pulses to stimulate the vagus nerve according to a predetermined program. In a second mode of operation, an operator may manually override the predetermined sequence of stimulation. The predetermined programs have different levels of control, which is password protected. The external stimulator may also be equipped with a telecommunications module to control the predetermined programs remotely. Excerpt(s): This invention relates generally to medical device used for adjunct (add-on) treatment for obesity, more specifically a medical device used for adjunct (add-on) therapy for obesity and compulsive eating disorders with electrical stimulation neuromodulation using an implanted lead-receiver and an external stimulator.... Obesity results from excessive accumulation of fat in the body. It is caused by ingestion of greater amounts of food than can be used by the body for energy. The excess food, whether fats, carbohydrates, or proteins, is then stored almost entirely as fat in the adipose tissue, to be used later for energy. There can be various causes of obesity including, psychogenic, neurogenic, genetic, and other metabolic related factors. Treatment of obesity depends on decreasing energy input below energy expenditure. Treatment has included among other things various drugs, starvation and even stapling or surgical resection of a portion of the stomach.... Observations on the profound effect of electrical stimulation of the vagus nerve on central nervous system (CNS) activity extends back to the 1930's. In 1988 it was reported in the American Journal of Physiology, that the afferent vagal fibers from the stomach wall increased their firing rate when the stomach was filled. Accordingly, extra-physiologic electrical stimulation of the vagus nerve, from just above the stomach level, should produce appetite supression by causing the patient to experience satiety. Web site: http://www.delphion.com/details?pn=US06611715__
Patents 265
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Aryl-substituted cyclobutylalkylamines for treating obesity Inventor(s): Martin; Keith Frank (Nottingham, GB), Heal; David John (Nottingham, GB) Assignee(s): Knoll Aktiengesesllschaft (Ludwigshafen, DE) Patent Number: 6,127,424 Date filed: April 27, 1998 Abstract: Use of aryl-substituted cyclobutylalkylamines and their pharmaceutically suitable salts for treating obesity and its accompanying disorders are disclosed. Excerpt(s): The invention relates to use of aryl-substituited cyclobutylalkylamines for treating obesity. DE 32 12 682 C2 discloses aryl-substituted cyclobutylalkylamines. The compounds disclosed therein are employed as antidepressants.... and their pharmaceutically suitable salts, for treating obesity and its accompanying disorders.... The compounds used according to the invention have the advantage of very good bioavailability and show a more favorable spectrum of side effects. Web site: http://www.delphion.com/details?pn=US06127424__
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Azaftig, a proteoglycan for monitoring cachexia and for control of obesity Inventor(s): Prasad; Chandan (New Orleans, LA), Figueroa, II; Julio E. (New Orleans, LA), Vijayagopal; Parakat (Kenner, LA) Assignee(s): Board of Supervisors of Louisiana State University and Agricultural and (Baton Rouge, LA) Patent Number: 6,274,550 Date filed: June 28, 1999 Abstract: A proteoglycan ("azaftig") with a molecular weight of approximately 24,000 Dalton has been isolated and partially characterized from the urine of cachectic cancer and non-cancer patients. Azaftig has been shown to bind to receptors on fat cell membranes, and to cause lipolysis. Azaftig does not bind to muscle cell membranes, or cause proteolysis in muscle tissue. Azaftig detection in urine or other body fluids will allow early identification of patients in which weight loss may become a problem. Azaftig may also aid fat loss in humans in which obesity is a threat to health. Excerpt(s): This invention pertains to the detection of a propensity for cachexia and to the control of obesity.... Cachexia is defined as significant weight loss. It occurs commonly in cancer patients and HIV-infected individuals, but can also be caused by hypercatabolism due to cardiac failure (especially, right-sided or biventricular failure), hepatic failure, renal failure, burns, inflammation (including sepsis), infection or tuberculosis. See R. B. Verdery, "Reversible and irreversible weight loss (cachexia) in the elderly," in Textbook of Internal Medicine, 2d Edition (V. T. DeVita et at. eds.), Ch. 523, pp. 2424-2425 (1992); K. I. Marton, "Approach to patient with unintentional weight loss," in Textbook of Internal Medicine, 2d Edition (V. T. DeVita et al. eds.), Ch. 444, pp. 21132115 (1992); R. M. Jordan et al., "Weight loss," in Internal Medicine, 4th Edition (J. H. Stein ed.), Ch. 152, pp. 1260-1262 (1994); C. P. Artz et al., "Burns: Including cold, chemical, and electrical injuries," in Textbook of Surgery, 11th Edition (D. C. Sabiston, Jr. ed.), Ch. 15, pp. 295-322 (1977); E. Braunwald, "Heart Failure," in Harrison's Principles of Internal Medicine, 13th Edition (K. J. Isselbacher ed.), Ch. 195, pp. 998-1009 (1994); and D. W. Foster, "Gain and loss in weight," in Harrison's Principles of Internal Medicine, 13th Edition (K. J. Isselbacher ed.), Ch. 40, pp. 221-223 (1994). Over 50% of cancer and
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HIV-infected patients experience an unintended weight loss of greater than 10% of their baseline weight. Moreover, this weight loss is associated with an increase in morbidity and mortality. Many cachectic patients manifest multiple physiological problems involving the immune system, muscular system, and hepatic function that can be directly related to loss of body weight or wasting. Therefore, understanding the mechanisms of cachexia in patients can lead to better treatment and consequently can have a substantial impact on the quality of life and survival of many cancer and HIV/AIDS patients. See G. O. Coodley et al., "The HIV Wasting Syndrome: a Review," Journal of Acquired Immune Deficiency Syndromes, vol. 7, pp. 681-694 (1994); L. M. Hecker et al., "Malnutrition in patients with AIDS," Nutrition Reviews, vol. 48, pp. 393401 (1990); N. M. Graham et al., "Clinical factors associated with weight loss related to infection with Human Immunodeficiency Virus Type 1 in the multicenter AIDS cohort study," American Journal of Epidemiology, vol. 137, pp. 439-46 (1993); and K. A. Nelson et al., "The cancer anorexia-cachexia syndrome," Journal of Clinical Oncology, vol. 12, pp. 213-25 (1994).... Despite the prevalence of weight loss in cancer patients, the mechanisms underlying the weight loss are unknown. Current explanations for cancer or AIDS-associated weight loss are divided into two general categories--(1) mechanisms that decrease food intake (anorexia); and (2) mechanisms that increase energy expenditure through altered or increased metabolism. Hecker et al., 1990. Any mismatch between energy intake and expenditure will result in a change in weight. Web site: http://www.delphion.com/details?pn=US06274550__ •
Combination anorexiant drug therapy for obesity using phentermine and an SSRI drug Inventor(s): Anchors; J. Michael (16220 Frederick Rd. Suite 210, Gaithersburg, MD 20877) Assignee(s): none reported Patent Number: 5,795,895 Date filed: June 13, 1997 Abstract: This is a new therapy and method used to treat moderate and severe exogenous obesity by combining generic phentermine with an SSRI (selective serotonin reuptake inhibitor) drug in specific doses for a brief or even a long duration, 12 months or more. The preferred drugs for the combination are fluoxetine hydrochloride(Prozac), sertraline (Zoloft), fluvoxamine maleate (Luvox) and trazodone hydrochloride (Desyrel). Excerpt(s): Abenhaim L, Moride Y, Brenot F, et al. Appetite-suppressant drugs and the risk of primary pulmonary hypertension. N Engl J Med. 1996;335:609-616.... Anchors M. Fluoxetine Is a Safer Alternative to Fenfluramine in the Medical Treatment of Obesity. Arch Int Med. 1997;157:1270.... Anchors M. Better Than Phen-Fen PRIMA Publishing, Sacramento Calif. 1997, 250 pages. Web site: http://www.delphion.com/details?pn=US05795895__
Patents 267
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Combination therapy for the treatment of diabetes and obesity Inventor(s): Smith; Roy G. (Westfield, NJ), Cascieri; Margaret A. (East Windsor, NJ), MacIntyre; Euan (Scotch Plains, NJ), MacNeil; Douglas J. (Westfield, NJ), Menke; John G. (Morganville, NJ) Assignee(s): Merck & Co., Inc. (Rahway, NJ) Patent Number: 5,908,830 Date filed: October 30, 1997 Abstract: The combination of a metabolic rate modifying agent (e.g., a.beta..sub.3 adrenergic receptor agonist) and a feeding behavior modifying agent (e.g., a NPY5 antagonist) is useful in the treatment of obesity and diabetes, either as compounds, pharmaceutically acceptable salts, pharmaceutical composition ingredients. Methods of treating obesity and diabetes are also described. Excerpt(s): The present invention provides a combination useful in the treatment of obesity and diabetes, either as compounds, pharmaceutically acceptable salts or pharmaceutical composition ingredients. Methods of treating obesity and diabetes are also disclosed. More particularly, the combination of the present invention comprises a metabolic rate modifying agent and a feeding behavior modifying agent; and the pharmaceutically acceptable salts and esters thereof.... Obesity, which can be defined as a body weight more than 20% above the ideal body weight, is a major health concern in Western societies, since it is accompanied by numerous complications such as hypertension, non-insulin dependent diabetes mellitus and arteriosclerosis, which in turn cause heart disease, stroke and premature death. Obesity is the result of a positive energy balance, as a consequence of increased ratio of caloric intake to energy expenditure. The molecular factors regulating food intake and body weight balance are incompletely understood. ›B. Staels et al., J. Biol. Chem. 270(27), 15958 (1995); F. Lonnquist et al., Nature Medicine 1(9), 950 (1995)!. Although the genetic and/or environmental factors leading to obesity are poorly understood, several genetic factors have recently been identified.... Early developments in this area produced compounds with greater agonist activity for the stimulation of lipolysis (.beta..sub.3 activity) than for stimulation of atrial rate (.beta..sub.1) and tracheal relaxation (.beta..sub.2). These early developments disclosed in Ainsworth et al., U.S. Pat. Nos. 4,478,849 and 4,396,627, were derivatives of phenylethanolamines. Web site: http://www.delphion.com/details?pn=US05908830__
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Compositions and methods, for the treatment of body weight disorders, including obesity Inventor(s): Tartaglia; Louis Anthony (Waterstown, MA) Assignee(s): Millennium Pharmaceuticals, Inc. (Cambridge, MA) Patent Number: 5,741,666 Date filed: August 23, 1994 Abstract: The present invention relates to methods and compositions for the treatment of body weight disorders, including, but not limited to, obesity. Specifically, the present invention identifies and describes genes which are differentially expressed in body weight disorder states, relative to their expression in normal, or non-body weight disorder states, and/or in response to manipulations relevant to appetite and/or weight
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regulation. Further, the present invention identifies and describes genes via the ability of their gene products to interact with gene products involved in body weight disorders and/or appetite and/or body weight regulation. Still further, the present invention provides methods for the identification and therapeutic use of compounds as treatments of body weight disorders. Additionally, the present invention describes methods for the diagnostic evaluation and prognosis of various body weight disorders, and for the identification of subjects exhibiting a predisposition to such conditions. Excerpt(s): The present invention relates to methods and compositions for the treatment of body weight disorders, including, but not limited to, obesity. Specifically, the present invention identifies and describes genes which are differentially expressed in body weight disorder states, relative to their expression in normal, or non-body weight disorder states, and also identifies genes which are differentially expressed in response to manipulations relevant to appetite and/or weight regulation. Further, the present invention identifies and describes genes via the ability of their gene products to interact with gene products involved in body weight disorders and/or to interact with gene products which are relevant to appetite and/or body weight regulation. Still further, the present invention provides methods for the identification and therapeutic use of compounds as treatments of body weight disorders. Additionally, the present invention describes methods for the diagnostic evaluation and prognosis of various body weight disorders, and for the identification of subjects exhibiting a predisposition to such conditions.... Body weight disorders, including eating disorders, represent major health problems in all industrialized countries. Obesity, the most prevalent of eating disorders, for example, is the most important nutritional disorder in the western world, with estimates of its prevalence ranging from 30% to 50% within the middle-aged population. Other body weight disorders, such as anorexia nervosa and bulimia nervosa which together affect approximately 0.2% of the female population of the western world, also pose serious health threats. Further, such disorders as anorexia and cachexia (wasting) are also prominent features of other diseases such as cancer, cystic fibrosis, and AIDS.... Obesity, defined as an excess of body fat relative to lean body mass, also contributes to other diseases. For example, this disorder is responsible for increased incidences of diseases such as coronary artery disease, stroke, and diabetes. Obesity is not merely a behavioral problem, i.e., the result of voluntary hyperphagia. Rather, the differential body composition observed between obese and normal subjects results from differences in both metabolism and neurologic/metabolic interactions. These differences seem to be, to some extent, due to differences in gene expression, and/or level of gene products or activity. The nature, however, of the genetic factors which control body composition are unknown, and attempts to identify molecules involved in such control have generally been empiric and the parameters of body composition and/or substrate flux are monitored have not yet been identified (Friedman, J. M. et al., 1991, Mammalian Gene 1:130-144). Web site: http://www.delphion.com/details?pn=US05741666__ •
Compositions containing compounds with adrenergic activity and vegetable extracts of Crataegus and gingko biloba for the treatment of overweight and obesity Inventor(s): Stankov; Bojidar M. (Milan, IT) Assignee(s): Ambros Pharma S.R.L. (Milan, IT) Patent Number: 6,447,818 Date filed: October 10, 2000
Patents 269
Abstract: Compositions containing compounds with adrenergic activity and an extract of Crataegus standardized in flavonoids, combined with an extract of Gingko biloba standardized in flavonglucosides in appropriate weight ratios are suitable for pharmaceutical administration or as food supplements for the treatment of weight loss and obesity in humans. The formulations are appropriate for the administration of the active ingredients in a form that increases patient compliance and the efficacy of the therapeutic or dietary intervention, but reduces the untoward effects of the compounds with adrenergic activity. Excerpt(s): This invention relates to compositions for the treatment of overweight and obesity.... The management of body weight is a complex phenomenon that generally varies according to nutritive equilibrium. The amount of energy introduced with the intake of food and that used by the organism for the maintenance of vital functions (metabolism, respiration, thermoregulation, movement etc.) determines the energetic balance, which, if positive for long-term periods, inevitably leads to increased body weight and obesity.... a) The loss of weight, obtained by a low-calorie diet, gives rise, as a defense mechanism, to an exacerbated attraction for food, especially carbohydrates which are transformed into fat by the organism. Subsequently, the temporary weight loss is replaced by a fast and often uncontrolled weight increase. Web site: http://www.delphion.com/details?pn=US06447818__ •
Compositions for the treatment of body weight disorders including obesity Inventor(s): Tartaglia; Louis Anthony (Watertown, MA) Assignee(s): Millennium Pharmaceuticals, Inc. (Cambridge, MA) Patent Number: 6,057,109 Date filed: December 14, 1998 Abstract: The present invention relates to methods and compositions for the treatment of body weight disorders, including, but not limited to, obesity. Specifically, the present invention identifies and describes genes which are differentially expressed in body weight disorder states, relative to their expression in normal, or non-body weight disorder states, and/or in response to manipulations relevant to appetite and/or weight regulation. Further, the present invention identifies and describes genes via the ability of their gene products to interact with gene products involved in body weight disorders and/or appetite and/or body weight regulation. Still further, the present invention provides methods for the identification and therapeutic use of compounds as treatments of body weight disorders. Additionally, the present invention describes methods for the diagnostic evaluation and prognosis of various body weight disorders, and for the identification of subjects exhibiting a predisposition to such conditions. Excerpt(s): The present invention relates to methods and compositions for the modulation of processes related to mammalian body weight regulation, including treatment of body weight disorders such as obesity and cachexia, and modulation of thermogenesis. Specifically, the present invention identifies and describes genes which are differentially expressed in body weight disorder states, relative to their expression in normal, or non-body weight disorder states, and also identifies genes which are differentially expressed in response to manipulations relevant to appetite and/or weight regulation. Further, the present invention identifies and describes genes via the ability of their gene products to interact with gene products involved in body weight disorders and/or to interact with gene products which are relevant to appetite and/or body
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weight regulation. Still further, the present invention provides methods for the identification and therapeutic use of compounds as treatments of body weight-related processes, including body weight disorders such as obesity and cachexia. Additionally, the present invention describes methods for the diagnostic evaluation and prognosis of various body weight disorders, and for the identification of subjects exhibiting a predisposition to such conditions.... The regulation of body fat in mammals is a complex process involving the regulation of not only appetite but also energy expenditure. An important component of energy expenditure is non-shivering thermogenesis (NST). In rodents, the majority of NST appears to occur in brown adipose tissue (BAT) via the uncoupling protein (UCP) (Cannon & Nedergaard, 1985, Essays in Biochem. 20:110-165; Himms-Hagen J., 1989, Prog. Lipid Res. 28:67-115). UCP is a proton channel located exclusively in the inner mitochondrial membrane of adipocytes of the BAT (Nicholls & Locke, 1984, Physiol. Rev. 64:1-64). By allowing protons to equilibrate across the inner mitochondrial membrane, UCP uncouples oxidative phosphorylation from ATP production and thus converts stored energy into heat rather than work (Klingenberg M., 1990, Trends Biochem. Sci. 15:108-112; Klaus S. et al., 1991, Int. J. Biochem. 23:791-801). UCP-mediated uncoupling is not only capable of increasing body temperature in coldacclimatized rodents and hibernating animals, but can also dissipate surplus caloric energy (Rothwell & Stock, 1986, In Brown Adipose Tissue. Trayhurn P., Nicholls D. G., Eds., London, Arnold, p. 269-298; Spiegelman & Flier, 1996, Cell 87:377-389; Hamann & Flier, 1996, Endocrinology 137:2129). A number of studies have now implicated UCP and brown adipose tissue as important regulators of body weight in rodents (Hamann & Flier, 1996, Endocrinology 137:2129; Lowell B. B. et al., 1993, Nature 366:740-742; Kopecky J. et al., 1995, J. Clin. Invest. 96:2914-2923; Cummings D. E. et al., 1996, Nature 382:622-626).... In humans, body weight homeostasis is poorly understood, but is also thought to involve regulated thermogenesis (Rothwell & Stock, 1981, Annu. Rev. Nutr. 1:235-56; Segal K. R. et al., 1992, J. Clin. Invest. 89:824-833; Jensen M. D. et al., 1995, Am. J. Physiol. 268:E433-438). However, the importance of the UCP in adult humans is questionable due to the low levels of BAT and consequently the low levels of UCP expression (Huttunen P. et al., 1981, Eur. J. Appl. Physiol. 46:339-345; Cunningham S. et al., 1985, Clin. Sci. 69:343-348; Schulz L., 1987, J. Am. Diet Assoc. 87:761-764; Santos G. C. et al., 1992, Arch. Pathol. Lab Med. 116:1152-1154). Web site: http://www.delphion.com/details?pn=US06057109__ •
Compositions for the treatment of body weight disorders, including obesity Inventor(s): Tartaglia; Louis Anthony (Watertown, MA) Assignee(s): Millennium Pharmaceuticals, Inc. (Cambridge, MA) Patent Number: 6,121,017 Date filed: October 8, 1997 Abstract: The present invention relates to methods and compositions for the treatment of body weight disorders, including, but not limited to, obesity. Specifically, the present invention identifies and describes genes which are differentially expressed in body weight disorder states, relative to their expression in normal, or non-body weight disorder states, and/or in response to manipulations relevant to appetite and/or weight regulation. Further, the present invention identifies and describes genes via the ability of their gene products to interact with gene products involved in body weight disorders and/or appetite and/or body weight regulation. Still further, the present invention provides methods for the identification and therapeutic use of compounds as treatments
Patents 271
of body weight disorders. Additionally, the present invention describes methods for the diagnostic evaluation and prognosis of various body weight disorders, and for the identification of subjects exhibiting a predisposition to such conditions. Excerpt(s): The present invention relates to methods and compositions for the modulation of processes related to mammalian body weight regulation, including treatment of body weight disorders such as obesity and cachexia, and modulation of thermogenesis. Specifically, the present invention identifies and describes genes which are differentially expressed in body weight disorder states, relative to their expression in normal, or non-body weight disorder states, and also identifies genes which are differentially expressed in response to manipulations relevant to appetite and/or weight regulation. Further, the present invention identifies and describes genes via the ability of their gene products to interact with gene products involved in body weight disorders and/or to interact with gene products which are relevant to appetite and/or body weight regulation. Still further, the present invention provides methods for the identification and therapeutic use of compounds as treatments of body weight-related processes, including body weight disorders such as obesity and cachexia. Additionally, the present invention describes methods for the diagnostic evaluation and prognosis of various body weight disorders, and for the identification of subjects exhibiting a predisposition to such conditions.... The regulation of body fat in mammals is a complex process involving the regulation of not only appetite but also energy expenditure. An important component of energy expenditure is non-shivering thermogenesis (NST). In rodents, the majority of NST appears to occur in brown adipose tissue (BAT) via the uncoupling protein (UCP) (Cannon & Nedergaard, 1985, Essays in Biochem. 20:110-165; Himms-Hagen J., 1989, Prog. Lipid Res. 28:67-115). UCP is a proton channel located exclusively in the inner mitochondrial membrane of adipocytes of the BAT (Nicholls & Locke, 1984, Physiol. Rev. 64:1-64). By allowing protons to equilibrate across the inner mitochondrial membrane, UCP uncouples oxidative phosphorylation from ATP production and thus converts stored energy into heat rather than work (Klingenberg M., 1990, Trends Biochem. Sci. 15:108-112; Klaus S. et al., 1991, Int. J. Biochem. 23:791-801). UCP-mediated uncoupling is not only capable of increasing body temperature in coldacclimatized rodents and hibernating animals, but can also dissipate surplus caloric energy (Rothwell & Stock, 1986, In Brown Adipose Tissue. Trayhurn P., Nicholls D. G., Eds., London, Arnold, p. 269-298; Spiegelman & Flier, 1996, Cell 87:377-389; Hamann & Flier, 1996, Endocrinology 137:2129). A number of studies have now implicated UCP and brown adipose tissue as important regulators of body weight in rodents (Hamann & Flier, 1996, Endocrinology 137:2129; Lowell B. B. et al., 1993, Nature 366:740-742; Kopecky J. et al., 1995, J. Clin. Invest. 96:2914-2923; Cummings D. E. et al., 1996, Nature 382:622-626).... In humans, body weight homeostasis is poorly understood, but is also thought to involve regulated thermogenesis (Rothwell & Stock, 1981, Annu. Rev. Nutr. 1:235-56; Segal K. R. et al., 1992, J. Clin. Invest. 89:824-83.3; Jensen M. D. et al., 1995, Am. J. Physiol. 268:E433-438). However, the importance of the UCP in adult humans is questionable due to the low levels of BAT and consequently the low levels of UCP expression (Huttunen P. et al., 1981, Eur. J. Appl. Physiol. 46:339-345; Cunningham S. et al., 1985, Clin. Sci. 69:343-348; Schulz L., 1987, J. Am. Diet Assoc. 87:761-764; Santos G. C. et al., 1992, Arch. Pathol. Lab Med. 116:1152-1154). Web site: http://www.delphion.com/details?pn=US06121017__
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Compounds for the treatment of obesity Inventor(s): Elliott; Richard L. (East Lyme, CT), Hank; Richard F. (No. Stonington, CT), Hammond; Marlys (Salem, CT) Assignee(s): Pfizer Inc. (New York, NY) Patent Number: 6,514,966 Date filed: January 4, 2001 Abstract: NPY antagonists, methods of using such NPY antagonists and pharmaceutical compositions containing such NPY antagonists. The NPY antagonists are useful for the treatment of NPY mediated disease/conditions including obesity. Excerpt(s): This invention relates to NPY antagonists, particularly NPY-5 antagonists, and pharmaceutical compositions containing such antagonists and the use of such antagonists to treat, for example, obesity, feeding disorders, as well as other NPY mediated diseases/conditions in mammals, including humans, dogs, cats and horses.... Neuropeptide Y (NPY), a 36 amino acid peptide neurotransmitter, is a member of the pancreatic polypeptide class of neurotransmitters/neurohormones which has been shown to be present in both the periphery and central nervous system. NPY is one of the most potent orexogenic agents known and has been shown to play a major role in the regulation of food intake in animals. At least 6 NPY receptor subclasses have been identified and cloned to date, with two of these subclasses, NPY-1 and NPY-5, thought to be the most important receptor subtypes modulating food intake and energy expenditure.... Various animal studies have shown that activation of neuropeptide Y receptors is related to stimulation of consummatory behavior, Food and Morley Peptides, 10:963-966 (1989), Leibowitz and Alexander, Peptides, 12:1251-1260 (1991), and Stanley et al. Peptides, 13:581-587 (1992), and to vasoconstriction, Wahlestedt et al. Regul. Peptides, 13:307-318 (1986), McCauley and Westfall J. Pharmacol. Exp. Ther. 261:863-868 (1992), and Grundemar et al. Br. J. Pharmacol. 105:45-50 (1992). Web site: http://www.delphion.com/details?pn=US06514966__
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Comprehensive pharmacologic therapy for treatment of obesity Inventor(s): Hinz; Martin C. (1150 - 88th Ave. West, Duluth, MN 55808) Assignee(s): none reported Patent Number: 6,403,657 Date filed: October 5, 1999 Abstract: The comprehensive pharmacologic therapy for treatment of obesity is a procedure which involves the administration of a desired therapeutic range of Diethylpropion and/or Phentermine in combination with a SSRI medication and nutritional supplementation for brief and long durations which may be 12 months or more. The preferred procedure involves the administration of drugs in combination which are identified as: Citalopram (Celexa) and Phentermine; Citalopram (Celexa) and Diethylpropion; Citalopram (Celexa), Phentermine, and Diethylpropion. In addition nutritional supplementation such as a multivitamin, 5-Hydroxytryptophan, vitamin B6, vitamin C, Tyrosine, Calcium, and Lysine may be used to enhance the performance of the weight loss treatment program. Excerpt(s): Safer than Phen-Fen (copyright 1997), Written by Michael Anchors, MD Ph.D. Pulmonary Vascular Disease, Medical Clinics of North America Nov. 6, 1997,
Patents 273
Written by Donald Heath, MD Ph.D.... The "Phen-pro" Diet Drug Combination Is Not Associated with Valvular Heart Disease. Jan. 12, 1998 Archives of Internal Medicine. Written by: Len Griffen, MD and Michael Anchors, MD Ph.D.... Fluoxetine (Prozac) and Other Drugs for Treatment of Obesity, Nov. 25, 1994 The Medical Letter. Web site: http://www.delphion.com/details?pn=US06403657__ •
Comprehensive pharmacologic therapy for treatment of obesity Inventor(s): Hinz; Martin C. (1150 - 88th Ave. W., Duluth, MN 55808) Assignee(s): none reported Patent Number: 6,548,551 Date filed: August 30, 2001 Abstract: The comprehensive pharmacologic therapy for treatment of obesity is a procedure which involves the administration of a desired therapeutic range of Diethylpropion and/or Phentermine in combination with a SSRI medication and nutritional supplementation for brief and long durations which may be 12 months or more. The preferred procedure involves the administration of drugs in combination which are identified as: Citalopram (Celexa) and Phentermine; Citalopram (Celexa) and Diethylpropion; Citalopram (Celexa), Phentermine, and Diethylpropion. In addition nutritional supplementation such as a multivitamin, 5-Hydroxytryptophan, vitamin B6, vitamin C, Tyrosine, Calcium, and Lysine may be used to enhance the performance of the weight loss treatment program. Excerpt(s): The medications stop working during therapy where at least 40% to 50% of patients quit losing weight (plateau) on an average of 3.3 months into therapy; and 5% to 8% of patients who receive drug therapy for weight problems experience the complication where the medications fail to assist in appetite suppression where the patient therefore does not lose significant weight.... In the past long term treatment, defined as treatment longer than 3 months to many years, with drugs has been a problem due to long term safety issues including, medication intolerability by the patient, medication side effects and most important ineffectiveness of the drugs or the cessation of benefit of the drugs which in turn causes the patient to fall out of appetite suppression and terminate weight loss.... A weight loss procedure using SSRI medication is disclosed in U.S. Pat. No. 5,795,895. The potential for patients to obtain goal weight loss under the process of U.S. Pat. No. 5,795,895 is low, and the failure of the drugs to provide a desired level of performance is at the heart of the problem. Web site: http://www.delphion.com/details?pn=US06548551__
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Creatine analogues for treatment of obesity Inventor(s): Kaddurah-Daouk; Rima (Belmont, MA) Assignee(s): Avicena Group, Inc. (Cambridge, MA) Patent Number: 5,998,457 Date filed: October 25, 1996 Abstract: The present invention relates to the use of creatine compounds for treating or preventing a metabolic disorder related to body weight control such as obesity, and it's associated diseases in a patient experiencing said disorder. The creatine compounds
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which can be used in the present method include (1) analogues of creatine which can act as substrates or substrate analogues for the enzyme creatine kinase; (2) compounds which can act as inhibitors of creatine kinase; (3) compounds which can modulate the creatine transporter (4) N-phosphocreatine analogues bearing transferable or nontransferable moieties which mimic the N-phosphoryl group. (5) compounds which modify the association of creatine kinase with other cellular components. Excerpt(s): The present invention provides for new use for creatine compounds (creatine analogues and compounds which modulate one or more of the structural or functional components of the creatine kinase/creatine phosphate system) as therapeutic agents. More particularly, the present invention provides a method of treating or preventing certain metabolic disorders of human and animal metabolism relating to aberrant body weight regulation as manifested in obesity and it's related disorders.... There are several metabolic diseases of human and animal metabolism, eg., obesity and severe weight loss that relate to energy imbalance--where caloric intake versus energy expenditure--is imbalanced. Obesity, which can be defined as a body weight more than 20% in excess of the ideal body weight, is a major health problem in Western affluent societies. It is associated with an increased risk for cardiovascular disease, hypertension, diabetes, hyperlipidaemia and an increased mortality rate. Obesity is the result of a positive energy balance, as a consequence of an increased ratio of caloric intake to energy expenditure. The molecular factors regulating food intake and body weight balance are incompletely understood. Five single-gene mutations resulting in obesity have been described in mice, implicating genetic factors in the etiology of obesity. (Friedman, J. M., and Leibel, R. L. Cell 69: 217-220 (1990)). In the ob mouse a single gene mutation, obese, results in profound obesity, which is accompanied by diabetes (Friedman, J. M., et. al. Genomics 11: 1054-1062 (1991)). Cross-circulation experiments have suggested that the ob mice are deficient of a blood-borne factor regulating nutrient intake and energy metabolism (Coleman, D. L. Diabetologia 14: 141-148 (1978)). Using positional cloning technologies, the mouse ob gene, and subsequently its human homologue, have been recently cloned (Zhang, Y., et. al., Nature 372: 425-432 (1994)). Daily intraperitoneal injections of either mouse or human recombinant OB protein reduced the body weight of obese mice ob/ob by 30% after 2 weeks of injection. The protein reduced food intake and increased energy expenditure in the ob/ob mice (Halaas et. al., Science 269: 543-546 (1995)).... Cachexia on the other hand is characterized by severe weight loss and imbalanced energy expenditure, examples being patients with cancer or HIV infections. Web site: http://www.delphion.com/details?pn=US05998457__ •
Detection of dinucleotide repeat polymorphism in exon 18 of LDL receptor gene for determining predisposition to obesity Inventor(s): Griffiths; Lynette Robyn (Burleigh Heads, AU) Assignee(s): Griffith University (Queensland, AU) Patent Number: 5,688,647 Date filed: December 8, 1995 Abstract: A method detects whether an individual is predisposed to obesity. The method includes the steps of (i) obtaining a sample containing human genomic DNA from the individual; (ii) detecting whether the genomic DNA in the sample has a 7 AT tandem repeat in exon 18 of the low density lipoprotein receptor gene on one or both chromosomes; and (iii) correlating the absence of the 7 AT tandem repeat on the chromosome or chromosomes with a predisposition to obesity in the individual.
Patents 275
Excerpt(s): This invention relates to a method for detecting individuals who are predisposed to obesity. This invention further relates to genetic techniques for detecting a low density lipoprotein receptor gene (LDLR) microsatellite polymorphism.... Obesity is a common nutritional disorder that affects approximately 30% of adults in the Western world. Obesity is a multifactorial condition in which both environmental and genetic factors are important determinants in susceptibility to body fat accumulation (Despres et al., 1992, Molecular and Cellular Biochemistry, 113, 151-169). Adoption studies have implicated genetic control, rather than childhood environment, as the main influence on the development of adult obesity (Sorensen, T. I. & Stunkard, A. J., 1993, Acta Psychiatrica Scandinavica, 370, 67-72). Obesity, essential hypertension, impaired glucose tolerance, non-insulin-dependent diabetes mellitus and dyslipidaemia tend to cluster in families. Collectively, these abnormalities constitute the multiple metabolic syndrome or Syndrome X, which is associated with cardiovascular disease (Kesaniemi et. al., 1992, Annals of Medicine (Helsinki), 24, 461-464).... Lipida and cholesterol ingested in an individuals' diet are essential for body maintenance. These molecules are transported through the body in lipoproteins. There are four types of lipoproteins each responsible for transporting varying amounts of lipid and cholesterol. It has been shown that lipoprotein concentration in the blood is proportional to abdominal fat disposition in obese individuals (Nishina et al., 1992, Proceeding of the National Academy of Science U.S.A., 89, 708-712). The low density lipoprotein (LDL) receptor is responsible for regulating LDL levels and hence cholesterol and plasma lipids in the blood. The gene encoding the LDL receptor (LDLR) is located at chromosome 19 position p13.2. Web site: http://www.delphion.com/details?pn=US05688647__ •
Dietary system high in oil intake for the treatment of obesity and for the lowering of saturated fats Inventor(s): McLean; Linsey (4267 S. State Rd., Davison, MI 48423) Assignee(s): none reported Patent Number: 5,484,623 Date filed: January 10, 1994 Abstract: A dietary system for the treatment of obesity and for the lowering of saturated fats in the blood. The system includes a diet that restricts the patient to the intake of certain foods in certain amounts and combines this intake with specific supplements. The prescribed foods comprise those low in saturated fats and carbohydrates, those having moderate amounts of proteins, and oils high in monounsaturates and certain fatty acids such as olive oil and canola oil. The supplements include prescribed amounts of vitamins and minerals. By providing the patient with a diet high in essential fatty acids, the glucagon-driven pathway of the patient is stimulated and less fat is stored by the body. In addition, more body fat is catalyzed for the production of energy for use by the body. Excerpt(s): The present invention relates to diets for humans. More particularly, the present invention relates to a dietary system for the treatment of obesity and for the lowering of saturated fats in the blood. The system includes a diet that restricts the patient to the intake of certain foods in certain amounts and combines this intake with specific supplements. The prescribed foods comprise those that are low in saturated fats and carbohydrates, those having moderate amounts of proteins, and oils high in monounsaturates and certain fatty acids. The supplements include selected vitamins and minerals.... The patient presenting with obesity is known to require a modified diet
276 Obesity
to effect weight reduction. This same patient also typically presents with a high concentration of saturated fat in the blood.... Whatever the underlying psychological or physiological basis the common belief is that for most cases of obesity overeating or eating the "wrong" foods are the main avenues to weight gain. Accordingly, conventional approaches to resolving obesity include both behavior modification and diet modification. The former approach requires significant psychological adjustment with varying results and the latter is much more common and includes a broad array of diets with many plans producing instantaneous results but being unworkable and even counterproductive over time. Web site: http://www.delphion.com/details?pn=US05484623__ •
Endoscopic stomach insert for treating obesity and method for use Inventor(s): Ellias; Yakub A. (2272 Renshaw Ave., Dayton, OH 45439) Assignee(s): none reported Patent Number: 5,868,141 Date filed: May 14, 1997 Abstract: An endoscopic stomach insert for treating obesity in humans by reducing the desire for eating, comprising a base-sized for passing through a human mouth and esophagus; a plurality of flexible blades coupled at one end thereof to the base and circumferentially arranged about the base central axis, where the blades are biased to extend substantially radially outward and downward from the base; and a retainer for releasably coupling the distal portions of the blades within close proximity to each other about the central axis of the base. The insert is thus adapted to be passed through the mouth and esophagus and into a human stomach, and upon releasing the retainer within the stomach, the blades are biased to flare outwardly into the form of a domeshaped cage, applying pressure to the stomach, and thus causing a sensation of fullness within the stomach and reducing the desire for eating. Excerpt(s): The present invention is an apparatus and method for treating obesity in humans, and particularly, a device for endoscopic insertion into the stomach of a human to cause a reduced desire for eating.... Obesity is arguably one of the most serious health problems in the United States, afflicting over 60 million people of all ages. Apart from physical and psychological effects, especially on the younger population, obesity predisposes to serious diseases such as coronary artery disease, hyperlipidemia, hypertension, and diabetes mellitus. The costs to the health system is a staggering $39 billion per year.... Weight reduction can be achieved either by increasing caloric expenditure through exercise and/or by reducing caloric intake. Reduced caloric intake can be achieved in a number of ways; surgical procedures to reduce the stomach capacity or increase the food transit time in the gastrointestinal tract, appetite suppressants like amphetamines or noradrenargic compounds, or other methods such as introducing balloons into the stomach. Surgical procedures to reduce the stomach capacity or increase food transit time in the gastrointestinal tract carry with them the risk of surgery as well as post-operative complications. The appetite suppressants act on the central nervous system and are associated with considerable morbidity and side effects. Balloon inserts have several disadvantages, which include failure due to bursting or dislodging, intestinal obstruction (blockage of the intestinal lumen), and the requirement of complicated devices and/or procedures to secure the balloons within the stomach.
Patents 277
Web site: http://www.delphion.com/details?pn=US05868141__ •
Fatty analogues for the treatment of obesity, hypertension and fatty liver Inventor(s): Berge; Rolf (B.o slashed.nes, NO) Assignee(s): Thia Medica AS (Bergen, NO) Patent Number: 6,441,036 Date filed: January 27, 2001 Abstract: The present invention relates to novel fatty acid analogous of the general forumla I: CH.sub.3 --[CH.sub.2 ].sub.m --[x.sub.i --CH.sub.2 ].sub.n --COOR, as defined in the specification, which can be used for the treatment and/or prevention of obesity, fatty liver and hypertension. Further, the invention relates to a nutritional composition comprising such fatty acid analogues, and a method for reducing the total weight, or the amount of adipose tissue in an animal. The invention also relates to a method for improving the quality of product such as meat, milk and eggs. Excerpt(s): The present invention relates to novel fatty acid analogous which can be used for the treatment and/or prevention of obesity, fatty liver and hypertension. Further, the invention relates to a nutritional composition comprising such fatty acid analogues, and a method for reducing the total weight, or the amount of adipose tissue in an animal. The invention also relates to a method for improving the quality of product such as meat, milk and eggs.... Hyperlipidemia and obesity afflict an increasing proportion of the population in Western societies and are associated with the development of serious conditions such as atherosclerosis, hypertension, fatty liver and insulin resistance. These conditions may eventually lead to the clinical manifestations of coronary heart diseases (CD) and non-insulin dependent diabetes mellitus (NIDDM).... Treatment with modified fatty acids represent a new way to treat these diseases. Web site: http://www.delphion.com/details?pn=US06441036__
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Fatty-acid monoesters of estrogens for the treatment of obesity and/or overweight Inventor(s): Alemany; Maria (Barcelona, ES) Assignee(s): Laboratorios S.A.L.V.A.T., S.A. (Esplugues de Llobregat, ES) Patent Number: 5,798,348 Date filed: October 30, 1996 Abstract: The pharmaceutical and/or cosmetic compositions for treatment of obesity and/or overweight contain an effective amount of a fatty-acid monoester of an estrogen and a fatty acid wherein the estrogen is estrone, diethylstilbestrol, estriol, estradiol or ethinyl estradiol and the fatty acid is oleic, linoleic, linolenic, stearic, palmitic, palmitoleic or arachidonic acids. The fatty-acid monoesters mimic the function of estrone monooleate, as a signal that informs the brain of the size of fat tissue mass. In preferred pharmaceutical and/or cosmetic compositions for intravenous injection the monoester is incorporated in a lipidic suspension, prepared from lipoproteins or from liposome components, such as soy oil and egg phospholipids. When administered to rats with a 15% of total adipose tissue, they produce weight reduction of about 10%, by a new and unexpected mechanism. They are useful for the treatment of obesity and/or overweight in mammals, with the advantages of high efficacy and low toxicity. New
278 Obesity
substantially pure fatty-acid monoesters including diethylstilbestrol monooleate are also described.
estrone
monooleate
and
Excerpt(s): This invention refers to products, compositions and uses thereof, for therapeutic and/or cosmetic treatment of obesity and/or overweight in mammals.... Treatment of obesity and/or overweight is a therapeutic or cosmetic problem of major importance that does not have a satisfactory solution yet. Attempts to solve the problem by reducing food intake or by doing physical exercise, are well known. But also known are the difficulties, limitations and general lack of success of all these approaches. Apparently the sheer complexity of mechanisms involved in the control of body mass allow little room for external manipulation, thus limiting the possible damage to body reserves by increased thermogenic stimulation or diminished energy intake.... In the therapeutic fight against obesity and/or overweight considerable research has been focused on trying to find some signal that informs the brain of the size of fat tissue mass. It is believed that such information is required by the brain to promote either the accumulation of fat reserves or their burning by the thermogenic system, via the natural homeostatic mechanisms set to maintain the body mass stable. According to a recent discovery based on a mutation of a gene, one such signal could be a protein named leptin (cf. Y. Zhang et al., Nature 1994, vol. 372, pp. 425-32). From this discovery the invention of using leptin for the preparation of a medicament for treating obesity by injection could be derived. But, even if this approach proves to be useful in the future, it would be very expensive because leptin must be prepared by genetic engineering. Web site: http://www.delphion.com/details?pn=US05798348__ •
Indoline derivatives and method of treating obesity Inventor(s): Bentley; Jonathan Mark (Oakdene Court, 613 Reading Court, Winnersh, Wokingham RG41 5UA, GB), Davidson; James Edward Paul (Oakdene Court, 613 Reading Court, Winnersh, Wokingham RG41 5UA, GB), Mansell; Howard Langham (Oakdene Court, 613 Reading Court, Winnersh, Wokingham RG41 5UA, GB), Monck; Nathaniel Julius Thomas (Oakdene Court, 613 Reading Court, Winnersh, Wokingham RG41 5UA, GB) Assignee(s): none reported Patent Number: 6,479,534 Date filed: October 15, 2001 Abstract: The present invention relates to indoline derivatives. These compounds are especially useful for the prevention and treatment of disorders of the central nervous system; damage to the central nervous system; cardiovascular disorders; gastrointestinal disorders; diabetes, sleep apnea, and especially for the treatment and prevention of obesity. Excerpt(s): The present invention relates to indoline derivatives, to processes and intermediates for their preparation, to pharmaceutical compositions comprising them and to their medicinal use. The active compounds of the present invention are useful in treating obesity, diabetes and other disorders.... It has been recognised that obesity is a disease process influenced by environmental factors in which the traditional weight loss methods of dieting and exercise need to be supplemented by therapeutic products (S. Parker, "Obesity: Trends and Treatments", Scrip Reports, PJB Publications Ltd, 1996).... Whether someone is classified as overweight or obese is generally determined on the basis of their body mass index (BMI) which is calculated by dividing body weight (kg)
Patents 279
by height squared (m.sup.2). Thus, the units of BMI are kg/m.sup.2 and it is possible to calculate the BMI range associated with minimum mortality in each decade of life. Overweight is defined as a BMI in the range 25-30 kg/m.sup.2, and obesity as a BMI greater than 30 kg/m.sup.2. There are problems with this definition in that it does not take into account the proportion of body mass that is muscle in relation to fat (adipose tissue). To account for this, obesity can also be defined on the basis of body fat content: greater than 25% and 30% in males and females, respectively. Web site: http://www.delphion.com/details?pn=US06479534__ •
Inflatable gastric device for treating obesity Inventor(s): Berson; Daniel (199 Kings Highway, Congers, NY 10920) Assignee(s): none reported Patent Number: 4,246,893 Date filed: July 5, 1978 Abstract: Apparatus for treating extreme obesity comprising means for compressing the stomach and reducing its capacity and procedures employing said apparatus. Excerpt(s): This invention relates to procedures and apparatus for treating obesity in human patients.... In the past, rather drastic surgical procedures have been employed to treat morbidly or mortally obese patients, i.e., patients whose body weight is at least twice their appropriate weight. One set of surgical procedures induces a pathophysiologic abnormality of the gastrointestinal tract by gastric or jejunoileal bypass operations in which as much as 95% of the tract is surgically bypassed. These procedures result in a patient who is a metabolic cripple having surgically induced malabsorption, and are associated with long term complications often requiring additional surgical procedures. The jejunoileal bypass, for example, has been used extensively in this country and around the world. This procedure bypasses about 95% of the small bowel, leaving about 40 cm. of functioning jejunum and ileum. The physiologic effect of this is massive diarrhea and malabsorption of nutrients, leading to weight loss secondary to poor absorption of nutrients, as well as aversion to eating. The procedure is performed an estimated five thousand to twenty thousand times per year in the United States, but has been abandoned by many institutions, including the Cleveland Clinic, because of unacceptable operative mortality averaging 6% nationwide, as well as severe complications including wound infection and breakdown, progressive liver failure, hypocalcemia, calcium oxalate urinary calculi and bypass enteropathy. Mechanical problems such as intestinal obstruction and hernia formation are frequent.... Approximately 32% of the patients having jejunoileal bypass operations are rehospitalized within one year. These operations have also been associated with liver dysfunctions most likely caused by the preferential absorption of carbohydrates in the remaining small bowel, with resulting relative protein starvation. Web site: http://www.delphion.com/details?pn=US04246893__
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Inhibition of adipose tissue development and obesity Inventor(s): Serrero; Ginette (Lake Placid, NY) Assignee(s): W. Alton Jones Cell Science Center, Inc. (Lake Placid, NY) Patent Number: 5,723,115 Date filed: December 2, 1993 Abstract: Epidermal growth factor (EGF), which can act as a potent inhibitor of adipocyte differentiation in vitro, affects adipose tissue differentiation in vivo and can suppress obesity. Methods are provided for inhibiting the differentiation of adipocyte precursor cells, and for treating or preventing obesity, which comprise administering an effective amount of a composition capable of binding to and activating the EGF receptor, preferably epidermal EGF or a functional derivative thereof, TGF.alpha., an antibody specific for the EGF receptor or an anti-idiotypic antibody specific for an idiotope on an antibody specific for EGF. Also provided is a method for determining the susceptibility of a subject to obesity or determining the presence of obesity associated with an abnormality in EGF or EGF receptor, which comprises measuring EGF in a body fluid or the amount or activity of EGF receptor protein or mRNA in adipocyte precursors. Excerpt(s): The invention in the field of cell biology, physiology and medicine relates to methods for treating obesity and methods for determine susceptibility to obesity.... Obesity has been declared a public health hazard by the National Institutes of Health. To combat this health problem, both prophylactic and therapeutic approaches are necessary. For prophylactic purposes, it would be useful to be able to predict and measure a person's propensity or susceptibility to obesity For therapeutic purposes, a means for interfering with the development or differentiation of adipocytes (fat cells) would be of great benefit. Furthermore, as a broader preventative approach to obesity, the ability to limit the fat content of food mammals would be of great importance. None of these desired objectives has been achieved. Early-onset obesity cannot be efficiently controlled by a weight reduction program once the obesity is apparent. Therefore, a means for early detection of early-onset obesity is imperative for its prevention.... The identification of the hormones controlling adipocyte proliferation and differentiation is very important for understanding normal adipose tissue development and for designing approaches for controlling abnormal states of adipose tissue development such as obesity. Several adipogenic cell lines able to undergo differentiation in vitro into fully mature adipocytes have served as model systems for investigating differentiation at the cellular and molecular levels (1-3). Using these cell lines, several hormones and growth factors have been shown to have adipogenic (3-5) or anti-adipogenic activities (6-9). Web site: http://www.delphion.com/details?pn=US05723115__
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Lipolytic composition and method of treating obesity Inventor(s): Traunecker; Werner (Munster-Sarmsheim, DE), Frolke; Wilhelm (Ingelheim am Rhein, DE), Kreuzer; Heinrich (Gau-Algesheim, DE), Kollmer; Hans P. (Wackernheim, DE) Assignee(s): Boehringer Ingelheim KG (Ingelheim am Rhein, DE) Patent Number: 4,499,106 Date filed: May 20, 1983
Patents 281
Abstract: Lipolytic pharmaceutical composition containing 1-(4-hydroxy-3dimethylamino-sulfonamidophenyl)-1-hydroxy-2-(1-phenoxy-iso propylamino)ethane or a pharmaceutically acceptable acid addition salt thereof as the active ingredient, and a method of combatting obesity therewith. Excerpt(s): This invention relates to pharmaceutical compositions which contain as the active ingredient the compound 1-(4-hydroxy-3-dimethylamino-sulfonamidophenyl)-1hydroxy-2-(1-phenoxy-iso propylamino)ethane (Me 693), and to a method of treating both generalized and also localized obesity in warm-blooded animals therewith.... It is known from West German Pat. No. 2,115,926 that a group of sulfonamides, which includes 1-(4-hydroxy-3-dimethylamino-sulfonamidophenyl)-1-hydroxy-2-(1-phenoxyiso propylamino)ethane (Me 693), having a dilating effect upon the peripheral blood vessels, influence blood pressure, increase the capacity of the heart, and have broncholytic properties.... Compounds which exhibit activities of this kind are known as.beta.-adrenergics. Known.beta.-adrenergics have, in addition to the properties mentioned above, a marked glycogenolytic effect on the skeletal muscle, which is accompanied by lactacidemia. Web site: http://www.delphion.com/details?pn=US04499106__ •
Medicament for treating obesity and improving lipid metabolism Inventor(s): Suzuki; Kunio (1238-8, Gomigaya, Tsurugashima-shi, Saitama 350-2202, JP), Shimizu; Takeshi (Saitama, JP), Nakata; Tadashi (Saitama, JP) Assignee(s): Riken (Saitama, JP), Suzuki; Kunio (Saitama, JP) Patent Number: 6,531,462 Date filed: January 7, 2002 Abstract: A medicament for preventive and therapeutic treatment of obesity and a disease with abnormal lipid metabolism which comprises a 24-alkylcholest-5-en-3-one as an active ingredient. Excerpt(s): The present invention relates to medicaments useful for preventive and/or therapeutic treatment of obesity, and to medicaments of improving lipid metabolism.... Obesity is caused by insufficient exercise of habitual hyperphagia, or by metabolic disturbance due to genetic causes or endocrine diseases and other. Obesity may be a risk factor that causes various adult diseases such as myocardial infarct or arterial sclerosis, and it may also be a cause for deteriorating these diseases. Therefore, early therapeutic and preventive treatment of obesity is very important. Diet therapies or exercise therapies have been applied heretofore as the treatment of mild obesity, and drug therapies are sometimes used for serious obesity in combination with these therapies.... Hormone drugs, metabolic accelerators and other have been used heretofore for drug therapies of obesity and lipid metabolic disorder. For example, androgens such as dehydroepiandrosterone and 3-keto-.DELTA..sup.9 -19-norsteroid are known to have anti-obesity action (Japanese Patent Unexamined Publication No. (Hei)2-275895/1990). These androgens are considered to activate intramuscular anabolism to induce the consumption of depot lipid. It is also known that 3-ketosteroids such as 4-cholesten-3one (Japanese Patent Unexamined Publication No. (Hei)5-170651/1993) and 5-cholesten3-one (Japanese Patent Unexamined Publication No. (Hei)7-165587/1995) have reducing activity on serum lipid and anti-obesity action. However, the aformentioned cholestenones, which have the enone structure derived from cholesterol, may possibly
282 Obesity
be absorbed and accumulated in the body, and therefore, they are not satisfactory medicaments from a viewpoint of safety. Web site: http://www.delphion.com/details?pn=US06531462__ •
Method and apparatus for reducing obesity Inventor(s): Berman; Edward J. (3426 N. Meridian, Indianapolis, IN 46208), Rowe; George A. (3426 N. Meridian, Indianapolis, IN 46208) Assignee(s): none reported Patent Number: 4,133,315 Date filed: December 27, 1976 Abstract: An apparatus for reducing obesity in human beings having an inflatable bag to which a flexible tube is attached. The bag is positioned in the stomach, usually by swallowing, and the tube extends up through the esophagus and out of a nasal cavity or out from the abdomen when a gastrostomy is performed. The bag is inflated by attachment of a supply of fluid to the end of the tube, and then the tube is closed so that the bag will maintain its inflated conditon. With a portion of the open cavity of the patient's stomach occupied by the inflated bag, the patient will sense a feeling of being "filled-up" with only a small amount of food intake. Excerpt(s): This invention relates in general to dietary devices for medical treatment of obesity.... Those who have a problem with obesity have few options available to them with respect to a solution. The typical approach is to rely on the person's willpower to stick to a particular diet or to use diet pills to try and reduce the desire for food. These may be effective measures, depending upon the individual, but if the person is either physically or mentally unable to control his weight gain, he may be subject to more drastic measures, such as surgical reduction of the size of the stomach or bypassing much of the small intestines. Unfortunately, such measures have resulted in death to the patient in a substantial number of cases. Even if death is not the result, the operation is often permanent and the patient is still subjected to the after-effects once the problem with obesity is corrected. One approach to correcting obesity involves reducing the desire for food. This can be accomplished by partially filling the stomach so as to produce the sensation of being "filled-up." One way of accomplishing this is to place an inflatable, elastomeric bag in the stomach and inflate the bag with fluid.... Inflatable bag and tube combination devices are known in the field of medicine and have experienced use by the medical profession in the treatment of gastric disorders such as stomach ulcers and hemorrhages in the upper gastrointestinal tract. Cook, U.S. Pat. No. 3,227,154 discloses a device in which the bag must be fully inflated so that its impressionablesettable outer surface can make impressions in the walls of cavities which have restricted outlets. Another use of inflatable bag and tube combination devices as disclosed by Gawura, U.S. Pat. No. 3,768,484 and Seaman, U.S. Pat. No. 3,174,481, is to transfer and retain a cooling solution at a particular internal location. The bag acts merely as a container for this solution and the characteristic of being inflatable allows a single bag to be used with a wide range of cavity sizes. These prior art references all disclose tubes with a plurality of passageways and a liquid to inflate the bag. Web site: http://www.delphion.com/details?pn=US04133315__
Patents 283
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Method and apparatus for treating obesity Inventor(s): Garren; Lloyd R. (P.O. Box 3738, Wilmington, DE 19807), Garren; Mary L. (P.O. Box 3738, Wilmington, DE 19807) Assignee(s): none reported Patent Number: 4,416,267 Date filed: December 10, 1981 Abstract: A stomach insert for treating obesity in humans by reducing the stomach volume comprises a flexible torus-shaped inflatable balloon having a central opening extending therethrough. At least a portion of the balloon has a self-sealing substance to facilitate puncture thereof with a needle for inflating the balloon and sealing of the puncture upon removal of the needle. The method herein comprises positioning the balloon inside the stomach of the person being treated for obesity so as to reduce the stomach volume. Excerpt(s): The present invention relates to the medical treatment of obesity in humans, and more particularly to apparatus and methods for curbing the appetite of persons being treated for obesity.... Extreme obesity is a major illness in the United States and other countries. Its complications include hypertension, diabetes, coronary artery disease, stroke, congestive heart failure, venous disease, multiple orthopedic problems and pulmonary insufficiency with markedly decreased life expectancy. Medical management including dietary, psychotherapy, medications and behavioral modification techniques have yielded extremely poor results in multiple trials. Several surgical techniques have been tried which have bypassed the absorptive surface of the small intestine or have been aimed at reducing the stomach size by either partition or bypass. These procedures have been proven both hazardous to perform in morbidly obese patients and have been fraught with numerous life-threatening postoperative complications. Moreover such operative procedures are often difficult to reverse.... Nonsurgical approaches for the treatment of obesity include voluntary dieting which is often unsuccessful since most persons do not possess sufficient willpower to limit the intake of food. Other approaches include the use of stomach fillers such as methyl cellulose, often taken in the form of tablets. The methyl cellulose expands in the stomach leaving the person with a filled-up feeling. Also, inflatable bag and tube combinations have been proposed wherein the bag is swallowed into the stomach and the tube attached thereto is used to periodically inflate the bag, particulary just prior to mealtime or during the meal. Once the person has eaten, the bag can be deflated all at once, or it can be deflated gradually over a period of a few hours so as to simulate the condition of digestion occurring and the gradual reduction of stomach contents. Web site: http://www.delphion.com/details?pn=US04416267__
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Method and appartus for treating obesity Inventor(s): Garren; Lloyd R. (P.O. Box 3738, Wilmington, DE 19807), Garren; Mary L. (P.O. Box 3738, Wilmington, DE 19807) Assignee(s): none reported Patent Number: 4,899,747 Date filed: September 6, 1983
284 Obesity
Abstract: A stomach insert for treating obesity in humans by reducing the stomach volume comprises a flexible, free floating and unattached, inflatable balloon, the balloon being inflatable to a volume effective to reduce the stomach volume of a person being treated. At least a portion of the balloon has a self-sealing substance to facilitate puncture thereof with insufflation means through which the balloon is inflated and to facilitate sealing of the puncture upon removal of the insufflation means. The method herein comprises positioning the balloon inside the stomach of the person being treated for obesity so as to reduce the stomach volume. Excerpt(s): The present invention relates to a medical treatment of obesity in humans, and more particularly to both apparatus and method for curbing the appetite of persons being treated for obesity.... Extreme obesity is a major illness in the United States and other countries. Its complications include hypertension, diabetes, coronary artery disease, stroke, congestive heart failure, venous disease, multiple orthopedic problems and pulmonary insufficiency with markedly decreased life expectancy. Medical management including dietary, psychotherapy, medications and behavioral modification techniques have yielded extremely poor results in multiple trials. Several surgical techniques have been tried which have bypassed the absorptive surface of the small intestine or have been aimed at reducing the stomach size by either partition or bypass. These procedures have been proven both hazardous to perform in morbidly obese patients and have been fraught with numerous life-threatening postoperative complications. Moreover such operative procedures are often difficult to reverse.... Nonsurgical approaches for the treatment of obesity include voluntary dieting which is often unsuccessful since most persons do not possess sufficient willpower to limit the intake of food. Other approaches include the use of stomach fillers such as methyl cellulose, often taken in the form of tablets. The methyl cellulose expands in the stomach leaving the person with a filled-up feeling. Also, inflatable bag and tube combinations have been proposed wherein the bag is swallowed into the stomach and the tube attached thereto is used to periodically inflate the bag, particularly just prior to mealtime or during the meal. Once the person has eaten, the bag can be deflated all at once, or it can be deflated gradually over a period of a few hours so as to simulate the condition of digestion occurring and the gradual reduction of stomach contents. Web site: http://www.delphion.com/details?pn=US04899747__ •
Method and composition for treating obesity and related disorders in animals comprising dehydroepiandrosterone (DHEA), or a derivative thereof, and an anorectic agent Inventor(s): Svec; Frank (Metairie, LA), Porter; Johnny (Metairie, LA) Assignee(s): Louisiana State University Medical Center Foundation (New Orleans, LA) Patent Number: 5,795,880 Date filed: December 30, 1996 Abstract: The invention describes a method and composition for treating obesity or related disorders in animals using an anorectic agent and dehydroepiandrosterone (DHEA). The composition effectively diminishes caloric intake, may alter metabolism, weight gain, or a combination thereof. Excerpt(s): A method and composition for treating obesity and related disorders in animals comprising dehydroepiandrosterone (DHEA), or a derivative thereof, and an anorectic agent.... This invention describes an effective method and composition for
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treating obesity and related disorders in humans and animals, such as dogs, cats, or any other suitable animal, using DHEA or a derivative thereof and an anorectic agent. The method and composition are useful in veterinary as well as human applications.... Obesity may be the major health problem of the Western world. Nearly 20% of the United States' adult population is overweight and its prevalence is rising. The medical and economic importance of obesity go far beyond effects on self-image. Obesity is the dominant risk factor for the expression of adult-onset diabetes mellitus, and thus leads to complications of cardiovascular, renal, and peripheral vascular disease. Obesity is also a leading factor in the development of complications after surgical procedures. Web site: http://www.delphion.com/details?pn=US05795880__ •
Method and composition for treating obesity comprising dehydroepiandrosterone (DHEA), or a derivative thereof, and an anorectic agent Inventor(s): Svec; Frank (Metairie, LA), Porter; Johnny (Metairie, LA) Assignee(s): Louisiana State Univ. Medical Center Foundation (New Orleans, LA) Patent Number: 5,527,788 Date filed: January 18, 1994 Abstract: The invention describes a method and composition for treating obesity or related disorders in animals using an anorectic agent and dehydroepiandrosterone (DHEA). The composition effectively diminishes caloric intake, may alter metabolism, weight gain, or a combination thereof. Excerpt(s): A method and composition for treating obesity and related disorders in animals comprising dehydroepiandrosterone (DHEA), or a derivative thereof, and an anorectic agent.... This invention describes an effective method and composition for treating obesity and related disorders in humans and animals, such as dogs, cats, or any other suitable animal, using DHEA or a derivative thereof and an anorectic agent. The method and composition are useful in veterinary as well as human applications.... Obesity may be the major health problem of the Western world. Nearly 20% of the United States' adult population is overweight and its prevalence is rising. The medical and economic importance of obesity go far beyond effects on self-image. Obesity is the dominant risk factor for the expression of adult-onset diabetes mellitus, and thus leads to complications of cardiovascular, renal, and peripheral vascular disease. Obesity is also a leading factor in the development of complications after surgical procedures. Web site: http://www.delphion.com/details?pn=US05527788__
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Method and composition for treating obesity, drug abuse, and narcolepsy Inventor(s): Hohenwarter; Mark (Mobile, AL) Assignee(s): Serotonin Industries of Charleston (Charleston, SC) Patent Number: 4,843,071 Date filed: December 5, 1986 Abstract: Compositions and methods are disclosed for the treatment of obesity, depression, drug abuse, and narcolepsy. The compositions comprise a norepinephrine precursor such as L-tyrosine or L-phenylalanine in combination with a norepinephrine re-uptake inhibitor such as desipramine. In another embodiment of the invention, the
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compositions further norepinephrine.
comprise
enzymatic
cofactors
for
the
biosynthesis
of
Excerpt(s): This invention relates to compositions comprising a norepinephrine precursor, such as L-tyrosine or L-phenylalanine in combination with a norepinephrine re-uptake inhibitor such as desipramine. The compositions are useful in controlling obesity, depression, drug abuse, and narcolepsy in animals. The invention also relates to said compositions further comprising one or more enzymatic cofactors for the biosynthesis of norepinephrine. This invention further relates to a method of controlling obesity, depression, drug abuse, or narcolepsy in an animal comprising administering an effective amount of the compositions of this invention to said animal.... The use of appetite supressants such as diethylproprion and phenylpropanolamine operate by directly and/or indirectly stimulating noradrenergic receptors in the brain. However, long-term use of these drugs is met with increasing tolerance in most patients, requiring increased dosage and more frequent administration to achieve continued appetite suppression. Tolerance to these products occurs as the result of a depletion of norepinephrine from storage sites in the neuron with the use of indirect-acting agents.... Catecholamines are stored in subcellular granules and released by exocytosis in the adrenal medulla and sympathetic nerve endings. The biosynthesis of catecholamines proceeds from the amino acid phenylalanine which is sequentially hydroxylated to form tyrosine, then 3,4-dihydroxyphenylalanine (DOPA). DOPA is decarboxylated to form dopamine. Hydroxylation on the beta position of the side chain forms norepinephrine. Web site: http://www.delphion.com/details?pn=US04843071__ •
Method for combating obesity Inventor(s): Munter; Klaus (Mannheim, DE), Kirchengast; Michael (Mannheim, DE) Assignee(s): Knoll Aktiengesellschaft (Ludwigshafen, DE) Patent Number: 6,197,780 Date filed: April 27, 2000 Abstract: Diseases caused by obesity are treated with endothelin receptor antagonists. Diseases treated include those frequently associated with obesity such as hypertension, type 2 diabetes, hyperlipidemia, chronic kidney failure, arteriosclerosis and gout. Excerpt(s): The present invention relates to a method for controlling obesity and diseases caused by obesity.... The peptide hormone endothelin is known for its strong vasoconstrictor properties. Endothelin receptor antagonists are therefore mainly being tested in cardiovascular pathologies.... The invention relates to the use of endothelin receptor antagonists for producing drugs for controlling obesity and diseases caused by obesity. Web site: http://www.delphion.com/details?pn=US06197780__
Patents 287
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Method for control of obesity, overweight and eating disorders Inventor(s): Clegg; Charles T. (1418 Thayer Ave., Los Angeles, CA 90024), Wallace; Garn A. (1647 Manning Ave., Los Angeles, CA 90024) Assignee(s): none reported Patent Number: 4,823,808 Date filed: July 6, 1987 Abstract: Methods for the treatment of obesity, overweight, compulsive overeating, emotional overeating, binge eating, bulimia and anorexia comprises the steps of monitoring physiological parameters in the esophageal and/or gastrointestinal tract which are associated with gastric relaxation, gastric filling, gastric contractions, gastric secretions, and gastric emptying. The measurement are transmitted either directly to a receiver or via radiotelemetry to a receiver. The receiver has a data processor associated therewith, and the data processor produces audio and/or visual feedback for the person under treatment to hear and/or see. This feedback is used for purposes of teaching behavior modification and other psychotherapeutic purposes. In the most simple form of the invention, a warning sound is generated by the data processor indicating when sufficient food has been ingested. This warning can be generated by the monitoring apparatus much sooner than the biological signal of fullness transmitted by the stomach to the brain of the person. The person can thereby discontinue eating before otherwise becoming unconsciously too full. Excerpt(s): The present invention relates generally to methods for the control of obesity, overweight, and eating disorders, including anorexia, bulimia, and compulsive overeating. In particular, the invention relates to methods for sensing the quantity of food consumed and/or the monitoring of various physiological changes during food ingestion and digestion, with the monitored data being presented visually or through auditory means or other sensations to a person who is participating in a program of treatment involving voluntary limitation of dietary intake and/or behavior modification.... Obesity has been treated in many ways, with the overall goal being to reduce ingestion below energy expenditure so as to result in a weight loss. Energy expenditure is increased by physical activity increases, and the physical activity further results in an increase in metabolic rate lasting beyond the period of exercise. Energy intake is reduced through dietary restriction or other means. Numerous theories exist regarding various topics which are believed to influence body weight, such as genetics, fat cell number behavior, and developmental psychology. Finally systems theory has also been used to partially account for difficulties with overweight, obesity, and eating disorders.... Currently used treatments for obesity and overeating include psychological interventions, dietetics, exercise, gastric balloons, stomach staping, jaw wiring, surgery, drugs and behavior modifications. An important of the psychological interventions may also include assessment and treatment of body image. Behavior modification, including assessment and treatment of body image, is a most effective treatment when combined with diet and exercise. Web site: http://www.delphion.com/details?pn=US04823808__
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Method for imparting ability of preventing obesity and impaired glucose tolerance to foods and foods and sugar preparations exhibiting such preventive effects Inventor(s): Wakabayashi; Shigeru (Takarazuka, JP), Hoshii; Yasuhiro (Fujiidera, JP) Assignee(s): Matsutani Chemical Industries Co., Ltd. (Hyogo, JP) Patent Number: 5,505,981 Date filed: August 3, 1993 Abstract: Preventing obesity and impaired glucose tolerance by incorporating indigestible dextrin containing at least 30% by weight of indigestible components into a food in an amount ranging from 1 g to 30 g per meal of the food. Excerpt(s): The present invention relates to a method for imparting an ability of preventing obesity and impaired glucose tolerance to foods, and a food and a sugar preparation exhibiting such preventive effects.... Recently, eating habits have been improved, but the population of patients suffering from geriatric diseases represented by obesity and diabetes increases steadily because of hypernutrition and unbalanced diet as well as lack of exercise. Under such social background, there have been developed various agents for inhibiting an increase in the blood-sugar level and excess insulin-secretion for preventing healthy person from suffering from obesity and/or diabetes or for treating patients requiring the control of the blood-sugar level such as those suffering from diabetes. As such agents, there have been known, for instance, Acarbose (available from Bayer Yakuhin, Ltd.) and A0-128 (available from Takeda Chemical Industries, Ltd.) which are substances having an effect of inhibiting the gastrointestinal absorption of sugar and starch and inhibitors for enzymes involved in digestion, but both of them are medicines and the ingestion or intake thereof for the preventive purpose becomes a cause of various problems. For instance, they suffer from a problem of safety, since they would be dangerous because of possible side-effects. Moreover, polymers of glucose moieties bonded through.alpha.-1,6-bonds such as isomaltotriose, dextran and pullulan have been known to have an effect of inhibiting an increase in the blood-sugar level in response to ingestion of sugar. Isomaltotriose and dextran as such are digested and absorbed and, in particular, dextran suffers from a problem of safety since it has been proved that dextran exhibits side-effects such as an effect of elongating the blood-coagulation time. On the other hand, pullulan can inhibit any increase in the blood-sugar level after the ingestion of sugar, but is substantially ineffective for the control of the blood-sugar level after the ingestion of glucose and maltose. Moreover, the effect thereof for controlling the insulin-secretion has not yet been proved. Furthermore, pullulan has been known to control an increase in the body weight when it is administered to a young rat and to inhibit the growth thereof.... On the other hand, the effect of insulin is very important for controlling the sugar-metabolism in patients suffering from diabetes, persons whose probability of suffering from diabetes is high or patients suffering from obesity and, therefore, it is needed for these persons or patients to protect, hold and/or enhance the effect of insulin. There have been used, for instance, solutions for transfusion and foods containing monosaccharides or sugar alcohols such as fructose, sorbitol and xylitol; disaccharides and their alcohols such as maltitol, maltose and leucrose; and glucose polymers (U.S. Pat. No. 3,928,135), capable of being digested in and absorbed by living bodies independent of the effect of insulin, for the prevention of temporal hyperglycemia after the ingestion of these sugars, for saving the insulin-secretion, for the supplementation of energy or for controlling the osmotic pressure of transfusion solutions. However, these mono- and poly-saccharides and their alcohols have high degrees of sweetness, but the quality of sweetness thereof is inferior to that of sugar. In addition, sugar alcohols often becomes a cause of diarrhea.
Patents 289
Moreover, it has been known that the glucose polymers do not stimulate any insulinsecretion when it is used in the form of a transfusion solution, but the transfusion is a medical act and cannot be commonly adopted. Web site: http://www.delphion.com/details?pn=US05505981__ •
Method for screening potential anti-obesity agents Inventor(s): Hamilton; Bradford S. (D7 - 245 Howland Avenue, Toronto, Ontario, CA), Roncari, deceased; Daniel A. K. (late of North York, CA), Roncari, executor; by Lubov (144 Esther Crescent, Thornhill, Ontario, CA) Assignee(s): none reported Patent Number: 5,783,408 Date filed: June 7, 1995 Abstract: A method for screening a compound as a potential anti-obesity agent by determining whether the compound stimulates micro motion of cells in vitro is described Excerpt(s): The present invention relates to a method for screening compounds having potential as anti-obesity agents.... Obesity is a significant health problem in many countries and has been extensively reviewed in the literature..sup.1,2,3,4,5,6 Obesity is frequently associated with such cardiovascular risk factors as dyslipidemias (particularly, elevated levels of very-low-density lipoprotein-triglycerides and depressed levels of high-density lipoproteins), hypertension, hyperinsulinemia, and non-insulin dependent diabetes mellitus..sup.1,2,3,4,5,6 Massive corpulence (body weight greater than 170% of reference or body mass index greater than 37 kg/m.sup.2) is also characterized by high morbidity and mortality..sup.1,2,6 Massive obesity, which features diffuse distribution of adiposity, is particularly associated with the mixed (central and obstructive) sleep-apnea syndrome, and at times the full hypoventilation syndrome, gallbladder disease, non-insulin dependent diabetes, trauma and psychosocial problems.... It has been estimated that approximately 34 million American adults were obese in 1980..sup.7 The economic costs in 1986 of obesity were estimated conservatively to be $39.3 billion. Web site: http://www.delphion.com/details?pn=US05783408__
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Method for the treatment of obesity Inventor(s): Hornkvist; Per-Erik (Goteborg, SE) Assignee(s): Imperial Chemical Industries plc (London, GB2) Patent Number: 4,933,340 Date filed: November 26, 1986 Abstract: The invention concerns the use of N-(2-[RS-2-hydroxy-3-(4hydroxyphenoxy)propylamino]ethyl)-morpholinoformam ide or a salt thereof in the production of a medicament for the treatment of obesity and/or related conditions in warm-blooded animals including man. Excerpt(s): This invention concerns a therapeutic agent for use in the treatment of obesity and/or related conditions such as obesity of maturity onset diabetes, affecting
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warm-blooded animals, especially humans or domestic animals. More particularly, the invention concerns the novel use of the known pharmaceutical agent xamoterol, its Senantiomer or a salt in the treatment of obesity and/or related conditions in humans or domestic animals, and in the manufacture of a new medicament for such use.... According to the invention there is provided a method for the treatment of obesity and/or related conditions in warm-blooded animals, such as humans or domestic animals which comprises the administration of a therapeutically effective amount of a therapeutic agent selected from N-(2-[RS-2-hydroxy-3-(4hydroxyphenoxy)propylamino]ethyl)morpholinoformami de of formula I (also known as xamoterol) and the S-laevorotatory enantiomer thereof, or of a pharmaceutically acceptable acid-addition salt of said agent, to humans or domestic animals requiring such treatment.... Particularly suitable pharmaceutically acceptable acid-addition salts include, for example, salts derived from a suitable inorganic acid, such as hydrochloric, hydrobromic, phosphoric and sulphuric acids, and salts derived from a suitable organic acid, such as oxalic, fumaric, lactic, acetic, salicylic, citric, benzoic, 2-naphthoic and adipic acid, 1,1-methylene-bis(2-hydroxy-3-naphthoic acid), and from an acidic synthetic resin, such as a sulphonated polystyrene resin. Web site: http://www.delphion.com/details?pn=US04933340__ •
Method for treating morbid obesity Inventor(s): Silverman; David E. (Palo Alto, CA), Stein; Alan (Moss Beach, CA) Assignee(s): SciMed Life Systems, Inc. (Maple Grove, MN) Patent Number: 6,540,789 Date filed: November 10, 2000 Abstract: A method for treating morbid obesity in a body of a mammal having a gastrointestinal tract extending through a stomach and a pyloric sphincter and a wall forming the stomach and pyloric sphincter. At least one implant is formed in the wall in the vicinity of the pyloric sphincter to inhibit emptying of the stomach. Excerpt(s): This invention pertains to the treatment of morbid obesity.... Numerous modalities are purported to treat morbid obesity. These include patient-specific dietary restrictions and nutritional supplementation, abdominoplasty or panniculectomy, gastric banding and/or stapling and the more invasive and surgically aggressive gastric bypass. There is a need for a method which is less invasive and more clinically efficacious in treating morbid obesity.... In general, it is an object of the present invention to provide a method for creating implants in natural body cavities accessible by natural body openings and more preferably in gastrointestinal tract passageways in order to treat morbid obesity. Web site: http://www.delphion.com/details?pn=US06540789__
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Method for treating obesity Inventor(s): Lassen; Joergen B. (Glostrup, DK) Assignee(s): A/S Ferrosan (Soberg, DK) Patent Number: 4,745,122 Date filed: December 4, 1985
Patents 291
Abstract: A method for treating obesity in humans or non-human animals, which method comprises administering an effective, non-toxic amount of paroxetine or a pharmaceutically acceptable salt thereof, to obese humans or animals and compositions for use in such treatment. Excerpt(s): The present invention relates to a method for the treatment of obesity and to a compound for use in such method.... U.S. Pat. No. 4,007,196 discloses the compound, ()-trans-4-(4'-fluorophenyl)-3-(3',4'-methylenedioxyphenoxymethyl)piperid ine, and, in Example 2, a process by which it can be prepared. The compound, which is referred to herein by its common name, paroxetine, is described in the patent as an inhibitor of 5hydroxytryptamine and, therefore, is of use in the treatment of depression. The patent also mentions that paroxetine is useful in the treatment of Parkinson's disease.... It has now been discovered that paroxetine also has activity against obesity. Web site: http://www.delphion.com/details?pn=US04745122__ •
Method for treatment of morbid obesity Inventor(s): Angelchik; Jean P. (1728 W. Glendale Ave., Phoenix, AZ 85021) Assignee(s): none reported Patent Number: 4,607,618 Date filed: January 11, 1985 Abstract: Morbid obesity is treated by implacement in the fundus of a hollow shaped appliance. The appliance is formed of semi-rigid skeleton members and is collapsible to a dimension and shape which can be inserted into the stomach through the esophagus and cardiac opening. Upon release of the collapsed device in the stomach, it autogenously re-assumes its normal uncollapsed shape. Excerpt(s): This invention pertains to medical treatment methods and apparatus useful therein.... In a more particular respect, the invention concerns a method for treating morbid obesity.... In another particular respect, the invention concerns an appliance useful in such treatment. Web site: http://www.delphion.com/details?pn=US04607618__
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Method for treatment of obesity Inventor(s): Viner; Norman (Ottawa, CA) Assignee(s): Synapse Pharmaceuticals International, Inc. (Ottawa, CA) Patent Number: 5,900,418 Date filed: February 10, 1997 Abstract: A method is provided for the control of obesity comprising administering to a mammal including humans suffering from obesity an acetylcholine esterase reactivator or prodrug derivative thereof optionally in association with an acetylcholine receptor antagonist. Excerpt(s): The present invention is directed to a method for the control and/or treatment of obesity.... It is well understood that obesity is a widespread problem. Obesity is linked to a variety of medical conditions including hypertension, diabetes, cardiovascular disease, etc. obesity is also linked to a variety of psychological
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maladjustments. By contemporary medical standards an obese person is judged to be overweight by at least 10 percent. At present, only a limited number of treatments are available to treat obesity. Exemplary treatments are disclosed in U.S. Pat. Nos. 3,867,539 (administration of histidine); 4,446,138 (administration of L-Dopa); 4,588,724 (administration of beta adrenergic stimulant or alpha-2 adrenergic inhibitor); 4,745,122 (administration of paroxetine); 5,019,594 (sympathomimetic drug and tyrosine); 5,300,298 (administration of 8-phenylxanthines); 5,403,851 (tryptamine); 5,567,714 (administration of neuropeptide Y); 5,573,774 (nicotinic metabolites); and 5,578,613 (administration of 2-phenyl-3-aroylbenzothiophenes). Amphetamine has also been used as an appetite suppressant.... Unfortunately, none of the above methods of treatment have been very successful. While such treatments may bring short-term relief to the person, long-term success has not been easily achieved. The cessation of tobacco use has frequently contributed to weight gain. Also, comorbid addictions, stress, psychiatric disorders and environmental factors may exacerbate the difficulty encountered by a particular person in alleviating obesity. It is believed, for example, that xenobiotic toxic agents such as pesticides, insecticides, fungicides, oxidants, solvents and other environmental toxins encountered by the person by various means (e.g., via drinking water and/or food impurities, etc.) may contribute to the inability of the person to control obesity. Web site: http://www.delphion.com/details?pn=US05900418__ •
Method for treatment of obesity using prolactin modulators and diet Inventor(s): Cincotta; Anthony H. (Andover, MA), Meier; Albert H. (Andover, MA) Assignee(s): The Board of Supervisors of Louisiana State University and Agriculture (Baton Rouge, LA), Ergo Research Corporation (Wakefield, RI) Patent Number: 5,760,047 Date filed: May 10, 1995 Abstract: The present invention is directed to an improvement in a method of weight and/or body-fat reduction comprising a (preferably moderate) reduction in the caloric intake of a subject in need of such treatment in combination with administration to said subject of a prolactin inhibitor. Additionally, the present invention is directed to an improvement in a method for altering and/or resetting prolactin profiles (and thereby controlling one or more metabolic disorders such as obesity, excessive body fat, hyperlipidemia, hyperlipoproteinemia, hyperglycemia, hypercholesterolemia, hyperinsulinemia, insulin resistance, glucose intolerance, and Type II diabetes) comprising administration to a subject in need of such treatment of a prolactin inhibitor at a predetermined time or times during a 24-hour period in combination with a (preferably moderate) reduction of the caloric intake of said subject. Excerpt(s): This invention relates to an improved method for the reduction in a subject, vertebrate animal or human, of weight and/or body fat stores. This method involves a reduction in caloric intake, in combination with the administration of a prolactin inhibitor.... In another aspect, this invention relates to an improved method for altering and/or resetting prolactin profiles of a vertebrate subject (including a human), by administering to such subjects a prolactin inhibitor in combination with restricting the caloric intake of the subject, thereby effecting an amelioration in abnormal metabolic indices of said subject.... The reduction of body weight and/or fat stores in man is of significant benefit, both cosmetically and physiologically. Whereas controlled diet and exercise can produce modest results in the reduction of weight and body fat deposits,
Patents 293
these results are often unsatisfactory due to the substantial reduction in metabolic rate which accompanies a reduced calorie diet. Further, although a loss in body weight is seen with reduced caloric intake, this loss is often temporary and/or due to a reduction in lean body weight (as opposed to loss of fat). Various studies have shown that most calorie restriction diets result in weight loss approximately 40% of which is body fat lost and the remainder is lean body mass loss. Web site: http://www.delphion.com/details?pn=US05760047__ •
Method for treatment or prevention of obesity Inventor(s): Clark; Ross G. (Pacifica, CA) Assignee(s): Genentech, Inc. (South San Francisco, CA) Patent Number: 5,597,797 Date filed: November 19, 1993 Abstract: A method is disclosed for treating obese mammals or preventing obesity from occurring in mammals. This method involves administering to the mammal an effective amount of growth hormone in combination with an effective amount of IGF-I. Preferably, the growth hormone is given so as to have a maintained, continual therapeutically effective presence in the blood, such as by continuous infusion or frequent injections, or by use of a long-acting formulation. Excerpt(s): This invention relates to a method of restoring ideal population-based body composition in obese mammals or preventing obesity especially in humans.... Obesity is a chronic disease that is highly prevalent in modern society and is associated not only with a social stigma, but also with decreased life span and numerous medical problems, including adverse psychological development, reproductive disorders such as polycystic ovarian disease, dermatological disorders such as infections, varicose veins, Acanthosis nigricans, and eczema, exercise intolerance, diabetes mellitus, insulin resistance, hypertension, hypercholesterolemia, cholelithiasis, osteoarthritis, orthopedic injury, thromboembolic disease, cancer, and coronary heart disease. Rissanen et al., British Medical Journal, 301: 835-837 (1990).... Obese subjects tend to have low basal levels of growth hormone (GH) and fail to secrete significant amounts of GH in response to a variety of stimuli, including growth hormone releasing hormone (GHRH). Williams, New Engl. J. Med., 311: 1403 (1984) Kopelman, Clin. Endocrinol., 23: 87 (1985); Kopelman, Clin. Endocrinol., 24: 157 (1986) Loche, Clin. Endocrinol., 27: 145 (19871) Ghigo et al., Metabolism, 41: 560-563 (1992). The GH responsiveness to GHRH in obese rats shows sexual dimorphism. Cocchi et al., Pharmacol. Res., 25: Suppl. 2, 336-337 (1992). This failure to secrete GH has been postulated to be the result of a hypothalamic disorder (Kopelman, 1986, supra), leading to a chronic state of somatostatin hypersecretion. Cordido, J. Clin. Endocrinol. Metab., 68: 290 (1989). This defect in GH secretion appears to be a result rather than a cause of obesity, since it is, at least in part, reversible with weight reduction. Web site: http://www.delphion.com/details?pn=US05597797__
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Method of controlling obesity with purified active principle of fruit of Synsepalum dulcificum Inventor(s): Henkin; Robert I. (Bethesda, MD), Giroux; Eugene L. (Strasbourg, FR) Assignee(s): The United States of America as represented by the Department of Health, (Washington, DC) Patent Number: 3,995,031 Date filed: July 23, 1974 Abstract: A process for the purification of the active principle of the fruit of the plant Synsepalum dulcificum is disclosed. The process includes contacting the fruit with a suspension of polyvinyl pyrrolidone, followed by adsorption of the active principle by means of chromatography procedures. By following the process in accordance with the present invention, proteases and tannins are substantially completely eliminated from the final product. The active principle of this fruit, when prepared in accordance with the present invention, has been found to be particularly useful in controlling obesity in human beings. Excerpt(s): The present invention relates to a process for purification of the active principle of the fruit of the plant Synsepalum dulcificum. Also disclosed is a method for the use of this active principle in the control of obesity.... The botanical plant species of Synsepalum dulcificum is indigenous to tropical West Africa, where it is often referred to as "miracle fruit." The plant, which grows in the form of a shrub, yields ripe red berries from December to June, the berries being ellipsoidal in shape and about 0.75 inch long, and composed of a thin layer of pulp surrounding a single large seed. These berries have the unique property of modifying the taste of sour foods to make such foods taste sweet after the fruit pulp has been chewed.... Previous methods for the purification of the active principle of plants such as Synsepalum dulcificum have been characterized by a complex series of steps involving bulky equipment and long periods of time for the separation of an active principle which in many cases has been of a low degree of purity, often containing contaminants such as proteases and tannins in relatively large amounts. Such prior art methods include those described by Inglett et al., J. Agri. Food Chem., 13:284 (1965), Brouwer et al., Nature 220:373 (1968) and Beidler et al., Science 161:1241 (1968). The method of Inglett et al. involves purification of the active principle of miracle fruit in phases A and B, with phase A involving successive treatment of the plant parts with petroleum ether, chloroform, ethyl acetate, acetone, absolute ethanol and water, and phase B including successive treatment with water, aqueous alcohol, absolute alcohol, acetone, chloroform and n-hexane, followed by hydrolysis of fractions A and B. By removal of inactive matter, a five-fold concentration of the active material was achieved. Web site: http://www.delphion.com/details?pn=US03995031__
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Method of preventing or alleviating mammalian obesity Inventor(s): Mikami; Toshiyuki (Ibaraki, JP), Spiegelman; Bruce (Waban, MA), Wright; Harold (Watertown, MA) Assignee(s): Sumitomo Chemical Company, Limited (Osaka, JP), Dana-Farber Cancer Institute, Inc. (Boston, MA) Patent Number: 6,033,656 Date filed: May 4, 1999
Patents 295
Abstract: The present invention provides methods of suppressing the activation of Peroxisome Proliferator-Activated Receptor gamma in a mammalian body by administering an effective amount of bisphenol A diglycidyl ether to a mammal, methods of suppressing the accumulation of fat in the mammalian fat cell or adipose tissue by administering an effective amount of bisphenol A diglycidyl ether to a mammal, methods of preventing or alleviating mammalian obesity by administering an effective amount of bisphenol A diglycidyl ether to a mammal, bisphenol A diglycidyl ether for use as an active pharmaceutical substance or composition for the treatment of obesity, and uses of bisphenol A diglycidyl either for the preparation of a pharmaceutical composition for the treatment of obesity. Excerpt(s): The present invention relates to a method of preventing or alleviating mammalian obesity.... Fat cells have the ability to store fat in their cells and are typically present in the adipose tisses of the subcutaneous abdominal region, the femoral region, the gluteal region, the pectoral region and the like, and the adipose tissues which are in the abdominal cavity and in the vicinity of the mesenterium, kidney, epididymis, and the like, which are in the body of a mammal, such as a human. For example, promoting the storage of fat in fat cells generally results in an obese mammal, which is generally accompanied by an increase in body fat content and an increase in the mass of adipose tissue which is typically in the abdominal cavity of the mammal. It is knovwn that such obesity thereby induces disorders such as the impairment in glucose tolerance [Journal of Clinical Investigation, vol.72, pp. 1150 (1983)], diabetes [National Diabetes Data Group: Diabetes in America. Bethesda, Md., U.S. Dept. of Health and Human Services, (1985), Diabetes Care, vol.19, pp.613 (1996), Diabetes & Metabolisme, vol.20, pp.375 (1994), Obesity: Advances in Understanding and Treatment, Published by IBC Biomedical Library, Chapter 3.1, (1996)], hyperglycemia, hyperlipemia, hypertension [Journal of Clinical Investigation, vol.72, pp. 1150 (1983)], coronary arterial diseases [Diabetes & Metabolisme, vol.20, pp.375 (1994)], obstructive arterial sclerosis and the like [WHO Expert Committee on Diabetes Mellitus. Second report, WHO Tech Rep 646 Geneva: World Health Organization (1980)].... The fat cells are generally produced by differentiating progenitor fat cells. To differentiate progenitor fat cells into fat cells, it is essential to activate a function of a protein called Peroxisome Proliferator-Activated Receptor gamma (hereinafter refereed to as "PPAR.gamma.")[Peter Tontonoz, et al., Cell, vol.79, 1147-1156, 1994]. For example, the accumulation of fat in a fat cell can occur from having a thiazolidinedione derivative bind to PPAR.gamma. in the progenitor fat cell so that PPAR.gamma. can be activated, which induces the differentiation of the progenitor fat cell to a fat cell, and which then further expresses genes associated with fat accumulation [Jurgen of M. Lehman, et al., Journal of Biological Chemistry, vol. 270, No. 22, 12953-12956, 1995]. PPAR.gamma. is a nuclear receptor type transcription regulating factor [Issenman and Green, Nature 347-645-650 (1990)]. Web site: http://www.delphion.com/details?pn=US06033656__ •
Method of reducing bodyweight and treating obesity Inventor(s): Remmereit; Jan (Volda, NO) Assignee(s): Natural Nutrition Ltd. AS (NO) Patent Number: 6,034,132 Date filed: March 19, 1998 Abstract: The present invention discloses method for reducing body weight and treating obesity. The method comprises administering a nutritionally effective amount of
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conjugated linoleic acid to a human. The conjugated linoleic acid may be provided in the form of a free fatty acid in a pill, or as a component of a prepared food product. Excerpt(s): This invention relates to the administration of a dietary supplement, conjugated linoleic acid, to induce bodyweight reduction, thereby providing a treatment for obesity.... Obesity is the most common disorder of the developed world. The ready availability of food in most areas, a shift to relatively sedentary lifestyles, and changing food sources have contributed to this problem.... Researchers have hypothesized that recent changes in food sources have led to an imbalance in the optimal ratio of fatty acid intake. These imbalances may influence obesity. Specifically, modern diets have increased amounts of omega-6 fatty acids as compared to omega-3 fatty acids, as noted in Simopoulos, "Evolutionary Aspects of Diet: Fatty Acids, Insulin Resistance and Obesity", in Obesity: New Directions in Assessment and Management, VanItallie and Simonpoulos ed., The Charles Press, Philadelphia, 241-61 (1995). Omega-6 fatty acids are represented by linoleic acid and omega-3 fatty acids are represented by alpha-linolenic acid. A balance between omega-6 and omega-3 fatty acids existed for most of human history and has now been changed to a ratio of about 20 to 25:1 in the favor of omega-6 fatty acids. This increase in omega-6 fatty acids is due the increased intake of vegetable oils and increased amounts saturated and monounsaturated fatty acids (depot fat) in domestic meat as compared to meat from wild game. The replacement of saturated fats with unsaturated fats has been widely recommended, resulting in increased intake of omega-6 fatty acids from vegetable oils and trans fatty acids from margarine. This means that humans have been exposed to pharmacological doses of omega-6 fatty acids from the first time in their evolutionary history. Web site: http://www.delphion.com/details?pn=US06034132__ •
Method of treating obesity Inventor(s): Klein; Ira (5 Windermere, Houston, TX 77063) Assignee(s): none reported Patent Number: 5,498,424 Date filed: November 30, 1994 Abstract: The present invention provides a simple, pharmacological method for treating obesity without risk of undesirable side effects. It has been discovered that intake of a megadose of a macrolide antibiotic creates an anorexigenic reaction in the human sufficient to result in weight loss. This method can also be used advantageously to assist non-obese persons in losing weight. The present invention relates to a method of treating obesity, comprising the steps of identifying a patient needing to lose weight and administering an appetite suppressing dose of a macrolide antibiotic compound to the patient. The dose of the macrolide antibiotic preferably ranges between a dose greater than a normal clinical dose used to treat bacterial infections and a maximum dose capable of being safely received by the patient without toxicity. In another preferred embodiment, the method includes the additional step of readministering the dose at an interval as required to maintain a desired level of appetite suppression throughout the treatment. In a preferred embodiment of the present invention, the macrolide antibiotic compound is clarithromycin. Excerpt(s): The present invention relates to methods of inducing weight loss in mammals, and in particular to methods of treating obesity.... Excess adiposity, in its extreme form obesity, is generally regarded as a disorder of energy regulation. This
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disorder is increasingly prevalent in industrialized nations because of the abundance of food and the reduced activity levels that accompany the movement of populations from rural to urban settings. Obesity is loosely defined as an excess of body fat over that needed to maintain health.... Obesity is associated with increased morbidity and mortality. Detrimental effects of obesity on health, include an increased risk of cardiovascular disease and the associated conditions of hypertension, diabetes, and hyperlipidemia. Millions of people are clinically obese (i.e., a Body Mass Index value above the 851 h percentile), and, in view of the deleterious effects of obesity on health, would benefit from treatment. Additionally, many people, although not clinically obese, can improve their health and well-being by losing weight. Web site: http://www.delphion.com/details?pn=US05498424__ •
Method of treating obesity by the oral administration of a predigested protein composition Inventor(s): Gans; Arnold M. (Closter, NJ), Goren; Alvin J. (North Bergen, NJ), Gorenberg; Eli M. (Fair Lawn, NJ) Assignee(s): Control Drug, Inc. (Port Reading, NJ) Patent Number: 4,042,687 Date filed: June 22, 1976 Abstract: A method of preventing obesity which comprises ingestion of a pre-digested protein composition formed from hydrolyzed gelatin to which has been added an effective amount of tryptophane, said composition containing all of the essential amino acids and having a palatable taste and odor. Excerpt(s): This invention relates to a method and composition for providing a highly efficient source of nutrition without undesirable side effects, and it especially relates to the provision of a source of protein in concentrated but highly palatable form.... One of the most significant aspects of the present invention is its utilization in the prevention of nutritional deficiency, and particularly that form of nutritional deficiency which is caused by disease or which is an undesirable condition in the treatment of a disease or surgical procedure.... The crucial effect in the body's response to nutritional deficiency or starvation is the preservation of the size and character of the body cell mass. The term "body cell mass" denotes the total mass of living, functioning, energy-exchanging, and mitotically active cells of the body comprising two large groups of tissues, namely skeletal muscle and visceral parenchyma. Web site: http://www.delphion.com/details?pn=US04042687__
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Method of treatment of obesity Inventor(s): Holloway; Brian R. (Congleton, GB2), Howe; Ralph (Macclesfield, GB2), Rao; Balbir S. (Holmes Chapel, GB2), Stribling; Donald (Prestbury, GB2) Assignee(s): Imperial Chemical Industries PLC (London, GB2) Patent Number: 4,937,267 Date filed: March 10, 1987 Abstract: A method of treatment of obesity or diabetes mellitus in a warm-blooded animal requiring such treatment which comprises administering to said animal an
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effective amount of the compound N-(2-[2-hydroxy-3-phenoxypropyl]aminoethyl)isobutyramide in racemic (R,S) or levorotatory optically active (S) form, or of a pharmaceutically acceptable acid-addition salt thereof. Excerpt(s): The invention concerns novel therapeutic agents having thermogenic properties for use in the treatment of obesity and/or related conditions such as diabetes mellitus especially of maturity onset, in warm-blooded animals such as man. More particularly, the invention provides a new method of treatment of obesity and/or related conditions involving administration of a known pharmaceutical agent and the use of said agent in the manufacture of a novel medicament.... According to the invention there is provided a method of treatment of obesity and/or a related condition affecting a warm-blooded animal which comprises administering to said animal an effective amount of the compound N-(2-[2-hydroxy-3phenoxypropyl]aminoethyl)isobutyramide of formula I (set out hereinafter) in racemic (R,S) or laevorotatory optically active (S) form, or a pharmaceutically acceptable acidaddition salt thereof.... The invention also provides the use of the compound of formula I in racemic (R,S) or laevorotatory optically active (S) form, or of a pharmaceutically acceptable salt thereof, in the manufacture of a novel medicament for the treatment of obesity and/or related conditions in warm-blooded animals, including man. Web site: http://www.delphion.com/details?pn=US04937267__ •
Methods and compositions for the diagnosis and treatment of body weight disorders, including obesity Inventor(s): Moore; Karen (Maynard, MA), Nagle; Deborah Lynn (Watertown, MA) Assignee(s): Millennium Pharmaceuticals, Inc. (Cambridge, MA) Patent Number: 6,274,339 Date filed: February 5, 1999 Abstract: The present invention relates to mammalian mahogany genes, including the human mahogany gene, which are novel genes involved in the control of mammalian body weight. The invention encompasses nucleotide sequences of the mahogany gene, host cell expression systems of the mahogany gene, and hosts which have been transformed by these expression systems, including transgenic animals. The invention also encompasses novel mahogany gene products, including mahogany proteins, polypeptides and peptides containing amino acid sequences mahogany proteins, fusion proteins of mahogany proteins polypeptides and peptides, and antibodies directed against such mahogany gene products. The present invention also relates to methods and compositions for the diagnosis and treatment of mammalian body weight disorders, including obesity, cachexia, and anorexia, and for the identification of subjects susceptible to such disorders. Further, the invention relates to methods of using the mahogany gene and gene products of the invention for the identification of compounds which modulate the expression of the mahogany gene and/or the activity of the mahogany gene product. Such compounds can be useful as therapeutic agents in the treatment of mammalian body weight disorders, including obesity, cachexia, and anorexia. Excerpt(s): The present invention relates to mammalian mahogany genes, including the human mahogany gene, which are novel genes involved in the control of mammalian body weight. The invention encompasses nucleotide sequences of the mahogany gene, host cell expression systems of the mahogany gene, and hosts which have been
Patents 299
transformed by these expression systems, including transgenic animals. The invention also encompasses novel mahogany gene products, including mahogany proteins, polypeptides and peptides containing amino acid sequences mahogany proteins, fusion proteins of mahogany proteins polypeptides and peptides, and antibodies directed against such mahogany gene products.... The present invention also relates to methods and compositions for the diagnosis and treatment of mammalian body weight disorders, including obesity, cachexia, and anorexia, and for the identification of subjects susceptible to such disorders. Further, the invention relates to methods of using the mahogany gene and gene products of the invention for the identification of compounds which modulate the expression of the mahogany gene and/or the activity of the mahogany gene product. Such compounds can be useful as therapeutic agents in the treatment of mammalian body weight disorders, including obesity, cachexia, and anorexia.... Obesity represents the most prevalent of body weight disorders, and it is the most important nutritional disorder in the western world, with estimates of its prevalence ranging from 30% to 50% within the middle-aged population. Other body weight disorders, such as anorexia nervosa and bulimia nervosa, which together affect approximately 0.2% of the female population of the western world, also pose serious health threats. Further, such disorders as anorexia and cachexia (wasting) are also prominent features of other diseases such as cancer, cystic fibrosis, and AIDS. Web site: http://www.delphion.com/details?pn=US06274339__ •
Methods and reagents for regulating obesity Inventor(s): Bernfield; Merton (Boston, MA), Reizes; Ofer (Newton, MA) Assignee(s): Children's Medical Center Corporation (Boston, MA) Patent Number: 6,284,729 Date filed: May 6, 1998 Abstract: It has now been demonstrated that syndecan binds to and interacts with MC4R, and thereby modulates neuropeptide regulation of body weight, via the agouti/MC4R signaling pathway. Transgenic animals were made initially using a construct including a cytomegalovirus promoter and the 3' untranslated region, including the polyadenylation site, of the bovine growth hormone gene, as well as cDNA encoding syndecan-1. The mice express the syndecan-1 transgene in many tissues, with expression in the brain occurring preferentially in their hypothalamus. These mice are characterized by elevated levels of circulating syndecan-1 ectodomain and exhibit enormous weight gain after reaching sexual maturity, but have a relatively normal distribution of fat, are completely healthy and heterozygotes reproduce, and show other indicators associated with obesity in humans. Agouti mice which are transgenic for syndecan-1 ectodomain demonstrate that syndecan-1 and agouti interact, potentiating obesity. The double heterozygote shows both an earlier onset, and greater extent, of obesity than either normal agouti or the original transgenic syndecan-1 mice.Based on these studies and animal models, one can design and test compounds regulating obesity. These mice are also useful in understanding the factors involved in weight regulation and in designing and screening for drugs which are involved in weight regulation and that can either enhance or reduce appetite and activity. Excerpt(s): Obesity is a well established risk factor for a number of potentially lifethreatening diseases such as atherosclerosis, hypertension, diabetes, stroke, pulmonary embolism, and cancer. Furthermore, it complicates numerous chronic conditions such as respiratory diseases, osteoarthritis, osteoporosis, gall bladder disease, and
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dyslipidemias. The enormity of this problem is best reflected in the fact that death rates escalate with increasing body weight. More than 50% of all-cause mortality is attributable to obesity-related conditions once the body mass index (BMI) exceeds 30 kg/m.sup.2, as seen in 35 million Americans. (Lee1992. JAMA. 268:2045-2049). By contributing to greater than 300,000 deaths per year, obesity ranks second only to tobacco smoking as the most common cause of potentially preventable death. (McGinnis 1993 MA.270:2207-2212). Accompanying the devastating medical consequences of this problem is the severe financial burden placed on the health care system in the United States. The estimated economic impact of obesity and its associated illnesses from medical expenses and loss of income are reported to be in excess of $68 billion/year. (Colditz G. 1992. Am J Clin Nutr. 55:503S-507S). This does not include the greater than $30 billion per year spent on weight loss foods, products, and programs. (Wolf 1994. Pharmacoeconomics. 5:34-37).... A major reason for the long-term failure of established approaches is their basis on misconceptions and a poor understanding of the mechanisms of obesity. Conventional wisdom maintained that obesity is a self-inflicted disease of gluttony. Comprehensive treatment programs, therefore, focused on behavior modifications to reduce caloric intake and increase physical activity using a myriad of systems. These methods have limited efficacy and are associated with recidivism rates exceeding 95%. (NIH Technology Assessment Conference Panel. 1993. Ann Intern Med. 119:764-770). Failure of short-term approaches, together with the recent progress made in elucidating the pathophysiology of obesity, have lead to a reappraisal of pharmacotherapy as a potential long-term, adjuvant treatment. (National Task Force on Obesity. 1996. JAMA. 276:1907-1915). The premise is that body weight is a physiologically controlled parameter similar to blood pressure and obesity is a chronic disease similar to hypertension. The goal of long-term (perhaps life long) medical therapy would be to facilitate both weight loss and subsequent weight maintenance in conjunction with a healthy diet and exercise. To assess this approach, the long-term efficacy of currently available drugs must be judged against that of nonpharmacological interventions alone. Currently, no single drug regimen emerges as superior in either promoting or sustaining weight loss. Although promising, the success of this approach is limited by the efficacy of currently available anorexiant drugs. Surgical interventions, such as gastric partitioning procedures, jejunoileal bypass, and vagotomy, have also been developed to treat severe obesity. (Greenway 1996. Endo Metab Clin N Amer. 25:1005-1027). Although these procedures induce similar rates of early weight loss as nonsurgical interventions, they have been shown to maintain a weight loss of up to 33% for more than 10 years. (Long 1994. Diabetes Care. 17:372-375). While still far from optimal, this is a substantial improvement over that achieved with behavioral and medical management alone. The superior long-term outcome with surgical procedures in attributed to the inherent permanence of the intervention which addresses the chronic nature of the disease. Although advantageous in the long run, the acute risk benefit ratio has reserved these invasive procedures for morbidly obese patients according to the NIH consensus conference on obesity surgery (BMI>40 kg/m.sup.2). (NIH Conference. 1991. Ann Intern Med. 115:956-961). Therefore, this is not an alternative for the majority of overweight patients unless and until they become profoundly obese and are suffering the attendant complications.... No one knows all of the mechanisms involved in regulation of weight gain, although it is believed that many genetic as well as environmental factors, including diet and exercise, play major, interrelated roles. A number of publications have reported the discovery of genes that have been "knocked out" or overexpressed in transgenic mice, resulting in affected animals becoming incredibly obese, or vice versa. See, for example, Ezzell, "Fat Times for Obesity Research: Tons of New Information, but How Does It All Fit Together" J. NIH Res. 7, 39-43 (October 1995). Researchers have reported the cloning of at least two
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distinct genes, Ob which encodes a protein "leptin" believed to cause weight reduction in obese animals, and Db, which is believed to cause weight gain in animals. Other genes which have been reported include the fat, tub, agouti, and melanocortin 4 receptor genes. Recent reviews relating to the insights regarding the mechanisms involved in obesity help to understand these complex pathways. See, for example, Trish Gura, Science 275, 752-753 (Feb. 7, 1997) and Jeffrey S. Flier, Proc. Natl. Acad. Sci. USA 94, 4242-4245 (April 1997). Leptin, discovered in 1994 by Jeffrey Friedman's team at Rockefeller University, NY, is a 16 kD protein produced by the obesity (ob) gene of mice. Homozygotes with defective ob genes are unable to reproduce, stay warm, or grow normally, and become grossly overweight. The receptor for leptin has now been identified and cloned. Defects in the receptor also result in grossly obese animals. The receptor is expressed in the brain primarily in four regions, including the arcuate nucleus. In humans, however, the linkage between obesity and overexpression of leptin does not seem to be closely correlated, and no individuals have been identified that have a mutated Ob receptor or gene. Another molecule which appears to be important in weight control is the appetite-stimulating neurotransmitter referred to as neuropeptide Y or "NPY". NPY levels are elevated in animals with decreased levels of leptin. Genetic studies with knockout NPY and ob/ob animals indicate that NPY plays a role in, but is not a controlling factor, in obesity. Another line of research has implicated a role in obesity for the melanocortin receptor ("MCR"). Two MCRs, MCR3 and MCR4, are produced in the arcuate nucleus of the hypothalamus, a prime target of leptin action as well as of NPY production. Synthetic peptides mimicking melanocortins which bind to MCR-4 suppress feeding. Animals in which the gene encoding MCR-4 has been knocked out show the opposite behavior, exhibiting high weight gain and high NPY expression. Web site: http://www.delphion.com/details?pn=US06284729__ •
Methods for identifying compositions for the treatment of body weight disorders, including obesity Inventor(s): Tartaglia; Louis Anthony (Watertown, MA) Assignee(s): Millennium Pharmaceuticals, Inc. (Cambridge, MA) Patent Number: 5,853,975 Date filed: February 26, 1997 Abstract: The present invention relates to methods and compositions for the treatment of body weight disorders, including, but not limited to, obesity. Specifically, the present invention identifies and describes genes which are differentially expressed in body weight disorder states, relative to their expression in normal, or non-body weight disorder states, and/or in response to manipulations relevant to appetite and/or weight regulation. Further, the present invention identifies and describes genes via the ability of their gene products to interact with gene products involved in body weight disorders and/or appetite and/or body weight regulation. Still further, the present invention provides methods for the identification and therapeutic use of compounds as treatments of body weight disorders. Additionally, the present invention describes methods for the diagnostic evaluation and prognosis of various body weight disorders, and for the identification of subjects exhibiting a predisposition to such conditions. Excerpt(s): The present invention relates to methods and compositions for the modulation of processes related to mammalian body weight regulation, including treatment of body weight disorders such as obesity and cachexia, and modulation of thermogenesis. Specifically, the present invention identifies and describes genes which
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are differentially expressed in body weight disorder states, relative to their expression in normal, or non-body weight disorder states, and also identifies genes which are differentially expressed in response to manipulations relevant to appetite and/or weight regulation. Further, the present invention identifies and describes genes via the ability of their gene products to interact with gene products involved in body weight disorders and/or to interact with gene products which are relevant to appetite and/or body weight regulation. Still further, the present invention provides methods for the identification and therapeutic use of compounds as treatments of body weight-related processes, including body weight disorders such as obesity and cachexia. Additionally, the present invention describes methods for the diagnostic evaluation and prognosis of various body weight disorders, and for the identification of subjects exhibiting a predisposition to such conditions.... The regulation of body fat in mammals is a complex process involving the regulation of not only appetite but also energy expenditure. An important component of energy expenditure is non-shivering thermogenesis (NST). In rodents, the majority of NST appears to occur in brown adipose tissue (BAT) via the uncoupling protein (UCP) (Cannon & Nedergaard, 1985, Essays in Biochem. 20:110-165; Himms-Hagen J., 1989, Prog. Lipid Res. 28:67-115). UCP is a proton channel located exclusively in the inner mitochondrial membrane of adipocytes of the BAT (Nicholls & Locke, 1984, Physiol. Rev. 64:1-64). By allowing protons to equilibrate across the inner mitochondrial membrane, UCP uncouples oxidative phosphorylation from ATP production and thus converts stored energy into heat rather than work (Klingenberg M., 1990, Trends Biochem. Sci. 15:108-112; Klaus S. et al., 1991, Int. J. Biochem. 23:791-801). UCP-mediated uncoupling is not only capable of increasing body temperature in coldacclimatized rodents and hibernating animals, but can also dissipate surplus caloric energy (Rothwell & Stock, 1986, In Brown Adipose Tissue. Trayhurn P., Nicholls D.G., Eds., London, Arnold, p. 269-298; Spiegelman & Flier, 1996, Cell 87:377-389; Hamann & Flier, 1996, Endocrinology 137:2129). A number of studies have now implicated UCP and brown adipose tissue as important regulators of body weight in rodents (Hamann & Flier, 1996, Endocrinology 137:2129; Lowell B. B. et al., 1993, Nature 366:740-742; Kopecky J. et al., 1995, J. Clin. Invest. 96:2914-2923; Cummings D. E. et al., 1996, Nature 382:622-626).... In humans, body weight homeostasis is poorly understood, but is also thought to involve regulated thermogenesis (Rothwell & Stock, 1981, Annu. Rev. Nutr. 1:235-56; Segal K. R. et al., 1992, J. Clin. Invest. 89:824-833; Jensen M. D. et al., 1995, Am. J. Physiol. 268:E433-438). However, the importance of the UCP in adult humans is questionable due to the low levels of BAT and consequently the low levels of UCP expression (Huttunen P. et al., 1981, Eur. J. Appl. Physiol. 46:339-345; Cunningham S. et al., 1985, Clin. Sci. 69:343-348; Schulz L., 1987, J. Am. Diet Assoc. 87:761-764; Santos G. C. et al., 1992, Arch. Pathol. Lab Med. 116:1152-1154). Web site: http://www.delphion.com/details?pn=US05853975__ •
Methods for the diagnosis of body weight disorders including obesity Inventor(s): Tartaglia; Louis Anthony (Watertown, MA) Assignee(s): Millennium Pharmaceuticals, Inc. (Cambridge, MA) Patent Number: 5,702,902 Date filed: August 23, 1995 Abstract: The present invention relates to methods and compositions for the treatment of body weight disorders, including, but not limited to, obesity. Specifically, the present invention identifies and describes genes which are differentially expressed in body
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weight disorder states, relative to their expression in normal, or non-body weight disorder states, and/or in response to manipulations relevant to appetite and/or weight regulation. Further, the present invention identifies and describes genes via the ability of their gene products to interact with gene products involved in body weight disorders and/or appetite and/or body weight regulation. Still further, the present invention provides methods for the identification and therapeutic use of compounds as treatments of body weight disorders. Additionally, the present invention describes methods for the diagnostic evaluation and prognosis of various body weight disorders, and for the identification of subjects exhibiting a predisposition to such conditions. Excerpt(s): The present invention relates to methods and compositions for the treatment of body weight disorders, including, but not limited to, obesity. Specifically, the present invention identifies and describes genes which are differentially expressed in body weight disorder states, relative to their expression in normal, or non-body weight disorder states, and also identifies genes which are differentially expressed in response to manipulations relevant to appetite and/or weight regulation. Further, the present invention identifies and describes genes via the ability of their gene products to interact with gene products involved in body weight disorders and/or to interact with gene products which are relevant to appetite and/or body weight regulation. Still further, the present invention provides methods for the identification and therapeutic use of compounds as treatments of body weight disorders. Additionally, the present invention describes methods for the diagnostic evaluation and prognosis of various body weight disorders, and for the identification of subjects exhibiting a predisposition to such conditions.... Body weight disorders, including eating disorders, represent major health problems in all industrialized countries. Obesity, the most prevalent of eating disorders, for example, is the most important nutritional disorder in the western world, with estimates of its prevalence ranging from 30% to 50% within the middle-aged population. Other body weight disorders, such as anorexia nervosa and bulimia nervosa which together affect approximately 0.2% of the female population of the western world, also pose serious health threats. Further, such disorders as anorexia and cachexia (wasting) are also prominent features of other diseases such as cancer, cystic fibrosis, and AIDS.... Obesity, defined as an excess of body fat relative to lean body mass, also contributes to other diseases. For example, this disorder is responsible for increased incidences of diseases such as coronary artery disease, stroke, and diabetes. Obesity is not merely a behavioral problem, i.e., the result of voluntary hyperphagia. Rather, the differential body composition observed between obese and normal subjects results from differences in both metabolism and neurologic/metabolic interactions. These differences seem to be, to some extent, due to differences in gene expression, and/or level of gene products or activity. The nature, however, of the genetic factors which control body composition are unknown, and attempts to identify molecules involved in such control have generally been empiric and the parameters of body composition and/or substrate flux are monitored have not yet been identified (Friedman, J. M. et al., 1991, Mammalian Gene 1:130-144). Web site: http://www.delphion.com/details?pn=US05702902__
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Methods for treating obesity and weight gain using optically pure (-)-bupropion Inventor(s): Young; James W. (Palo Alto, CA) Assignee(s): Sepracor (Marlborough, MA) Patent Number: 6,110,973 Date filed: January 28, 1999 Abstract: Methods are disclosed utilizing the optically pure (-)-isomer of bupropion, which is a potent drug for treating obesity and weight gain. Excerpt(s): This invention relates to methods of treatment and pharmaceutical compositions employing the compound (-)-bupropion.... Many organic compounds exist in optically active forms, i.e., they have the ability to rotate the plane of plane-polarized light. In describing an optically active compound, the prefixes D and L or R and S are used to denote the absolute configuration of the molecule about its chiral center(s). The prefixes (+) and (-) or d and l are employed to designate the sign of rotation of planepolarized light by the compound, with (-) or l meaning that the compound is levorotatory. A compound prefixed with (+) or d is dextrorotatory. For a given chemical structure, these compounds, called stereoisomers, are identical except that they are mirror images of one another. A specific stereoisomer may also be referred to as an enantiomer, and a mixture of such isomers is often called an enantiomeric or racemic mixture.... Stereochemical purity is of importance in the field of pharmaceuticals, where 16 of the 20 most prescribed drugs exhibit chirality. A case in point is provided by the Lform of the.beta.-adrenergic blocking agent, propranolol, which is known to be 100 times more potent than the D-enantiomer. Web site: http://www.delphion.com/details?pn=US06110973__
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Methods of producing weight loss and treatment of obesity Inventor(s): Kozachuk; Walter E. (Kensington, MD) Assignee(s): none reported Patent Number: 6,191,117 Date filed: July 10, 2000 Abstract: Methods are disclosed for the acute and chronic treatment of obesity using drugs whose mechanism includes the interaction and antagonism of the kainate/AMPA receptor. Methods are disclosed for employing the drug topiramate (topomax) as monotherapy or in combination therapy with lamotrigene, valproic acid, valproic acid and carbamezepine combination, or felbamate (felbatol). Excerpt(s): The present invention relates to pharmaceutical compositions, whose mechanisms of action(s) are at the kainate/AMPA receptor that can be used to treat the medical condition of obesity.... Obesity is one of the most common medical disorders, which affects 30-40% of the population of which 10% may be severe and morbid. Complications of obesity include insulin resistance, diabetes mellitus, hypertension, cardiovascular disease, pseudotumor cerebri, hyperlipidemia, sleep apnea, cancer, pulmonary hypertension, cholecystitis, and osteoarthritis. The mortality from obesity is estimated at 300,000 to 400,000 per annum in the United States. Obesity in humans is commonly measured by the BMI (body mass index) which is the weight in kilograms divided by the height in meters squared. The degree of obesity is determined by comparisons against standard deviations above the means for males and females. The
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exact etiology of obesity is unknown but occurs when energy intake exceeds energy expenditure. The amount and distribution of body fat may have some genetic predisposition and be under some hormonal control. Hypothalamic structures, which have complex interconnections with the limbic system and other brain structures, control appetite. Some neurochemicals known to be involved in appetite control include: leptin, a substance released from adipose tissue, GLP-1 (glucagon-like peptidel) which promotes satiety, and neuropeptide-Y, a potent stimulator of appetite.... The present invention proposes a theory of obesity in which dysfunction of the AMPA/kainate and/or NMDA is a contributing etiology. Administration of drugs whose mechanism or action is antagonism of the AMPA/kainate receptor, with or without the combination of glycine-site antagonists, is proposed as a treatment for obesity. Web site: http://www.delphion.com/details?pn=US06191117__ •
Methods of screening for modulators of uncoupling protein-2 (UCP-2) as potential treatments for obesity Inventor(s): Lind; Peter (Uppsala, SE), Walum; Erik (.ANG.kersberga, SE) Assignee(s): Pharmacia & Upjohn AB (Stockholm, SE) Patent Number: 6,001,578 Date filed: June 26, 1998 Abstract: The invention relates to a method for treatment of obesity, metabolic syndrome and/or non-insulin dependent diabetes mellitus by administering a drug capable of modulating the regulation of UCP-2, the use of a drug capable of modulating the regulation of UCP-2 for the production of drug for treatment of obesity, metabolic syndrome and/or non-insulin dependent diabetes mellitus and pharmaceutical composition comprising a pharmaceutically effective amount of such a drug. The invention is also related to methods for screening for potential drugs against obesity, metabolic syndrome and/or non-insulin dependent diabetes mellitus and the use of cDNA probe for determination of upregulation of UCP-2 for potential drugs against obesity, metabolic syndrome and/or non-insulin dependent diabetes mellitus. Excerpt(s): The present invention relates to method for treatment of obesity, metabolic syndrome and/or non-insulin dependent diabetes mellitus by administering a drug capable of modulating the regulation of UCP-2. The present invention also relates to the use of a drug capable of modulating the regulation of UCP-2 for the production of a drug for treatment of obesity, metabolic syndrome and/or non-insulin dependent diabetes mellitus. The present invention also relates to method for screening for potential drugs against obesity, metabolic syndrome and/or non-insulin dependent diabetes mellitus comprising the measurement of UCP-2 activity by biochemical, chemical or physical methods.... Obesity is a disease with strongly increasing prevalence, and has reached epidemic proportions in the industrialized world. This disease is essentially characterized by an unbalance between energy intake and expenditure, which, without interference, leads to an endless increase in adipose tissue mass and body weight.... Appetite and energy intake are influenced by several hormonal effectors and neurotransmitters acting in the peripheral as well as the central nervous system. Examples of neurotransmitters acting to increase appetite and, concomitantly, body weight, are neuropeptide Y, melanin concentrating hormone, galanin, as well as glucocorticoid hormones. Examples of hormones or neurotransmitters that counteract feeding and stimulate reduction in adipose mass are
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melanocortin, corticotropin releasing factor, as well as the recently described peptide hormone leptin. Web site: http://www.delphion.com/details?pn=US06001578__ •
Methods of treating obesity with purine related compounds Inventor(s): LaNoue; Kathryn F. (Hershey, PA) Assignee(s): The Pennsylvania Research Corporation (University Park, PA) Patent Number: 5,300,298 Date filed: May 6, 1992 Abstract: There is disclosed a method of treating obesity in warm-blooded animals, including humans, as well as a method of increasing the muscle mass to fat ratio in farm animals. The methods entail administering to an animal in need thereof, an effective amount of certain 8-phenylxanthines substituted in the 3- or 4-position of the phenyl group by an alkenylene, alkenyleneoxy, alkynylene or alkynyleneoxy bearing a terminal acetic grouping. Excerpt(s): The present invention pertains to a method of treating obesity in warmblooded animals, including humans, and to methods of increasing the ratio of muscle mass to fat in farm animals.... U.S. Pat. No. 4,879,296, issued Nov. 7, 1989 and U.S. Pat. No. 4,981,857, issued Jan. 1, 1991, disclose purine derivatives of Formula I described below, which are useful in the present invention. Methods of preparing the compounds are disclosed in both U.S. Pat. Nos. 4,879,296 and 4,981,857. The patents also disclose that the compounds provided therein are useful in human and veterinary therapy, particularly for conditions associated with the cell surface effects of adenosine. Even so, there is no disclosure in either U.S. patent that the compounds provided therein are useful as anti-obesity agents, or as agents capable of increasing the ratio to muscle mass to fat in farm animals. Instead, both patents are concerned with using the compounds disclosed therein in the treatment or prophylaxis of AIDS and other retroviral infections and for pathophysiological disorders arising from the cell surface effects of adenosine. Such pathophysiological disorders caused by adenosine/cell surface interaction are disclosed in both U.S. patents as including those arising within the cardiovascular, gastrointestinal or neuroendocrine systems, including heart block, asthma, and irritable bowel syndrome. U.S. Pat. No. 4,879,269 and 4,981,857 are each incorporated herein by reference, in their entirety.... The present invention provides a method of treating obesity in warm-blooded animals. In particular, the present invention provides a method of treating obesity (e.g., adult onset obesity, lifelong obesity and morbid obesity.sup.7) in humans. The method entails administering to a patient in need thereof, an effective amount of one of the anti-obesity agents encompassed by Formula I, as shown below. Such compounds are advantageously administered to a patient in need thereof in the form of a pharmaceutical composition, in combination with a pharmaceutically acceptable carrier. Web site: http://www.delphion.com/details?pn=US05300298__
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Methods of treating or preventing weight gain, obesity, and related disorders Inventor(s): Jerussi; Thomas P. (19 Garvey Rd., Framingham, MA 01701), Senanayake; Chrisantha H. (11 Old Farm Cir., Shrewsbury, MA 01545), Fang; Qun K. (35 Atwood St., Wellesley, MA 02181) Assignee(s): none reported Patent Number: 6,538,034 Date filed: December 4, 2001 Abstract: Methods are disclosed for the treatment and prevention of obesity, weight gain, and eating disorders. The methods comprise the administration of racemic or optically pure sibutramine metabolites and pharmaceutically acceptable salts, solvates, and clathrates thereof. Excerpt(s): The invention relates to methods of using, and compositions comprising, dopamine reuptake inhibitors and, in particular, racemic and optically pure metabolites of sibutramine.... Sibutramine, chemically named [N-1-[1-(4-chlorophenyl)cyclobutyl]-3methylbutyl]-N,N-dimethylamine, is a neuronal monoamine reuptake inhibitor which was originally disclosed in U.S. Pat. Nos. 4,746,680 and 4,806,570. Sibutramine inhibits the reuptake of norepinephrine and, to a lesser extent, serotonin and dopamine. See, e.g., Buckett et al., Prog. Neuro-psychopharm. & Biol. Psychiat., 12:575-584, 1988; King et al., J. Clin. Pharm., 26:607-611 (1989).... Racemic sibutramine is sold as a hydrochloride monohydrate under the tradename MERIDIA.RTM., and is indicated for the treatment of obesity. Physician's Desk Reference.RTM. 1494-1498 (53.sup.rd ed., 1999). The treatment of obesity using racemic sibutramine is disclosed, for example, in U.S. Pat. No. 5,436,272. Web site: http://www.delphion.com/details?pn=US06538034__
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Novel anti-obesity compounds and method of use Inventor(s): Ruhe; Rodney C. (1000 Willmar Ave., SW., Willmar, MN 56201) Assignee(s): none reported Patent Number: 4,897,390 Date filed: July 21, 1987 Abstract: The present invention provides novel compounds for controlling mammalian obesity by simultaneous action upon caloric intake and caloric expenditure. This is accomplished by the administration of pharmaceutically acceptable and therapeutically active analogs of.alpha.-HET and.beta.-HET, having a methyl group at the 3.beta. position to avoid metabolically induced conjugation of the molecule to an inactive species while retaining the structural integrity of the molecule. Excerpt(s): This invention relates generally to the use of steroid compounds in the reduction of mammalian obesity. In particular, this invention relates to the synthesis and use of etiocholanone derivatives as anti-obesity agents.... Weight reduction is accomplished when the body takes in fewer calories than it expends. Thus, all weight control measures involve strategies for either reducing caloric intake, or, increasing energy expenditure. For example, diets achieve weight reduction by directing an individual to consume food sufficient to maintain nutritional balance but insufficient to maintain body weight. U.S. Pat. No. 4,137,327 to Marshall claims an analogous process whereby a mixture of albumin and oxethazine is swallowed prior to eating. The mixture
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purportedly clings to the walls of the stomach and anesthetizes the nerve endings which activate digestive fluids. The process thereby permits eating without caloric intake. On the other hand, exercise or activity programs achieve weight reduction by increasing the body's rate of caloric expenditure. Such programs are effective when they specify normal levels of food consumption and greater than normal levels of exercise.... It follows that the most efficient weight reduction strategy would simultaneously decrease caloric intake while increasing caloric expenditure. To this end, dehydroepiandrosterone ("DHEA") is a promising antiobesity agent. The exact mechanism by which DHEA effects weight loss is not known. However, experimental evidence suggests that DHEA inhibits particular metabolic enzymes (and thus caloric intake) while simultaneously increasing the overall metabolic rate (and therefor caloric expenditure). Web site: http://www.delphion.com/details?pn=US04897390__ •
Ob receptor and methods for the diagnosis and treatment of body weight disorders, including obesity and cachexia Inventor(s): Tartaglia; Louis A. (Watertown, MA), Tepper; Robert I. (Weston, MA), Culpepper; Janice A. (Brookline, MA) Assignee(s): Millennium Pharmaceuticals, Inc. (Cambridge, MA) Patent Number: 6,548,269 Date filed: April 26, 1996 Abstract: The present invention relates to the discovery, identification and characterization of nucleotides that encode Ob receptor (ObR), a receptor protein that participates in mammalian body weight regulation. The invention encompasses obR nucleotides, host cell expression systems, ObR proteins, fusion proteins, polypeptides and peptides, antibodies to the receptor, transgenic animals that express an obR transgene, or recombinant knock-out animals that do not express the ObR, antagonists and agonists of the receptor, and other compounds that modulate obR gene expression or ObR activity that can be used for diagnosis, drug screening, clinical trial monitoring, and/or the treatment of body weight disorders, including but not limited to obesity, cachexia and anorexia. Excerpt(s): The present invention relates to the discovery, identification and characterization of nucleotides that encode Ob receptor (ObR), a receptor protein that participates in mammalian body weight regulation. The invention encompasses obR nucleotides, host cell expression systems, ObR proteins, fusion proteins, polypeptides and peptides, antibodies to the receptor, transgenic animals that express an obR transgene, or recombinant knock-out animals that do not express the ObR, antagonists and agonists of the receptor, and other compounds that modulate obR gene expression or ObR activity that can be used for diagnosis, drug screening, clinical trial monitoring, and/or the treatment of body weight disorders, including but not limited to obesity, cachexia and anorexia.... Obesity represents the most prevalent of body weight disorders, and it is the most important nutritional disorder in the western world, with estimates of its prevalence ranging from 30% to 50% within the middle-aged population. Other body weight disorders, such as anorexia nervosa and bulimia nervosa which together affect approximately 0.2% of the female population of the western world, also pose serious health threats. Further, such disorders as anorexia and cachexia (wasting) are also prominent features of other diseases such as cancer, cystic fibrosis, and AIDS.... Obesity, defined as an excess of body fat relative to lean body mass, also contributes to other diseases. For example, this disorder is responsible for increased incidences of
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diseases such as coronary artery disease, stroke, and diabetes. (See, e.g., Nishina, P. M. et al., 1994, Metab. 43:554-558.) Obesity is not merely a behavioral problem, i.e., the result of voluntary hyperphagia. Rather, the differential body composition observed between obese and normal subjects results from differences in both metabolism and neurologic/metabolic interactions. These differences seem to be, to some extent, due to differences in gene expression, and/or level of gene products or activity (Friedman, J. M. et al., 1991, Mammalian Gene 1:130-144). The epidemiology of obesity strongly shows that the disorder exhibits inherited characteristics (Stunkard, 1990, N. Eng. J. Med. 322:1483). Moll et al. have reported that, in many populations, obesity seems to be controlled by a few genetic loci (Moll et al. 1991, Am. J. Hum. Gen. 49:1243). In addition, human twin studies strongly suggest a substantial genetic basis in the control of body weight, with estimates of heritability of 80-90% (Simopoulos, A. P. & Childs B., eds., 1989, in "Genetic Variation and Nutrition in Obesity", World Review of Nutrition and Diabetes 63, S. Karger, Basel, Switzerland; Borjeson, M., 1976, Acta. Paediatr. Scand. 65:279-287). Web site: http://www.delphion.com/details?pn=US06548269__ •
Obesity associated genes Inventor(s): North; Michael (La Jolla, CA), Nishina; Patsy (Bar Harbor, ME), NobenTrauth; Konrad (Bar Harbor, ME), Naggert; Juergen (Bar Harbor, ME) Assignee(s): Sequana Therapeutics, Inc. (La Jolla, CA), The Jackson Laboratory (Bar Harbor, ME) Patent Number: 5,776,762 Date filed: September 17, 1996 Abstract: The gene responsible for the autosomal recessive mouse obesity mutation tub was identified by positional cloning. The homologous human gene is also provided. The genes are used to produce tubby protein; in screening for compositions that modulate the expression or function of the tubby protein; and in studying associated physiological pathways. The DNA is further used as a diagnostic for genetic predisposition to obesity, retinal degeneration or cochlear degeneration. The mutation responsible for the tub phenotype is a G to T transversion that abolishes a donor splice site in the 3' coding region and results in a larger transcript containing the unspliced intron. A second, prematurely truncated transcript arises from the introduction of a premature polyadenylation site in the unspliced intron. Excerpt(s): The field of this invention is genes associated with obesity in mammals.... Human obesity is a widespread and serious disorder, affecting a high percentage of the adult population in developed countries. In spite of an association with heart disease, type II diabetes, cancer, and other conditions, few persons are able to permanently achieve significant weight loss. Failure to treat obesity may be at least partially attributed to the complexity of the disease. Genetic, psychological and environmental factors all play a role in individual patterns of weight gain or loss, making it exceedingly difficult to define the contribution of any single element.... An understanding of the genetic factors that underlie obesity may aid in treatment. However, defining the exact genetic loci involved in a human polygenic trait requires extensive family studies. Because there are so many genes that can affect the single trait of obesity, in humans it may be virtually impossible to statistically determine the contribution of one locus. An attempt at such mapping studies can be further complicated by the interaction and linkage of genes. Also, environmental effects cannot be assumed to be the same for all
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genotypes. As an alternative to the complexities of human genetic mapping, animal models may be useful. Web site: http://www.delphion.com/details?pn=US05776762__ •
Obesity protein analog compounds and formulations thereof Inventor(s): Hoffmann; James Arthur (Greenwood, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,831,017 Date filed: January 24, 1997 Abstract: The present invention provides novel compounds, which comprise an obesity protein analog complexed with a divalent metal cation, pharmaceutical formulations thereof, and methods of using such compounds for treating obesity, and disorders associated with obesity such as diabetes, cardiovascular disease and cancer. Excerpt(s): This application claims the benefit of U.S. Provisional Application No. 60/011,055, filed Jan. 25, 1996.... The present invention is in the field of human medicine, particularly in the treatment of obesity and disorders associated with obesity. More specifically, the present invention relates to compounds and formulations of an obesity protein analog.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout the world. According to recent statistics, more than 25% of the United States population and 27% of the Canadian population are overweight. Kuczmarski, Amer. J. of Clin. Nutr. 55: 495S-502S (1992); Reeder et. al., Can. Med. Ass. J., 23: 226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society. Web site: http://www.delphion.com/details?pn=US05831017__
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Obesity treatment tools and methods Inventor(s): Deem; Mark E. (Mountain View, CA), Sutton; Douglas S. (Pacifica, CA), Gifford, III; Hanson S. (Woodside, CA), Andreas; Bernard H. (Redwood City, CA), French; Ronald G. (Santa Clara, CA) Assignee(s): Satiety, Inc. (Redwood City, CA) Patent Number: 6,558,400 Date filed: May 30, 2001 Abstract: Various obesity treatment tools and methods are described herein, as well as treatments for other gastric-related diseases, e.g., GERD. Treatment includes reducing the size of the stomach pouch to limit the caloric intake as well as to provide an earlier feeling of satiety. This may be done by creating a smaller gastric pouch within the stomach directly from the interior of the stomach itself. The smaller pouches may be made through the use of individual anchoring devices, rotating probes, or volume reduction devices. A pyloroplasty procedure may also be performed to render the pyloric sphincter incompetent. A gastric bypass procedure may additionally be
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performed using atraumatic magnetic anastomoses devices so that sugars and fats are passed directly to the bowel while bypassing the stomach. Many of these procedures may be done in a variety of combinations. Treatment may create enforced behavioral modifications by discouraging the ingestion of high-caloric foods. Excerpt(s): The present invention relates generally to tools and methods for the treatment of obesity. More particularly, the present invention relates to tools and methods for performing less traumatic gastroplasty procedures.... Obesity is considered a major health problem with annual associated costs reaching $100 billion in the U.S. alone. Morbid obesity is a condition of obesity with the presence of a secondary debilitating progressive disease and is generally associated with a body mass index (BMI).gtoreq.40 kg/m.sup.2. While the basic mechanism of obesity is simply an imbalance between caloric intake and burn rate, the underlying factors are varied and complex and conservative attempts at sustained weight loss with this population are almost always unsuccessful. Often, there are genetic and other biological influences that may override environmental causes. Consequently, obesity is a disease that eludes a simple treatment, with a recurrence rate above 90% for those who attempt to lose weight. Moreover, long-term results using conservative treatments for morbid obesity are generally unsuccessful and are typically associated with further loss of self-esteem with the regaining of weight. Hypertension, cardiovascular disease, diabetes, along with a host of other comorbidities all make morbid obesity second only to smoking as a preventable cause of death.... Surgical procedures for obesity date back to 1889 (Billroth) with the earliest peer reviewed procedure being the jejuno-ileal bypass in 1954 (Kreman). A successful procedure is commonly defined as one that results in at least 50% excess weight loss at 2 years. Today, the most commonly done operation is the Roux-en-Y gastric bypass (RYGB), with around 35,000 performed annually in the U.S. Other forms of bariatric surgery include Fobi pouch, bilio-pancreatic diversion, and gastroplasty or "stomach stapling". The single existing procedure that involves an implanted device is the Lap-Band, which is a laparoscopically installed inflatable cuff that is placed around the top of the stomach just below the lower esophageal sphincter (LES). This device affects satiety only (no reduced caloric absorption). Because there is more to obesity than simple overeating, it is unlikely that Lap-Band by itself will ever be as effective as a surgery that includes other physiologic feedback mechanisms. Web site: http://www.delphion.com/details?pn=US06558400__ •
Oxadiazole benzenesulfonamides as selective.beta..sub.3 Agonist for the treatment of Diabetes and Obesity Inventor(s): Biftu; Tesfaye (Westfield, NJ), Fisher; Michael H. (Ringoes, NJ), Feng; Danqing Dennis (Branchburg, NJ), Kuo; Chan-Hwa (South Plainfield, NJ), Liang; GuiBai (Scotch Plains, NJ), Naylor; Elizabeth M. (Scotch Plains, NJ), Weber; Ann E. (Scotch Plains, NJ) Assignee(s): Merck & Co., Inc. (Rahway, NJ) Patent Number: 6,034,106 Date filed: June 4, 1997 Abstract: Oxadiazole substituted benzenesulfonamides are selective.beta..sub.3 adrenergic receptor agonists with very little.beta..sub.1 and.beta..sub.2 adrenergic receptor activity and as such the compounds are capable of increasing lipolysis and energy expenditure in cells. The compounds thus have potent activity in the treatment of Type II diabetes and obesity. The compounds can also be used to lower triglyceride
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levels and cholesterol levels or raise high density lipoprotein levels or to decrease gut motility. In addition, the compounds can be used to reduced neurogenic inflammation or as antidepressant agents. The compounds are prepared by coupling an aminoalkylphenyl-sulfonamide with an appropriately substituted epoxide. Compositions and methods for the use of the compounds in the treatment of diabetes and obesity and for lowering triglyceride levels and cholesterol levels or raising high density lipoprotein levels or for increasing gut motility are also disclosed. Excerpt(s):.beta.-Adrenoceptors have been subclassified as.beta..sub.1 and.beta..sub.2 since 1967. Increased heart rate is the primary consequence of.beta..sub.1 -receptor stimulation, while bronchodilation and smooth muscle relaxation typically result from.beta..sub.2 stimulation. Adipocyte lipolysis was initially thought to be solely a.beta..sub.1 -mediated process. However, more recent results indicate that the receptormediating lipolysis is atypical in nature. These atypical receptors, later called.beta..sub.3 -adrenoceptors, are found on the cell surface of both white and brown adipocytes where their stimulation promotes both lipolysis (breakdown of fat) and energy expenditure.... Early developments in this area produced compounds with greater agonist activity for the stimulation of lipolysis (.beta..sub.3 activity) than for stimulation of atrial rate (.beta..sub.1) and tracheal relaxation (.beta..sub.2). These early developments disclosed in Ainsworth et al., U.S. Pat. Nos. 4,478,849 and 4,396,627, were derivatives of phenylethanolamines.... Such selectivity for.beta..sub.3 -adrenoceptors could make compounds of this type potentially useful as antiobesity agents. In addition, these compounds have been reported to show antihyperglycemic effects in animal models of non-insulin-dependent diabetes mellitus. Web site: http://www.delphion.com/details?pn=US06034106__ •
Percutaneous intragastric balloon catheter for the treatment of obesity Inventor(s): De Hoyos Garza; Andres (Mexico City, MX) Assignee(s): none reported Patent Number: 6,454,785 Date filed: February 23, 2001 Abstract: The present invention relates to a percutaneous intragastric balloon catheter for the treatment of obesity. The invention occupies a portion of the gastric cavity causing a feeling of satiety and decreasing the consumption of food by an obese patient. This invention consists in a percutaneous intragastric balloon that is placed in a nonsurgically form. The percutaneous intragastric balloon catheter is collocated by percutaneous endoscopic gastrotomy (PEG). The invention comprises an affixed valve for regulating the amount of fluid introduced or evacuated from the percutaneous intragastric balloon. Excerpt(s): This invention relates to gastrostomy devices for use in the treatment of obesity. More particularly, the invention relates to percutaneous balloon catheters positioned in the stomach for medical treatment of morbid obesity in humans.... Morbid obesity is a chronic medical illness defined as overweight of 50 to 100 percent above the ideal body weight. Obesity is a major medical problem affecting millions of people worldwide. In addition to the phychosocial stigmas associated with the condition or disease, many serious health ramifications may develop. Hypertension, hyperlipidemia, exacerbation of diabetes mellitus, heart disease, degenerative arthritis, and Pickwickian syndrome. Certain types of cancer, gallstones, varicose veins, thromboembolism and
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hernias are more common among overweight individuals. In addition, morbid obesity can lead to psychosocial difficulties such as depression, loss of self-esteem and decreased employability.... To date, numerous attempts have been made to cause weight loss in morbidly obese patients. None of them have been entirely successful. The weight loss methods can be broadly divided into behavioral modification, vigorous exercise, use of pharmaceuticals, medical diets, surgical procedures and devices. Web site: http://www.delphion.com/details?pn=US06454785__ •
Peroral apparatus for morbid obesity treatment Inventor(s): Angelchik; Jean P. (1728 W. Glendale Ave., Phoenix, AZ 85021) Assignee(s): none reported Patent Number: 4,648,383 Date filed: July 22, 1985 Abstract: Apparatus for peroral treatment of morbid obesity includes a collapsible intragastric appliance which can be temporarily deformed to pass through the esophagus and cardiac opening of the stomach and to autogenously assume a normal shape after it is received in the stomach to stimulate neuro-receptors in the sub-mucosa of the gastric fundus. Means are provided for detachably connecting the appliance to the lower end of an elongate, semi-rigid inserter rod which is passed through an aperture formed in the appliance to effect the detachable connection. Downward pressure on the inserter rod forces the collapsed appliance through the esophagus and cardiac opening into the stomach and slight upward force of the inserter rod is thereafter applied to detach the rod from the appliance. Excerpt(s): This invention relates to apparatus for peroral treatment of morbid obesity without surgery.... In still another aspect, the invention concerns such improved apparatus in which a collapsible intra-gastric appliance is emplaced in the gastric fundus with improved convenience and reduced discomfort for the patient.... In still another aspect the invention relates to peroral emplaceable applicances for treatment of morbid obesity which may have biodegradable parts which dissolve under normal stomach conditions after a preselected time to permit the remains of the appliance to be passed from the body through the intestines, such that removal of the appliance by surgery is unnecessary. Web site: http://www.delphion.com/details?pn=US04648383__
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Pharmaceutical composition for treatment of obesity Inventor(s): Langer; Salomon (Paris, FR) Assignee(s): Synthelabo (Paris, FR) Patent Number: 4,791,119 Date filed: September 9, 1987 Abstract: A method of treatment of obesity which comprises administering to a subject liable thereto or suffering therefrom an effective dose of 4-(2naphthylmethoxy)piperidine.
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Excerpt(s): The present invention relates to pharmaceutical compositions.... 4-(2naphthylmethoxy)piperidine is described in French Patent of Addition No. 81/19,025 (2,514,353) dated Oct. 9, 1981, to Pat. No. 80/09,513, as having antidepressant properties.... We have suprisingly found, according to the present invention, that 4-(2naphthylmethoxy)piperidine possesses anorexigenic properties and that it may therefore be employed in the treatment of obesity. Web site: http://www.delphion.com/details?pn=US04791119__ •
Polypeptide for obesity and type II diabetes mellitus Inventor(s): Shuldiner; Alan R. (Columbia, MD), Walston; Jeremy (Baltimore, MD), Silver; Kristi (Baltimore, MD), Roth; Jesse (Baltimore, MD) Assignee(s): The Johns Hopkins University School of Medicine (Baltimore, MD) Patent Number: 5,877,283 Date filed: June 15, 1998 Abstract: The present invention provides a novel polypeptide characterized by a nonconservative missense mutation, Trp64Arg, in the.beta.3-adrenergic receptor (.beta.3AR) that increases susceptibility to obesity and non-insulin dependent diabetes mellitus (NIDDM; type II diabetes). Also provided are methods of diagnosis and methods of treatment of subjects having or at risk of having type II diabetes/obesity. Excerpt(s): This invention relates generally to non-insulin dependent diabetes mellitus (NIDDM) (type II) and obesity, and specifically to a novel Trp64Arg mutation in the.beta.3-adrenergic receptor that increases susceptibility to obesity and type II diabetes.... Non-insulin dependent diabetes mellitus (NIDDM) is one of the most common inherited diseases in man with an estimated prevalence in Caucasian populations of 8-10% (Harris, et al., Diabetes, 36:523-534, 1987). Although most forms of NIDDM do not exhibit simple Mendelian inheritance, the contribution of heredity is well recognized (Rotter, et al., Diabetes Mellitus: Theory and Practice, 378-413, 1990). The genetic basis of a few rare monogenic syndromes of NIDDM have been elucidated, but together, these syndromes account for a very small minority of cases (Taylor, et al., Endocrine Rev., 13:566-595, 1992; Froguel, et al., N. Engl. J. Med., 328:697-702, 1993; Steiner, et al., Diabetes Care, 13:600-609, 1990; and Kadowaki, et al., N. Engl. J. Med., 330:962-968, 1994). It is likely that the common forms of NIDDM are complex and heterogenous, and result when a pool of mutant genes, each of which contributes modestly and in a subtle way, interact with each other and with environmental, aging and behavioral influences to lead to the expression of the disease. This pool of genes may vary between populations and among individuals within a population, despite the illusion of a clinically homogenous phenotype.... Obesity is a known risk factor for the development of NIDDM (Barrett-Conner, E., Epidemiol. Rev., 11:172-181, 1989; and Knowler, et al., Am. J. Clin. Nutr., 53:1543-1551, 1991), and although less well studied than NIDDM, also has clear genetic determinants (Bouchard, C., World Rev. Nutr. Diet, 72:68-77, 1993; and Stunkard, et al., N. Engl. J. Med., 314:193-197,1986). Potential candidate genes for obesity (and therefore also NIDDM) include those that influence energy expenditure. In adult Pima Indians, resting metabolic rate (RMR) is familial (Bogardus, et al., N. Engl. J Med, 315:96-100, 1986 ), and in prospective studies, a low RMR is a risk factor for weight gain and obesity (Ravussin, et al., N. Engl. J Med, 318:467-472, 1988). Studies in other populations (Bouchard, et al., Metabolism, 38:364370, 1989; and Griffith, et al., Lancet, 336:76-78, 1990), as well as in animal models (Coleman, D. L., Diabetes, 31:1-6, 1992), support the relationship between heredity, low
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RMR and obesity. In rodents, RMR is regulated by the sympathetic nervous system and acts through modulation of thermogenesis in brown adipose tissue (Lowell, et al., Nature, 366:740-749, 1993). Although humans do not have anatomically distinct deposits of brown adipose tissue, the identification of human uncoupling protein, a molecular marker widely regarded as being specific for brown adipose tissue, suggests that modulation of thermogenesis in adipose tissue may also be important in humans (Cassard, et al., J. Cell Biochem., 43:255-264, 1990). Web site: http://www.delphion.com/details?pn=US05877283__ •
Polypeptides involved in body weight disorders, including obesity Inventor(s): Tartaglia; Louis Anthony (Waterstown, MA) Assignee(s): Millennium Pharmaceuticals, Inc. (Cambridge, MA) Patent Number: 5,861,485 Date filed: June 6, 1995 Abstract: The present invention relates to methods and compositions for the treatment of body weight disorders, including, but not limited to, obesity. Specifically, the present invention identifies and describes genes which are differentially expressed in body weight disorder states, relative to their expression in normal, or non-body weight disorder states, and/or in response to manipulations relevant to appetite and/or weight regulation. Further, the present invention identifies and describes genes via the ability of their gene products to interact with gene products involved in body weight disorders and/or appetite and/or body weight regulation. Still further, the present invention provides methods for the identification and therapeutic use of compounds as treatments of body weight disorders. Additionally, the present invention describes methods for the diagnostic evaluation and prognosis of various body weight disorders, and for the identification of subjects exhibiting a predisposition to such conditions. Excerpt(s): The present invention relates to methods and compositions for the treatment of body weight disorders, including, but not limited to, obesity. Specifically, the present invention identifies and describes genes which are differentially expressed in body weight disorder states, relative to their expression in normal, or non-body weight disorder states, and also identifies genes which are differentially expressed in response to manipulations relevant to appetite and/or weight regulation. Further, the present invention identifies and describes genes via the ability of their gene products to interact with gene products involved in body weight disorders and/or to interact with gene products which are relevant to appetite and/or body weight regulation. Still further, the present invention provides methods for the identification and therapeutic use of compounds as treatments of body weight disorders. Additionally, the present invention describes methods for the diagnostic evaluation and prognosis of various body weight disorders, and for the identification of subjects exhibiting a predisposition to such conditions.... Body weight disorders, including eating disorders, represent major health problems in all industrialized countries. Obesity, the most prevalent of eating disorders, for example, is the most important nutritional disorder in the western world, with estimates of its prevalence ranging from 30% to 50% within the middle-aged population. Other body weight disorders, such as anorexia nervosa and bulimia nervosa which together affect approximately 0.2% of the female population of the western world, also pose serious health threats. Further, such disorders as anorexia and cachexia (wasting) are also prominent features of other diseases such as cancer, cystic fibrosis, and AIDS.... Obesity, defined as an excess of body fat relative to lean body mass, also contributes to
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other diseases. For example, this disorder is responsible for increased incidences of diseases such as coronary artery disease, stroke, and diabetes. Obesity is not merely a behavioral problem, i.e., the result of voluntary hyperphagia. Rather, the differential body composition observed between obese and normal subjects results from differences in both metabolism and neurologic/metabolic interactions. These differences seem to be, to some extent, due to differences in gene expression, and/or level of gene products or activity. The nature, however, of the genetic factors which control body composition are unknown, and attempts to identify molecules involved in such control have generally been empiric and the parameters of body composition and/or substrate flux are monitored have not yet been identified (Friedman, J. M. et al., 1991, Mammalian Gene 1:130-144). Web site: http://www.delphion.com/details?pn=US05861485__ •
Process and device for treating obesity and syndromes related to motor disorders of the stomach of a patient Inventor(s): Cigaina; Valerio (Via 4 Novembre 3a, 31050 Villorba (Treviso) Assignee(s): none reported Patent Number: 5,423,872 Date filed: May 26, 1993 Abstract: The process for treating obesity and syndromes related to motor disorders of the stomach of a patient consists in artificially altering, by means of sequential electrical pulses and for preset periods of time, the natural gastric motility of the patient to prevent emptying or to slow down gastric transit. Excerpt(s): The present invention relates to a process and to a device for treating obesity and syndromes related to motor disorders of the stomach of a patient. As is known, the treatment of obesity related to hyperalimentation, i.e. to a subject who introduces food in excess of his actual caloric requirements (energy expenditure related to motor activity, work, environmental activity, etc.) is based on psychotherapeutic, pharmacological or dietary provisions or, in selected cases (pathogenic obesity), on surgical provisions.... The modern surgical orientation (surgery is the only therapy that ensures real results in patients who have exceeded obesity values close to, or in excess of, 40 BMI, i.e. the ratio of weight to the square of the height) entails the reduction of gastric compliance, with the aim of limiting the subject's ability to ingest food, or of reducing the food absorption surface by shortening or bypassing part of the digestive canal; both aims are sought in some surgical procedures.... All of the surgical procedures currently in use have some immediate and/or delayed risks and surgery must thus be considered as an extreme solution. Web site: http://www.delphion.com/details?pn=US05423872__
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Process for electrostimulation treatment of morbid obesity Inventor(s): Cigaina; Valerio (Treviso, IT) Assignee(s): Transneuronix, Inc. (Mt. Arlington, NJ) Patent Number: 6,615,084 Date filed: November 15, 2000
Patents 317
Abstract: An improved process using electrostimulation for treating obesity, especially morbid obesity, and other syndromes related to motor disorders of the stomach is provided. The improved method of this invention provides electrostimulation on the lesser curvature of the stomach, preferably on the lower or distal end of the lesser curvature, which provides improved control of obesity and other syndromes related to motor disorders of the stomach. In one embodiment, the process employs stimulation of the lesser curvature at a rate of about 2 to about 14 pulses/minute with each pulse lasting about 0.5 to about 4 seconds such that there is a pause of about 3 to about 30 between the pulses. Preferably, the pulse rate is about 12 pulses/minute with each pulse lasting about 2 seconds with a pause of about 3 seconds between pulses. Preferably, the pulse amplitude is about 0.5 to about 15 milliamps. More preferable, each pulse consists of a train of micro-bursts with a frequency of about 5 to about 100 sec.sup.-1. Excerpt(s): The present invention relates to an improved process using electrostimulation for treating obesity, especially morbid obesity, and other syndromes related to motor disorders of the stomach. The improved method of this invention provides electrostimulation on the lesser curvature of the stomach which provides improved control of obesity and other syndromes related to motor disorders of the stomach.... The modern surgical orientation with regard to obesity generally entails the reduction of gastric compliance, with the aim of limiting the subject's ability to ingest food, or of reducing the food absorption surface by shortening or bypassing part of the digestive canal; both aims are sought in some surgical procedures. Until recently, surgery was the only therapy that ensures real results in patients who have exceeded obesity values close to or greater than about 40 BMI (ratio of weight to the square of the height).... All of the major surgical procedures (e.g., removal or blocking off of a portion of the stomach) currently in use have some immediate and/or delayed risks. Thus, surgery is usually considered as an extreme solution when all less invasive procedures fail. Furthermore, even surgical treatment fails in some cases, thereby requiring the surgeon to restore the original anatomical situation. Web site: http://www.delphion.com/details?pn=US06615084__ •
Process for preparing anti-obesity protein Inventor(s): MacKellar; Warren C. (Plainfield, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,614,379 Date filed: April 26, 1995 Abstract: The present invention is directed to a novel process of preparing an antiobesity protein using dipeptidyl-aminopeptidase isolated from the cellular slime mold, Dictyostelium discodeum. The process produces an anti-obesity protein in high yield. Excerpt(s): This invention is in the field of biotechnology. More specifically, this invention concerns a process for preparing an anti-obesity protein of SEQ ID NO: 1 using dipeptidyl-aminopeptidase isolated from the slime mold, Dictyostelium discoideum.... Obesity, and especially upper body obesity, is a common and very serious public health problem in the United States and throughout the world. According to recent statistics, more than 25% of the United States population and 27% of the Canadian population are over weight. Kuczmarski, Amer. J. of Clin. Nut. 55: 495S-502S (1992); Reeder et. al., Can. Med. Ass. J., 23:226-233 (1992). Upper body obesity is the strongest risk factor known for type II diabetes mellitus, and is a strong risk factor for
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cardiovascular disease and cancer as well. Recent estimates for the medical cost of obesity are $150,000,000,000 world wide. The problem has become serious enough that the surgeon general has begun an initiative to combat the ever increasing adiposity rampant in American society.... Much of this obesity induced pathology can be attributed to the strong association with dyslipidemia, hypertension, and insulin resistance. Many studies have demonstrated that reduction in obesity by diet and exercise reduces these risk factors dramatically. Unfortunately, these treatments are largely unsuccessful with a failure rate reaching 95%. This failure may be due to the fact that the condition is strongly associated with genetically inherited factors that contribute to increased appetite, preference for highly caloric foods, reduced physical activity, and increased lipogenic metabolism. This indicates that people inheriting these genetic traits are prone to becoming obese regardless of their efforts to combat the condition. Therefore, a pharmacological agent that can correct this adiposity handicap and allow the physician to successfully treat obese patients in spite of their genetic inheritance is needed. Web site: http://www.delphion.com/details?pn=US05614379__ •
Process for preparing obesity protein analogs Inventor(s): Atkinson; Paul Robert (Indianapolis, IN), Foster; Lisa Kay (Greenwood, IN), Furman; Thomas Charles (Indianapolis, IN), MacKellar; Warren Cameron (Plainfield, IN) Assignee(s): Eli Lilly and Company (Indianapolis, IN) Patent Number: 5,840,517 Date filed: March 24, 1997 Abstract: The present invention is directed to an improved process for preparing in high yield an obesity protein analog using a dipeptidylaminopeptidase isolated from the slime mold, Dictyostelium discoideum. Excerpt(s): 1. Field of the Invention.... This invention is in the field of enzyme technology. More specifically, this invention concerns a process for preparing an obesity protein analog using dipeptidylaminopeptidase isolated from the slime mold, Dictyostelium discoideum.... 2. Background Information. Web site: http://www.delphion.com/details?pn=US05840517__
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Prolonged acting appetite suppressant and anti-obesity compositions containing amphetamine adipate, dextroamphetamine adipate, amphetamine sulfate and dextroamphetamine sulfate as the active agents Inventor(s): Cohen; Louis (Yonkers, NY) Assignee(s): Delco Chemical Company, Inc. (Mount Vernon, NY) Patent Number: 4,049,791 Date filed: January 26, 1976 Abstract: A prolonged acting appetite suppressant and anti-obesity composition in oral administration form which comprises an effective amount of a synergistic combination of amphetamine adipate, dextroamphetamine adipate, amphetamine sulfate and dextroamphetamine sulfate in equal or substantially equal amounts as the active agents
Patents 319
in combination with a pharmaceutically acceptable carrier and is useful in suppressing one's appetite and in treating obesity. Excerpt(s): The present invention is concerned with prolonged-acting appetite suppressant and anit-obesity compositions. More particularly, the present invention is concerned with compositions in oral administration form which comprise an effective amount of a combination of at least two active agents selected from the group consisting of amphetamine adipate, dextroamphetamine adipate, amphetamine sulfate and dextroamphetamine sulfate in combination with a pharmaceutically-acceptable solid vehicle or carrier.... The compositions are preferably in the form of tablets or capsules.... The compositions of the present invention are effective for diminishing the rate of excretion by prolonging blood levels above the minimum effective concentration while avoiding peak concentrations and those side effects which may be encountered with respect to prior known amphetamine preparations. The use of a combination of the active agents set forth above have a stabilizing effect on the enzyme d-amino oxidase thereby prolonging appetite-suppressant effect of amphetamine and dextroamphetamine in the treatment of exogenous obesity while reducing undesired or adverse side effects encountered with amphetamine and dextroamphetamine. Web site: http://www.delphion.com/details?pn=US04049791__ •
Stereotactic hypothalamic obesity probe Inventor(s): Howard, III; Matthew A. (Iowa City, IA) Assignee(s): The University of Iowa Research Foundation (Iowa City, IA) Patent Number: 6,129,685 Date filed: June 27, 1997 Abstract: Apparatus and methods for regulating the appetite of an individual suffering from morbid obesity, the apparatus including a plurality of stimulation electrodes arranged longitudinally on at least one electrode support shaft for insertion within the hypothalamus for outputting electrical discharges to specific sites within the hypothalamus. Each of the plurality of stimulation electrodes may be independently controlled. Electrical discharge of various frequencies transmitted from one or more of the plurality of stimulation electrodes, and delivered to a region of the hypothalamus that is involved with either stimulating or inhibiting appetite, may be used to regulate appetite in the individual. Alternatively, an individual's appetite may be regulated by the microinfusion from at least one microinfusion catheter of an appropriate quantity of a suitable drug to a distinct site or region within the hypothalamus. Excerpt(s): This invention relates generally to an apparatus and method for delivering and detecting electrical signals to/from the patient's brain. In one embodiment, this invention also relates to an apparatus and method for performing ablative surgery on a patient. In particular the invention is concerned with an apparatus and method for performing brain surgery; and more particularly the invention is concerned with an apparatus and method for performing brain surgery by monitoring and selectively inactivating specific regions within the brain. The invention is also concerned with an apparatus and method for delivering therapeutic drugs, and more particularly is concerned with an apparatus and method for delivering therapeutic drug to a specific region within a patient's brain tissues, by monitoring and selectively delivering a drug to the target tissue. In one embodiment, this invention also relates to an apparatus and method for selective electrical stimulation of a patient's hypothalamus for the purpose of
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appetite regulation. In yet another embodiment, this invention relates to an apparatus and method for localized drug treatment for the purpose of appetite regulation by drug microinfusion into certain regions of the hypothalamus.... Prior to the nineteenth century, physicians and scientists believed the brain was an organ with functional properties distributed equally through its mass. Localization of specific functions within subregions of the brain was first demonstrated in the 1800's, and provided the fundamental conceptual framework for all of modern neuroscience and neurosurgery.... As it became clear that brain subregions served specific functions such as movement of the extremities, and touch sensation, it was also noted that direct electrical stimulation of the surface of these brain regions could cause partial reproduction of these functions. Morgan, J. P., "The first reported case of electrical stimulation of the human brain," J. History of Medicine, January 1982:51-63, 1982; Walker, A. E., "The development of the concept of cerebral localization in the nineteenth century," Bull. Hist. Med., 31:99-121, 1957. Web site: http://www.delphion.com/details?pn=US06129685__ •
Substituted benzylidene hydrazines for treating hyperglycemia, obesity and inflammation Inventor(s): Houlihan; William J. (Mountain Lakes, NJ), Manning; Robert E. (Mountain Lakes, NJ) Assignee(s): Sandoz, Inc. (E. Hanover, NJ) Patent Number: 3,982,020 Date filed: September 5, 1972 Abstract: Substituted benzylidene hydrazines e.g. N-(4-phenylbenzylidene)-N'-amidino hydrazine and their use as hypoglycemic-antihyperglycemic agents, anti-obesity agents and anti-inflammatory agents. Excerpt(s): This invention relates to substituted benzylidene hydrazines. More particularly, it relates to novel N-(4-substituted benzylidene)-N' amidino hydrazines and acid addition salts thereof. The invention also relates to the use of these and other substituted benzylidene hydrazines as hypoglycemic-antihyperglycemic agents, antiobesity agents and anti-inflammatory agents to pharmaceutical compositions containing the compounds as an active ingredient thereof, and the method of using such compositions for the treatment of hyperglycemia, obesity and inflammation.... 4. both R.sup.1 and R.sup.5 are methyl only, when R.sub.2, R.sub.3 and R.sub.4 are other than hydrogen.... Where R.sup.1, R.sup.2, R.sup.3, R.sup.4 and R.sup.5 are as defined above. Web site: http://www.delphion.com/details?pn=US03982020__
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Substituted or unsubstituted 2-phenylbenzimidazoles as anti-obesity agents Inventor(s): Houlihan; William J. (Mt. Lakes, NJ) Assignee(s): Sandoz, Inc. (E. Hanover, NJ) Patent Number: 4,212,876 Date filed: June 21, 1978 Abstract: Certain substituted or unsubstituted 2-phenylbenzimidazoles, e.g., 1-methyl-2phenylbenzimidazole, are useful as anti-obesity agents.
Patents 321
Excerpt(s): This invention relates to the pharmaceutical activity of substituted or unsubstituted 2-phenylbenzimidazoles. More particularly, this invention concerns the use of substituted or unsubstituted 2-phenylbenzimidazoles in the treatment of obesity. The invention also relates to pharmaceutical compositions containing these compounds as an active ingredient thereof.... R.sub.2 represents hydrogen, fluoro or chloro.... The compounds of formula (I) above are known and may be prepared according to methods disclosed in the literature from known materials. The present invention contemplates only the novel use of such compounds as anti-obesity agents. Web site: http://www.delphion.com/details?pn=US04212876__ •
Substituted phenyl sulfonamides as selective.beta. 3 agonists for the treatment of diabetes and obesity Inventor(s): Fisher; Michael H. (Ringoes, NJ), Mathvink; Robert J. (Jersey City, NJ), Ok; Hyun O. (Edison, NJ), Parmee; Emma R. (Hoboken, NJ), Weber; Ann E. (Scotch Plains, NJ) Assignee(s): Merck & Co., Inc. (Rahway, NJ) Patent Number: 5,451,677 Date filed: December 15, 1993 Abstract: Substituted phenylsulfonamides are selective.beta..sub.3 adrenergic receptor agonists with very little.beta..sub.1 and.beta..sub.2 adrenergic receptor activity and as such the compounds are capable of increasing lipolysis and energy expenditure in cells. The compounds thus have potent activity in the treatment of Type II diabetes and obesity. The compounds can also be used to lower triglyceride levels and cholesterol levels or raise high density lipoprotein levels or to decrease gut motility. In addition, the compounds can be used to reduced neurogenic inflammation or as antidepressant agents. The compounds are prepared by coupling an aminoalkylphenyl-sulfonamide with an appropriately substituted alkyl epoxide. Compositions and methods for the use of the compounds in the treatment of diabetes and obesity and for lowering triglyceride levels and cholesterol levels or raising high density lipoprotein levels or for increasing gut motility are also disclosed. Excerpt(s):.beta.-Adrenoceptors have been subclassified as.beta..sub.1 and.beta..sub.2 since 1967. Increased heart rate is the primary consequence of.beta..sub.1 -receptor stimulation, while bronchodilation and smooth muscle relaxation typically result from.beta..sub.2 stimulation. Adipocyte lipolysis was initially thought to be solely a.beta..sub.1 -mediated process. However, more recent results indicate that the receptormediating lipolysis is atypical in nature. These atypical receptors, later called.beta..sub.3 -adrenoceptors, are found on the cell surface of both white and brown adipocytes where their stimulation promotes both lipolysis (breakdown of fat) and energy expenditure.... Early developments in this area produced compounds with greater agonist activity for the stimulation of lipolysis (.beta..sub.3 activity) than for stimulation of atrial rate (.beta..sub.1) and tracheal relaxtion (.beta..sub.2)- These early developments disclosed in Ainsworth et al., U.S. Pat. Nos. 4,478,849 and 4,396,627, were derivatives of phenylethanolamines.... Such selectivity for.beta..sub.3 -adrenoceptors could make compounds of this type potentially useful as antiobesity agents. In addition, these compounds have been reported to show antihyperglycemic effects in animal models of non-insulin-dependent diabetes mellitus. Web site: http://www.delphion.com/details?pn=US05451677__
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Substituted sulfonamides as selective.beta..sub.3 agonists for the treatment of diabetes and obesity Inventor(s): Fisher; Michael H. (Ringoes, NJ), Naylor; Elizabeth M. (Scotch Plains, NJ), Ok; Dong (Edison, NJ), Weber; Ann E. (Scotch Plains, NJ), Shih; Thomas (Edison, NJ), Ok; Hyun (Edison, NJ) Assignee(s): Merck & Co., Inc. (Rahway, NJ) Patent Number: 5,561,142 Date filed: May 22, 1995 Abstract: Substituted sulfonamides are selective.beta..sub.3 adrenergic receptor agonists with very little.beta..sub.1 and.beta..sub.2 adrenergic receptor activity and as such the compounds are capable of increasing lipolysis and energy expenditure in cells. The compounds thus have potent activity in the treatment of Type II diabetes and obesity. The compounds can also be used to lower triglyceride levels and cholesterol levels or raise high density lipoprotein levels or to decrease gut motility. In addition, the compounds can be used to reduced neurogenic inflammation or as antidepressant agents. The compounds are prepared by coupling an aminoalkylphenyl-sulfonamide with an appropriately substituted epoxide. Compositions and methods for the use of the compounds in the treatment of diabetes and obesity and for lowering triglyceride levels and cholesterol levels or raising high density lipoprotein levels or for increasing gut motility are also disclosed. Excerpt(s):.beta.-Adrenoceptors have been subclassified as.beta..sub.1 and.beta..sub.2 since 1967. Increased heart rate is the primary consequence of.beta..sub.1 -receptor stimulation, while bronchodilation and smooth muscle relaxation typically result from.beta..sub.2 stimulation. Adipocyte lipolysis was initially thought to be solely a.beta..sub.1 -mediated process. However, more recent results indicate that the receptormediating lipolysis is atypical in nature. These atypical receptors, later called.beta..sub.3 -adrenoceptors, are found on the cell surface of both white and brown adipocytes where their stimulation promotes both lipolysis (breakdown of fat) and energy expenditure.... Early developments in this area produced compounds with greater agonist activity for the stimulation of lipolysis (.beta..sub.3 activity) than for stimulation of atrial rate (.beta..sub.1) and tracheal relaxation (.beta..sub.2). These early developments disclosed in Ainsworth et al., U.S. Pat. Nos. 4,478,849 and 4,396,627, were derivatives of phenylethanolamines.... Such selectivity for.beta..sub.3 -adrenoceptors could make compounds of this type potentially useful as antiobesity agents. In addition, these compounds have been reported to show antihyperglycemic effects in animal models of non-insulin-dependent diabetes mellitus. Web site: http://www.delphion.com/details?pn=US05561142__
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Substituted sulfonamides as selective.beta.-3 agonists for the treatment of diabetes and obesity Inventor(s): Fisher; Michael H. (Ringoes, NJ), Naylor; Elizabeth M. (Scotch Plains, NJ), Parmee; Emma R. (Hoboken, NJ), Shih; Thomas (Edison, NJ), Ok; Hyun (Edison, NJ), Weber; Ann E. (Scotch Plains, NJ) Assignee(s): Merck & Co., Inc. (Rahway, NJ) Patent Number: 5,705,515 Date filed: July 25, 1996
Patents 323
Abstract: Substituted sulfonamides are selective.beta..sub.3 adrenergic receptor agonists with very little.beta..sub.1 and.beta..sub.2 adrenergic receptor activity and as such the compounds are capable of increasing lipolysis and energy expenditure in cells. The compounds thus have potent activity in the treatment of Type II diabetes and obesity. The compounds can also be used to lower triglyceride levels and cholesterol levels or raise high density lipoprotein levels or to decrease gut motility. In addition, the compounds can be used to reduced neurogenic inflammation or as antidepressant agents. The compounds are prepared by coupling an aminoalkylphenyl-sulfonamide with an appropriately substituted epoxide. Compositions and methods for the use of the compounds in the treatment of diabetes and obesity and for lowering triglyceride levels and cholesterol levels or raising high density lipoprotein levels or for increasing gut motility are also disclosed. Excerpt(s):.beta.-Adrenoceptors have been subclassified as.beta..sub.1 and.beta..sub.2 since 1967. Increased heart rate is the primary consequence of.beta..sub.1 -receptor stimulation, while bronchodilation and smooth muscle relaxation typically result from.beta..sub.2 stimulation. Adipocyte lipolysis was initially thought to be solely a.beta..sub.1 -mediated process. However, more recent results indicate that the receptormediating lipolysis is atypical in nature. These atypical receptors, later called.beta..sub.3 -adrenoceptors, are found on the cell surface of both white and brown adipocytes where their stimulation promotes both lipolysis (breakdown of fat) and energy expenditure.... Early developments in this area produced compounds with greater agonist activity for the stimulation of lipolysis (.beta..sub.3 activity) than for stimulation of atrial rate (.beta..sub.1) and tracheal relaxation (.beta..sub.2). These early developments disclosed in Ainsworth et al., U.S. Pat. Nos. 4,478,849 and 4,396,627, were derivatives of phenylethanolamines.... Such selectivity for.beta..sub.3 -adrenoceptors could make compounds of this type potentially useful as antiobesity agents. In addition, these compounds have been reported to show antihyperglycemic effects in animal models of non-insulin-dependent diabetes mellitus. Web site: http://www.delphion.com/details?pn=US05705515__ •
Susceptibility gene for obesity and type II diabetes mellitus Inventor(s): Shuldiner; Alan R. (Columbia, MD), Walston; Jeremy (Baltimore, MD), Silver; Kristi (Baltimore, MD), Roth; Jesse (Baltimore, MD) Assignee(s): The Johns Hopkins University School of Medicine (Baltimore, MD) Patent Number: 5,766,851 Date filed: May 19, 1995 Abstract: The present invention provides a novel polypeptide characterized by a nonconservative missense mutation, Trp64Arg, in the.beta.3-adrenergic receptor (.beta.3AR) that increases susceptibility to obesity and non-insulin dependent diabetes mellitus (NIDDM; type II diabetes). Also provided are methods of diagnosis and methods of treatment of subjects having or at risk of having type II diabetes/obesity. Excerpt(s): This invention relates generally to non-insulin dependent diabetes mellitus (NIDDM) (type II) and obesity, and specifically to a novel Trp64Arg mutation in the.beta.3-adrenergic receptor that increases susceptibility to obesity and type II diabetes.... Non-insulin dependent diabetes mellitus (NIDDM) is one of the most common inherited diseases in man with an estimated prevalence in Caucasian populations of 8-10% (Harris, et al., Diabetes, 36:523-534, 1987). Although most forms of
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NIDDM do not exhibit simple Mendelian inheritance, the contribution of heredity is well recognized (Rotter, et al., Diabetes Mellitus: Theory and Practice, 378-413, 1990). The genetic basis of a few rare monogenic syndromes of NIDDM have been elucidated, but together, these syndromes account for a very small minority of cases (Taylor, et al., Endocrine Rev., 13:566-595, 1992; Froguel, et al., N. Engl. J. Med., 328:697-702, 1993; Steiner, et al., Diabetes Care, 13:600-609, 1990; and Kadowaki, et al., N. Engl. J. Med., 330:962-968, 1994). It is likely that the common forms of NIDDM are complex and heterogenous, and result when a pool of mutant genes, each of which contributes modestly and in a subtle way, interact with each other and with environmental, aging and behavioral influences to lead to the expression of the disease. This pool of genes may vary between populations and among individuals within a population, despite the illusion of a clinically homogenous phenotype.... Obesity is a known risk factor for the development of NIDDM (Barrett-Conner, E., Epidemiol. Rev., 11:172-181, 1989; and Knowler, et al., Am. J. Clin. Nutr., 53:1543-1551, 1991), and although less well studied than NIDDM, also has clear genetic determinants (Bouchard, C., World Rev. Nutr. Diet, 72:68-77, 1993; and Stunkard, et al., N. Engl. J. Med., 314:193-197, 1986). Potential candidate genes for obesity (and therefore also NIDDM) include those that influence energy expenditure. In adult Pima Indians, resting metabolic rate (RMR) is familial (Bogardus, et al., N. Engl. J. Med., 315:96-100, 1986), and in prospective studies, a low RMR is a risk factor for weight gain and obesity (Ravussin, et al., N. Engl. J. Med., 318:467-472, 1988). Studies in other populations (Bouchard, et al., Metabolism, 38:364370, 1989; and Griffith, et al., Lancet, 336:76-78, 1990), as well as in animal models (Coleman, D. L., Diabetes, 31:1-6, 1992), support the relationship between heredity, low RMR and obesity. In rodents, RMR is regulated by the sympathetic nervous system and acts through modulation of thermogenesis in brown adipose tissue (Lowell, et al., Nature, 366:740-749, 1993). Although humans do not have anatomically distinct deposits of brown adipose tissue, the identification of human uncoupling protein, a molecular marker widely regarded as being specific for brown adipose tissue, suggests that modulation of thermogenesis in adipose tissue may also be important in humans (Cassard, et al., J. Cell Biochem., 43:255-264, 1990). Web site: http://www.delphion.com/details?pn=US05766851__ •
System for preventing and curing osteoporosis and obesity Inventor(s): Hirano; Shinnosuke (Kanagawa, JP) Assignee(s): Kohgen Kizai Kabushiki Kaisha (Yokohama, JP) Patent Number: 5,836,997 Date filed: November 25, 1996 Abstract: A system for preventing and curing osteoporosis and obesity, which has a mat essentially consisting of a first sheet made from a semiconductive or insulating material and having a volume resistivity of less than 10.sup.4.OMEGA..cm and a second sheet made from a semiconductive or insulating material, laminated on the first sheet and having a volume resistivity of 10.sup.4.OMEGA..cm or more; an electric power source; an electrical circuit to apply DC voltage of 25-800 to the first sheet; and a control unit. A normal person or patient is made contact with the mat, so as to put his body in electrostatic field to be formed on the mat. In another embodiment, a third sheet of a material having a volume resistivity of more than 10.sup.12.OMEGA..cm is used such that the first sheet is sandwiched between the third and second sheets.
Patents 325
Excerpt(s): The present invention relates to a system for preventing and curing osteoporosis and obesity, by putting a human body in an electrostatic field.... In recent years, medical techniques have greatly advanced to prolong the average span of human life and as a result, so-called "adult and senior diseases" tend to increase. Therefore, it has been emphasized in the medical world that so-called "Health medical science" will be required, in which each individual controls his health by himself to prevent a disease or pays his possible effort to overcome the diseases.... Among the diseases, osteoporosis has often been found in senior persons and women in menopause and it has been said that number of the patients with this disease reaches 6 million or more, even in Japan only. Web site: http://www.delphion.com/details?pn=US05836997__ •
Thiazole benzenesulfonamides as.beta.3 agonists for treatment of diabetes and obesity Inventor(s): Mathvink; Robert J. (Red Bank, NJ), Parmee; Emma R. (Highland Park, NJ), Tolman; Samuel (Jersey City, NJ), Weber; Ann E. (Scotch Plains, NJ) Assignee(s): Merck & Co., Inc. (Rahway, NJ) Patent Number: 6,011,048 Date filed: January 15, 1998 Abstract: Thiazole substituted benzenesulfonamides are.beta..sub.3 adrenergic receptor agonists with very little.beta..sub.1 and.beta..sub.2 adrenergic receptor activity and as such the compounds are capable of increasing lipolysis and energy expenditure in cells. The compounds thus have potent activity in the treatment of Type II diabetes and obesity. The compounds can also be used to lower triglyceride levels and cholesterol levels or raise high density lipoprotein levels or to decrease gut motility. In addition, the compounds can be used to reduced neurogenic inflammation or as antidepressant agents. The compounds are prepared by coupling an aminoalkylphenyl-sulfonamide with an appropriately substituted epoxide. Compositions and methods for the use of the compounds in the treatment of diabetes and obesity and for lowering triglyceride levels and cholesterol levels or raising high density lipoprotein levels or for decreasing gut motility are also disclosed. Excerpt(s):.beta.-Adrenoceptors have been subclassified as.beta..sub.1 and.beta..sub.2 since 1967. Increased heart rate is the primary consequence of.beta..sub.1 -receptor stimulation, while bronchodilation and smooth muscle relaxation typically result from.beta..sub.2 stimulation. Adipocyte lipolysis was initially thought to be solely a.beta..sub.1 -mediated process. However, more recent results indicate that the receptor mediating lipolysis is atypical in nature. These atypical receptors, later called.beta..sub.3 -adrenoceptors, are found on the cell surface of both white and brown adipocytes where their stimulation promotes both lipolysis (breakdown of fat) and energy expenditure.... Early developments in this area produced compounds with greater agonist activity for the stimulation of lipolysis (.beta..sub.3 activity) than for stimulation of atrial rate (.beta..sub.1) and tracheal relaxation (.beta..sub.2). These early developments disclosed in Ainsworth et al., U.S. Pat. Nos. 4,478,849 and 4,396,627, were derivatives of phenylethanolamines.... Such selectivity for.beta..sub.3 -adrenoceptors could make compounds of this type potentially useful as antiobesity agents. In addition, these compounds have been reported to show antihyperglycemic effects in animal models of non-insulin-dependent diabetes mellitus.
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Web site: http://www.delphion.com/details?pn=US06011048__ •
Treatment for obesity Inventor(s): Horrobin; David F. (Montreal, CA) Assignee(s): Efamol Limited (London, GB2) Patent Number: 4,393,049 Date filed: June 10, 1981 Abstract: Use of.gamma.-linolenic acid and related materials alone or with zinc or.beta.lactam antibiotics to treat obesity. Excerpt(s): This invention relates to the treatment of obesity primarily, but not exclusively, in the field of human medicine.... Considerable interest has been shown in recent years in the use of prostaglandin (PG) precursors in medicine.... Prior art within this general area includes the following patents and papers. Web site: http://www.delphion.com/details?pn=US04393049__
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Treatment of insulin resistance in obesity linked type II diabetes using antagonist to TNF-alpha function Inventor(s): Hotamisligil; Gokhan S. (Charlestown, MA), Spiegelman; Bruce M. (Waban, MA) Assignee(s): Dana-Farber Cancer Institute, Inc. (Boston, MA) Patent Number: 5,730,975 Date filed: June 8, 1994 Abstract: An induction of TNF-.alpha. mRNA expression has been observed in adipose tissue from four different insulin resistant rodent models of obesity and diabetes. TNF.alpha. protein was also elevated locally and systemically. Neutralization of TNF-.alpha. in obese fa/fa rats caused a significant increase in the peripheral uptake of glucose in response to insulin. A method of treating an animal suffering from insulin resistance in obesity linked Type II diabetes mellitus is disclosed. The method includes providing a therapeutic agent that includes an antagonist to TNF-.alpha. function in a pharmaceutically acceptable carrier substance and administering a pharmacologically effective amount of the therapeutic agent to the animal. Excerpt(s): Obesity and diabetes are among the most common human health problems in industrialized societies. Obesity, which is the result of an imbalance between caloric intake and energy expenditure, is highly correlated with insulin resistance and diabetes in experimental animals and humans. However, the molecular mechanisms that are involved in obesity-diabetes syndromes are not clear. Since adipose tissue is the major site for energy storage and mobilization, many investigators have focused on finding abnormalities in adipocyte physiology or metabolism (Plata-Salaman, Brain Behav. Immun. 3:193, 1989; Lardy et al., Annu. Rev. Biochem. 59:689, 1990).... It has been shown that several cytokines such as tumor necrosis factor (TNF)-.alpha. have direct effects on adipocyte metabolism as well as other important metabolic actions (Le et al., Lab. Invest. 56:234, 1987; Dinarello, Immunol. Lett. 16:227, 1987; Kunkel et al., Crit. Rev. Immunol. 9:93, 1989;Grunfeld et al., Biotherapy 3:143, 1991). TNF-.alpha. acts in vitro on murine adipocytes to suppress expression of most adipose specific genes including enzymes
Patents 327
involved in lipogenesis (Kawakami et al., Proc. Natl. Acad. Sci. USA 79:912, 1982; Price et al., Arch. Biochem. Biophys. 251:738, 1986). However, some of these effects are not observed in primary cultures of human or rat adipocytes (Grunfeld et al., Biotherapy 3:143, 1991; Kern, J. Lipid Res. 29:909, 1988).... In vivo, TNF-.alpha. expression has been associated with catabolic states leading to a "wasting syndrome," termed cachexia (Beutler et al., Nature 316:552, 1985; Beutler et al., Science 232:977, 1986; Beutler et al., Nature 320:584, 1986; Oliff et al., Cell 50:555, 1987; Beutler et al., Ann. Rev. Immunol. 7:625, 1989), but this effect of TNF-.alpha. has been challenged by several groups of investigators (Semb et al., J. Biol. Chem. 262:8390, 1987; Grunfeld et al., J. Lipid Res. 30:579, 1989; Feingold et al., J. Clin. Invest. 83:1116, 1989; Patton et al., J. Clin. Invest. 80:1587 (1987); Kettlehut et al., J. Clin. Invest. 81:1384, 1988; Tracey et al., J. Clin. Invest. 86:2014, 1990; Socher et al., J. Exp. Med. 167:1957, 1988; Mullen et al., Proc. Soc. Exp. Biol. Med. 193:318, 1990; Teng et al., Proc. Natl. Acad. Sci. USA 88:3535, 1991; for reviews see C. Grunfeld et al., Cancer Res. 49:2554, 1989; Fiers, FEBS 285:199, 1991). Web site: http://www.delphion.com/details?pn=US05730975__ •
Treatment of insulin resistance in obesity linked type II diabetes using antagonists to TNF-.alpha. function Inventor(s): Hotamisligil; Gokhan S. (Charlestown, MA), Spiegelman; Bruce M. (Waban, MA) Assignee(s): Dana-Farber Cancer Institute, Inc. (Boston, MA) Patent Number: 6,015,558 Date filed: March 10, 1998 Abstract: An induction of TNF-.alpha. mRNA expression has been observed in adipose tissue from four different insulin resistant rodent models of obesity and diabetes. TNF.alpha. protein was also elevated locally and systemically. Neutralization of TNF-.alpha. in obese fa/fa rats caused a significant increase in the peripheral uptake of glucose in response to insulin. A method of treating an animal suffering from insulin resistance in obesity linked Type II diabetes mellitus is disclosed. The method includes providing a therapeutic agent that includes an antagonist to TNF-.alpha. function in a pharmaceutically acceptable carrier substance and administering a pharmacologically effective amount of the therapeutic agent to the animal. Excerpt(s): Obesity and diabetes are among the most common human health problems in industrialized societies. Obesity, which is the result of an imbalance between caloric intake and energy expenditure, is highly correlated with insulin resistance and diabetes in experimental animals and humans. However, the molecular mechanisms that are involved in obesity-diabetes syndromes are not clear. Since adipose tissue is the major site for energy storage and mobilization, many investigators have focused on finding abnormalities in adipocyte physiology or metabolism (Plata-Salaman, Brain Behav. Immun. 3:193, 1989; Lardy et al., Annu. Rev. Biochem. 59:689, 1990).... It has been shown that several cytokines such as tumor necrosis factor (TNF)-.alpha. have direct effects on adipocyte metabolism as well as other important metabolic actions (Le et al., Lab. Invest. 56:234, 1987; Dinarello, Immunol. Lett. 16:227, 1987; Kunkel et al., Crit. Rev. Immunol. 9:93, 1989; Grunfeld et al., Biotherapy 3:143, 1991). TNF-.alpha. acts in vitro on murine adipocytes to suppress expression of most adipose specific genes including enzymes involved in lipogenesis (Kawakami et al., Proc. Natl. Acad. Sci. USA 79:912, 1982; Price et al., Arch. Biochem. Biophys. 251:738, 1986). However, some of these effects are not observed in primary cultures of human or rat adipocytes (Grunfeld et al., Biotherapy
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3:143, 1991; Kern, J. Lipid Res. 29:909, 1988).... In vivo, TNF-.alpha. expression has been associated with catabolic states leading to a "wasting syndrome," termed cachexia (Beutler et al., Nature 316:552, 1985; Beutler et al., Science 232:977, 1986; Beutler et al., Nature 320:584, 1986; Oliff et al., Cell 50:555, 1987; Beutler et al., Ann. Rev. Immunol. 7:625, 1989), but this effect of TNF-.alpha. has been challenged by several groups of investigators (Semb et al., J. Biol. Chem. 262:8390, 1987; Grunfeld et al., J. Lipid Res. 30:579, 1989; Feingold et al., J. Clin. Invest. 83:1116, 1989; Patton et al., J. Clin. Invest. 80:1587 (1987); Kettlehut et al., J. Clin. Invest. 81:1384, 1988; Tracey et al., J. Clin. Invest. 86:2014, 1990; Socher et al., J. Exp. Med. 167:1957, 1988; Mullen et al., Proc. Soc. Exp. Biol. Med. 193:318, 1990; Teng et al., Proc. Natl. Acad. Sci. USA 88:3535, 1991; for reviews see C. Grunfeld et al., Cancer Res. 49:2554, 1989; Fiers, FEBS 285:199, 1991). Web site: http://www.delphion.com/details?pn=US06015558__ •
Treatment of obesity Inventor(s): Ng; Frank Man-Woon (Kew, AU), Natera; Siria Helen-Anna (Mount Waverly, AU), Jiang; Woei-Jia (Clayton, AU) Assignee(s): Monash University (Clayton, AU) Patent Number: 5,869,452 Date filed: November 15, 1994 Abstract: A method for the treatment of obesity in an animal such as a human, comprises administering to the animal an effective amount of a peptide which comprises the carboxyl-terminal sequence of a growth hormone, particularly the carboxyl-terminal sequence of human growth hormone containing amine acid residues 177-191. A pharmaceutical composition for use in the treatment of obesity is also disclosed. Excerpt(s): This invention relates to the treatment of obesity in animals. In particular, the invention relates to the treatment of obesity in humans, although it is to be understood that the present invention also extends to the treatment of obesity in non-human mammals, for example, for the improvement of meat qualities in farm animals used in food production.... The critical role of human growth hormone (hGH) in postnatal growth in humans is well recognised. Less obvious is the impact of this hormone on the regulation of lipid and carbohydrate metabolism, due to lack of detailed molecular studies.... It is well documented that the predominant form of hGH is a globular protein with a molecular weight of 22,000 daltons (22-KD) and consists of 191 amino acid residues in a single-chain, folded by 2 disulphide bonds with a small loop at the carboxyl terminus between residues 182 and 189. Recent crystallographic studies also show that the hGH molecule contains four anti-parallel.alpha.-helices which are arranged in a left-twisted, tightly-packed helical bundle.sup.1. The concept that there are discrete functional domains within the hGH molecule responsible for specific metabolic actions of the hormone is generally accepted. The amino-terminus has been identified as the functional domain responsible for the insulin-like actions of the hGH molecule.sup.2,3. Web site: http://www.delphion.com/details?pn=US05869452__
Patents 329
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Treatment of obesity Inventor(s): Ng; Frank Man-Woon (Kew, AU), Natera; Siria Helen Anna (Mount Waverly, AU), Jiang; Woei-Jia (Clayton, AU) Assignee(s): Metabolic Pharmaceuticals, Inc. (Toorak, AU) Patent Number: 6,335,319 Date filed: February 8, 1999 Abstract: A method for the treatment of obesity in an animal such as a human, comprises administering to the animal an effective amount of a peptide which comprises the carboxyl-terminal sequence of a growth hormone, particularly the carboxyl-terminal sequence of human growth hormone containing amine acid residues 177-191. A pharmaceutical composition for use in the treatment of obesity is also disclosed. Excerpt(s): This invention relates to the treatment of obesity in animals. In particular, the invention relates to the treatment of obesity in humans, although it is to be understood that the present invention also extends to the treatment of obesity in non-human mammals, for example, for the improvement of meat qualities in farm animals used in food production.... The critical role of human growth hormone (hGH) in postnatal growth in humans is well recognised. Less obvious is the impact of this hormone on the regulation of lipid and carbohydrate metabolism, due to lack of detailed molecular studies.... It is well documented that the predominant form of hGH is a globular protein with a molecular weight of 22,000 daltons (22-KD) and consists of 191 amino acid residues in a single-chain, folded by 2 disulphide bonds with a small loop at the carboxyl terminus between residues 182 and 189. Recent crystallographic studies also show that the hGH molecule contains four anti-parallel.alpha.-helices which are arranged in a left-twisted, tightly-packed helical bundle.sup.1. The concept that there are discrete functional domains within the hGH molecule responsible for specific metabolic actions of the hormone is generally accepted. The amino-terminus has, been identified as the functional domain responsible for the insulin-like actions of the hGH molecule.sup.2,3. Web site: http://www.delphion.com/details?pn=US06335319__
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Treatment of obesity and diabetes using sapogenins Inventor(s): Applezweig; Norman (New York, NY) Assignee(s): Progenics, Inc. (New York, NY) Patent Number: 4,680,289 Date filed: June 5, 1985 Abstract: Obesity and diabetes obesity syndromes are treated with 5.beta.-sapogenin or.DELTA..sup.5 sapogenin. Excerpt(s): This invention is related to U.S. patent application Ser. No. 683,423, filed Dec. 19, 1984 for Treatment of Obesity, Diabetes and Other Symptoms of Hypercorticoidism Using Etiocholanolones, and to U.S. patent application Ser. No. 515,354, filed on July 19, 1983 for "Method for Treating Diabetes Using DHEA Components" and the contents of these applications are incorporated herein by reference.... The major function of the adrenal gland is to regulate metabolism in the body so that an intermittent intake of food can be regulated to maintain a constant metabolite supply to the cells. This is
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accomplished by producing steroid hormones which can control the conversion of incoming nutrients, such as aminoacids, glucose and fats into storage depots from which they can thereafter be released or interchanged, allowing a continuous flow of optimum energy and growth factors to the cells.... One category of steroids is known as the adrenal androgens. Dehydroepiandrosterone (DHEA) is the principal representative of this category. The adrenal androgens which have an anabolic action are produced with puberty, reach a peak in early adulthood and then, beyond the age of 50, decline to very low levels. Web site: http://www.delphion.com/details?pn=US04680289__ •
Treatment of obesity and essential hypertension and related disorders Inventor(s): Cooper; Garth J. S. (Solana Beach, CA), Leighton; Brendan (Eynsham, GB2) Assignee(s): Amylin Pharmaceuticals, Inc. (San Diego, CA) Patent Number: 5,364,841 Date filed: June 21, 1993 Abstract: The administration of antagonists and blockers of amylin or CGRP or both for the treatment of obesity and essential hypertension and associated lipid disorders and atherosclerosis. Excerpt(s): The field of the invention is medicine, and more particularly, the effect of amylin antagonists and amylin blockers on glucose metabolism in peripheral tissues as a treatment for obesity and essential hypertension and associated lipid disorders and atherosclerosis.... Publications and other materials including patent applications used to illuminate the specification are incorporated herein by reference.... A 37-amino acid peptide called amylin has been isolated, purified, sequenced and characterized. The present invention discloses the use of amylin antagonists and amylin receptor blockers to control glucose and lipid metabolism for the treatment of obesity and essential hypertension and associated lipid abnormalities and atherosclerosis. Web site: http://www.delphion.com/details?pn=US05364841__
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Treatment of obesity, diabetes and other symptoms of hypercorticoidism using etiocholanolones Inventor(s): Coleman; Douglas L. (Seal Harbor, ME), Applezweig; Norman (New York, NY) Assignee(s): Jackson Lab. (Bar Harbor, ME), Progenics, Inc. (New York, NY) Patent Number: 4,666,898 Date filed: December 19, 1984 Abstract: Obesity, diabetes obesity syndromes and associated hypercorticoidism are treated with.alpha. and/or.beta.-etiocholanolone. Excerpt(s): The major function of the adrenal gland is to regulate metabolism in the body so that an intermittent intake of food can be regulated to maintain a constant metabolite supply to the cells. This is accomplished by producing steroid hormones which can control the conversion of incoming nutrients, such as aminoacids, glucose and fats into storage depots from which they can thereafter be released or interchanged,
Patents 331
allowing a continuous flow of optimum energy and growth factors to the cells.... The steroid hormones are divided mainly into three classes. The first is glucocorticoids (cortisol), also known as gluconeogenic or diabetogenic steriods, which can convert aminoacids into glucose for direct use or store the glucose as glycogen for later use. Cortisol can therefore have an anti-anabolic effect through the depletion of aminoacids needed for protein synthesis and a diabetogenic effect through the direct release of glucose from the glycogen store.... A glucocorticoid excess, resulting from an excess of the pituitary hormone, adrenal cortico-trophic hormone (ACTH), which controls cortisol production, causes Cushing's Syndrome, an uncommon disease. Intake of an excess amount of cortisol from pharmacological use of steroids can also cause Cushing's Syndrome or Cushingoid-like disorders (hypercorticosteroidism, or more briefly hypercorticoidism) which are progeric in that they resemble the symptoms of the diseases of aging, e.g. obesity, hypertension, diabetes, renal stones, osteoporosis, mental disorder, menstrual disturbance, susceptibility to infection and poor wound healing. Web site: http://www.delphion.com/details?pn=US04666898__ •
Treatments for obesity and methods for identifying compounds useful for treating obesity Inventor(s): Hadcock; John R. (East Lyme, CT), Swick; Andrew G. (East Lyme, CT) Assignee(s): Pfizer Inc. (New York, NY) Patent Number: 6,451,783 Date filed: January 16, 2001 Abstract: The present invention provides a method of treating obesity, sexual dysfunction (including erectile dysfunction), diabetes, insulin resistance, hyperinsulinemia, Syndrome X, adrenal dysfunction, hypertension, hypercholesterolemia, atherosclerosis, hyperlipoproteinemia, hypertriglyceridemia, or substance abuse, the method comprising the step of administering to a patent having or at risk of having one of the above-mentioned diseases a therapeutically effective amount of a compound that attenuates the binding of agouti-related protein to melanocortin receptors, but does not attenuate the binding of.alpha.-melanocyte stimulating hormone to melanocortin receptors. The present invention also provides a method of identifying a compound that is useful for the treatment or prevention of obesity, sexual dysfunction (including erectile dysfunction), diabetes, insulin resistance, hyperinsulinemia, Syndrome X, adrenal dysfunction, hypertension, hypercholesterolemia, atherosclerosis, hyperlipoproteinemia, hypertriglyceridemia, or substance abuse, the method comprising the steps of: 1) determining if a compound affects the binding of agoutirelated protein to melanocortin receptors; 2) determining if a compound affects the binding of.alpha.-melanocyte stimulating hormone to melanocortin receptors; and 3) selecting a compound that attenuates the binding of agouti-related protein to melanocortin receptors, but does not affect the binding of.alpha.-melanocyte stimulating hormone to melanocortin receptors. Excerpt(s): The present invention provides methods of treating obesity, sexual dysfunction (including erectile dysfunction), diabetes, insulin resistance, hyperinsulinemia, Syndrome X, adrenal dysfunction, hypertension, hypercholesterolemia, atherosclerosis, hyperlipoproteinemia, hypertriglyceridemia, or substance abuse, the methods comprising the step of administering to a patient having or at risk of having one of the above-mentioned diseases or conditions a therapeutically effective amount of a compound that attenuates the binding of agouti-related protein to
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melanocortin receptors, but does not attenuate the binding of.alpha.-melanocyte stimulating hormone to melanocortin receptors.... The present invention also provides methods of identifying a compound that is useful for the treatment of obesity, sexual dysfunction (including erectile dysfunction), diabetes, insulin resistance, hyperinsulinemia, Syndrome X, adrenal dysfunction, hypertension, hypercholesterolemia, atherosclerosis, hyperlipoproteinemia, hypertriglyceridemia, or substance abuse, the methods comprising the steps of: 1) determining if a compound affects the binding of agouti-related protein to melanocortin receptors; 2) determining if a compound affects the binding of.alpha.-melanocyte stimulating hormone to melanocortin receptors; and 3) selecting a compound that attenuates the binding of agouti-related protein to melanocortin receptors, but does not attenuate the binding of cc-melanocyte stimulating hormone to melanocortin receptors.... Obesity is a devastating disease. In addition to harming physical health, obesity can wreak havoc on mental health because obesity affects self-esteem, which ultimately can affect a person's ability to interact socially with others. Unfortunately, obesity is not well understood, and societal stereotypes and presumptions regarding obesity only tend to exacerbate the psychological effects of the disease. Because of the impact of obesity on individuals and society, much effort has been expended to find ways to treat obesity, but little success has been achieved in the long-term treatment and/or prevention of obesity. Web site: http://www.delphion.com/details?pn=US06451783__ •
Use of agonists of the peroxisome proliferator activated receptor alpha for treating obesity Inventor(s): Willson; Timothy Mark (Durham, NC) Assignee(s): Glaxo Wellcome Inc. (Research Triangle Park, NC) Patent Number: 6,028,109 Date filed: September 28, 1998 Abstract: The use of agonists of the peroxisome proliferator activated receptor alpha (PPAR.alpha.) for the manufacture of a medicament for the treatment of obesity and methods of treating obesity comprising the administration of a therapeutic amount of a PPAR.alpha. agonist. Excerpt(s): The present invention is concerned with medicaments, and more particularly medicaments for use in the treatment of obesity.... Obesity can be described as a state of excessive accumulation of body fat, and is widely considered to be a major public health problem, being associated with substantially increased morbidity and mortality, as well as psychological problems, reduced economic achievement, and discrimination. Examples of health and social problems thought to be caused or exacerbated by obesity include coronary heart disease, stroke, obstructive sleep apnoea, diabetes mellitus, gout, hyperlipidemia, osteoarthritis, reduced fertility, impaired psychosocial function, reduced physical agility and increased risk of accidents, impaired obstetrical performance, reduced economic performance and discrimination and prejudice.... Causes of obesity remain unclear, however whether obesity is of genetic origin or is promoted by a genotype-environment interaction, or both, it remains true that energy intake must have exceeded metabolic and physical (work) energy expenditure for there to have been surplus energy available for fat deposition. There remains considerable uncertainty, however, over the relative importance of different mechanisms in achieving this positive energy balance.
Patents 333
Web site: http://www.delphion.com/details?pn=US06028109__ •
Use of an NK-1 receptor antagonist and an SSRI for treating obesity Inventor(s): Hefti; Franz Fridolin (Much Hadham, GB) Assignee(s): Merck Sharp & Dohme Limited (Hoddesdon, GB) Patent Number: 6,162,805 Date filed: October 22, 1999 Abstract: The present invention relates to the use of an NK-1 receptor antagonist and a selective serotonin reuptake inhibitor for the treatment or prevention of obesity. Excerpt(s): This invention relates to the treatment or prevention of obesity by the administration of a combination of a NK-1 receptor antagonist and a selective serotonin reuptake inhibitor.... Obesity is a chronic disease that is highly prevalent in modern society and is associated not only with a social stigma, but also with decreased life span and numerous medical problems, including adverse psychological development, reproductive disorders such as polycystic ovarian disease, dermatological disorders such as infections, varicose veins, Acanthosis nigricaits, and eczema, exercise intolerance, diabetes mellitus, insulin resistance, hypertension, hypercholesterolemia, cholelithiasis, osteoarthritis, orthopedic injury, thromboembolic disease, cancer, and coronary heart disease. Rissanen et al, British Medical Journal, 301:835-837 (1990).... Treatment regimens for obesity typically include the use of selective serotonin reuptake inhibitors (SSRIs). SSRIs alter the synaptic availability of serotonin through their inhibition of presynaptic reaccumulation of neuronally released serotonin. The SSRI, fluoxetine, has found to be of use in the treatment of obesity. Web site: http://www.delphion.com/details?pn=US06162805__
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Use of CNTF (ciliary neurotrophic factor) receptor activators for the treatment of obesity Inventor(s): Ciliberto; Gennaro (Rome, IT), Costa; Patrizia (Rome, IT), Paonessa; Giacomo (Rome, IT), Lazzaro; Domenico (Rome, IT), Gloaguen; Isabelle (Scoppito L'Aquila, IT), Di Marco; Annalise (Rieti, IT), De Martis; Anna (Rome, IT), Laufer; Ralph (Rome, IT), Cortese; Riccardo (Rome, IT) Assignee(s): Istituto di Ricerche di Biologia Molecolare P. Angeletti S.p.A. (Pomezia, IT) Patent Number: 6,565,869 Date filed: July 19, 1999 Abstract: The present invention refers to the use of hCNTF (human ciliary neurotrophic factor), mutants thereof or other molecules that activate the CNTF receptor, for the preparation of drugs for the treatment of obesity and associated disease, for example hyperglycemia. FIG. 1 shows the anti-obesity effect of hCNTF and leptin on body weight (left panels) and on food intake (right panels) in genetically obese mice and in mice with diet-induced obesity (DIO). Excerpt(s): The present application is the national stage under 35 U.S.C. 371 of PCT/IT97/00283, filed Nov. 18, 1997.... The subject of the present invention is the use of molecules that activate the CNTF (ciliary neurotrophic factor) receptor--such as hCNTF (human CNTF) or mutants of hCNTF--as active principles in the formulation of
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pharmaceutical compositions suitable for the treatment of obesity and of related diseases. The term hCNTF mutant is intended to mean an amino acid sequence that can in theory be derived from hCNTF by substitution of one or more amino acids.... Obesity, which affects >30% of the adult population in the industrial world, is a major public health problem, since it is associated with type II diabetes, hypertension, hyperlipidemia and increased mortality rate. Obesity is the result of a positive energy balance, as a consequence of an increased ratio of caloric intake to energy expenditure. Treatment is generally unsuccessful due to the operation of mechanisms that restore adipose mass after both intentional or unintentional changes (1). The lipostasis theory postulates that the size of the body fat depot is regulated by a feedback loop, constituted by adipocytederived circulating molecules that act on the hypothalamus to decrease appetite and increase energy expenditure (2). Web site: http://www.delphion.com/details?pn=US06565869__ •
Use of droloxifene for the treatment of protastic disease, endometriosis and obesity Inventor(s): Thompson; David D. (Gales Ferry, CT) Assignee(s): Pfizer Inc. (New York, NY) Patent Number: 5,852,059 Date filed: January 6, 1997 Abstract: This invention provides a method for treating a condition or disease selected from endometriosis, obesity, benign prostatic hypertrophy and prostatic carcinoma in mammals which comprises administering to said mammal an amount of droloxifene or a pharmaceutically acceptable salt thereof which is effective in treating said condition or disease. Excerpt(s): Droloxifene is a known compound disclosed in U.S. Pat. No. 5,047,431 in which it is disclosed as an anti-tumor agent, particularly for treatment and prevention of cancer of the breast. Droloxifene is also useful for the relief of bone diseases caused by the deficiency of estrogen or the like, which are often observed in women after menopause or those with the ovaries removed. U.S. Pat. No. 5,254,594.... Gill-Sharma, et al., J. Reproduction and Fertility (1993) 99, 395, disclose that tamoxifen at 200 and 400 mg/kg/day reduces the weights of the testes and secondary sex organs in male rats.... Neubauer, et al., The Prostate 23: 245 (1993) teach that raloxifene treatment of male rats produced regression of the ventral prostate. Web site: http://www.delphion.com/details?pn=US05852059__
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Viral obesity methods and compositions Inventor(s): Atkinson; Richard L. (Fitchburg, WI), Dhurandhar; Nikhil V. (Madison, WI) Assignee(s): Obetech, LLC (Fitchburg, WI) Patent Number: 6,127,113 Date filed: April 6, 1998 Abstract: A source of viral induced obesity has been discovered. A virus known as AD36P has been found to be associated with obesity in both animals and humans. Diagnostic DNA sequences are presented so that DNA based tests for the presence of the obesity associated virus can be conducted.
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Excerpt(s): This invention concerns obesity in humans caused by viruses and methods and compositions for diagnosing, treating and preventing this disease.... The invention also concerns methods and compositions for reducing levels of triglycerides and cholesterol in humans.... More particularly, the invention concerns methods and compositions for diagnosing whether obesity in a human is caused by a virus or whether a person is susceptible to becoming obese because of having been infected with and obesity-causing virus, methods for testing or screening body fluids (e.g., donated human blood) for the presence of obesity-causing viruses, methods for treating and preventing viral obesity in humans, methods for preparing vaccine compositions for treating and preventing viral obesity in humans, such vaccine compositions themselves, and viruses which cause viral obesity in humans. Web site: http://www.delphion.com/details?pn=US06127113__
Patent Applications on Obesity As of December 2000, U.S. patent applications are open to public viewing.10 Applications are patent requests which have yet to be granted. (The process to achieve a patent can take several years.) The following patent applications have been filed since December 2000 relating to obesity: •
2-amino-benzoxazinone derivatives for the treatment of obesity Inventor(s): Palmer, Richard Michael John; (Beckenham, GB), Dunk, Christopher Robert; (Ely, GB), Mitchell, Timothy John; (Cambridge, GB), Downham, Robert; (Cambridge, GB), Hodson, Harold Francis; (Beckenham, GB), Carr, Beverley Jane; (Royston, GB) Correspondence: Choate, Hall & Stewart; Exchange Place; 53 State Street; Boston; MA; 02109; US Patent Application Number: 20030013707 Date filed: July 6, 2001 Abstract: The use of a compound comprising formula (I): 1(I)or a salt, ester, amide or prodrug therof in the inhibition of an enzyme whose preferred mode of action is to catalyse the hydrolysis of an ester functionality, e.g. in the control and inhibition of unwanted enzymes in products and processes. The compounds are also useful in medicine e.g. in the treatment of obesity and related conditions. The invention also relates to novel compounds within formula (I), to processes for preparing them and pharmaceutical compositions containing them.In formula (I) A is a 6-membered aromatic or heteroaromatic ring; andR.sup.1 is a branched or unbranched alkyl (optionally interrupted by one or more oxygen atoms), alkenyl, alkynyl, cycloalkyl, cycloalkenyl, aryl, arylalkyl, reduced arylalkyl, arylalkenyl, heteroaryl, heteroarylalkyl, heteroarylalkenyl, reduced aryl, reduced heteroaryl, reduced heteroarylalkyl or a substituted derivative of any of the foregoing groups. Excerpt(s): This application is a continuation of international application number PCT/GB00/00031, filed on Jan. 6, 2000, entitled "2-Amino-Benzoxazinone Derivatives for the Treatment of Obesity", which PCT application claims priority to GB 9900416.0, filed on Jan. 8, 1999, and the entire contents of each of these is hereby incorporated by reference.... The present invention provides known and novel compounds, their use in
10
This has been a common practice outside the United States prior to December 2000.
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the inhibition of an enzyme whose preferred mode of action is to catalyse the hydrolysis of an ester functionality (in vivo, as the enzyme naturally occurs), their use in medicine, and particularly in the prevention and/or treatment of obesity or an obesity-related disorder. Also provided are methods for the prevention and/or treatment of obesity or an obesity-related disorder and for promoting/aiding non-medical weight loss and the use of the compounds in the manufacture of a medicament for the aforementioned indications. In respect of novel compounds the invention also provides processes for their manufacture, compositions containing them, and methods for manufacturing such compositions.... In the last 20 years, there has been an increasing trend in obesity in the populations of the developed world. The increased incidence of obesity is due in part to the ready availability of food in numerous retail outlets and westernised diets that have high saturated fat and lower fibre contents such that the food is energy dense. The lifestyle of the populations of the developed world has also become more sedentary with the increased mechanisation of society and the steady reduction of manual labour intensive industries. There now exists an energy imbalance between the energy intake from calorie dense foods and the reduced energy expenditure required for a sedentary lifestyle. Some of the excess energy intake is stored as fat in the adipose tissue, the accumulation of which over a period of time results in obesity and can be a significant contributory factor to other diseases and disorders. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
2-Oxy-benzoxazinone derivatives for the treatment of obesity Inventor(s): Palmer, Richard Michael John; (Kent, GB), Downham, Robert; (Cambridge, GB), Mitchell, Timothy John; (Cambridge, GB), Hodson, Harold Francis; (Beckenham, GB), Carr, Beverley Jane; (Royston, GB), Dunk, Christopher Robert; (Ely, GB) Correspondence: Choate, Hall & Stewart; Exchange Place; 53 State Street; Boston; MA; 02109; US Patent Application Number: 20030027821 Date filed: July 6, 2001 Abstract: The use of a compound comprising formula (I): 1(I)or a salt, ester, amide or prodrug therof in the inhibition of an enzyme whose preferred mode of action is to catalyse the hydrolysis of an ester functionality, e.g. in the control and inhibition of unwanted enzymes in products and processes. The compounds are also useful in medicine e.g. in the treatment of obesity and related conditions. The invention also relates to novel compounds within formula (I), to processes for preparing them and pharmaceutical compositions containing them.In formula (I) A is a 6-membered aromatic or heteroaromatic ring; and R.sup.1 is a branched or unbranched alkyl (optionally interrupted by one or more oxygen atoms), alkenyl, alkynyl, cycloalkyl, cycloalkenyl, aryl, arylalkyl, reduced arylalkyl, arylalkenyl, heteroaryl, heteroarylalkyl, heteroarylalkenyl, reduced aryl, reduced heteroaryl, reduced heteroarylalkyl or a substituted derivative of any of the foregoing groups. Excerpt(s): This application is a continuation of international application number PCT/GB00/00032, filed on Jan. 6, 2000, entitled "2-Oxy-Benzoxazinone Derivatives for the Treatment of Obesity", which PCT application claims priority to GB 9900413.7, filed on Jan. 8, 1999, and GB 9917294.2, filed on Jul. 22, 1999, and the entire contents of each of these is hereby incorporated by reference.... The present invention provides known and novel compounds, their use in the inhibition of an enzyme whose preferred mode of action is to catalyse the hydrolysis of an ester functionality (in vivo, as the enzyme
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naturally occurs) their use in medicine, and particularly in the prevention and/or treatment of obesity or an obesity-related disorder. Also provided are methods for the prevention and/or treatment of obesity or an obesity-related disorder and for promoting/aiding non-medical weight loss and the use of the compounds in the manufacture of a medicament for the aforementioned indications. In respect of novel compounds the invention also provides processes for their manufacture, compositions containing them and methods for manufacturing such compositions.... In the last 20 years, there has been an increasing trend in obesity in the populations of the developed world. The increased incidence of obesity is due in part to the ready availability of food in numerous retail outlets and westernised diets that have high saturated fat and lower fibre contents such that the food is energy dense. The lifestyle of the populations of the developed world has also become more sedentary with the increased mechanisation of society and the steady reduction of manual labour intensive industries. There now exists an energy imbalance between the energy intake from calorie dense foods and the reduced energy expenditure required for a sedentary lifestyle. Some of the excess energy intake is stored as fat in the adipose tissue, the accumulation of which over a period of time results in obesity and can be a significant contributory factor to other disease and disorders. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Acute and chronic electrical signal therapy for obesity Inventor(s): Darvish, Nissim; (Tzrufa, IL), Ben-Haim, Shlomo; (Cesarea, IL), Ben Arie, Yaakov; (Haifa, IL), Belsky, Ziv; (Haifa, IL), Mika, Yuval; (Zichron Yaakov, IL), Flesler, Melina; (Misgav, IL) Correspondence: William H. Dippert; Cowan, Liebowitz & Latman, P. C. 1133 Avenue of the Americas; New York; NY; 10036-6799; US Patent Application Number: 20020161414 Date filed: December 11, 2000 Abstract: Apparatus is provided for treating a condition such as obesity. The apparatus includes a set of one or more electrodes, which are adapted to be applied to one or more respective sites in a vicinity of a body of a stomach of a patient. A control unit is adapted to drive the electrode set to apply to the body of the stomach a signal, configured such that application thereof increases a level of contraction of muscle tissue of the body of the stomach, and decreases a cross-sectional area of a portion of the body of the stomach for a substantially continuous period greater than about 3 seconds. Excerpt(s): The present invention relates generally to treatment of obesity, and specifically to invasive techniques and apparatus for treating obesity.... Invasive treatments for obesity are often recommended for patients with a body mass index (mass/height.sup.2 [kg/m.sup.2]) which is greater than 35 or 40. For such patients, their weight is commonly associated with increased risk of heart disease, diabetes, and arthritis. Preferably, the invasive treatments are accompanied by changes in lifestyle, such as improved eating habits and an appropriate exercise regimen.... U.S. Pat. No. 6,067,991 to Forsell, U.S. Pat. No. 5,601,604 to Vincent, and U.S. Pat. No. 5,234,454 to Bangs, and U.S. Pat. Nos. 5,449,368, 5,226,429 and 5,074,868 to Kuzmak, which are incorporated herein by reference, describe mechanical instruments for implantation in or around the stomach of an obese patient. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Administration of estradiol metabolites for the treatment or prevention of obesity, metabolic syndrome, diabetes, and vascular and renal disorders Inventor(s): Tofovic, Stevan P. (Pittsburgh, PA), Jackson, Edwin K. (Pittsburgh, PA), Dubey, Raghvendra K. (Glenshaw, PA) Correspondence: Mary-Elizabeth Buckles; REED SMITH, LLP; Suite 1100 - East Tower; 1301 K Street, N.W. Washington; DC; 20005; US Patent Application Number: 20030050294 Date filed: August 19, 2002 Abstract: Methods are provided for preventing or treating risk factors for cardiovascular disease in an individual, comprising administering a therapeutically effective amount of a composition comprising an estradiol metabolite to said individual. Such risk factors include obesity, the metabolic syndrome, diabetes mellitus, vascular disorders, and renal disorders. Preferred estradiol metabolites include 2-methoxyestradiol, 4methoxyestradiol, 2-hydroxyestradiol, and 4-hydroxyestradiol or prodrugs thereof. The compositions may also be in the form of a controlled release formulation. Methods are also provided for use of estradiol metabolites to treat or prevent insulin resistance, vascular endothelial dysfunction, hyperlipidemia, hypertension, diabetic nephropathy, proteinuria and reducing leptin levels. In addition, the methods provide a method of stabilizing glucose levels. These treatments may be used in either gender because of their lack of a feminizing estrogenic effect. Excerpt(s): This application claims priority from U.S. Provisional Application No. 60/312,741 filed Aug. 17, 2001.... The present invention relates generally to methods and compositions for use in the prevention or treatment of risk factors for cardiovascular diseases such as obesity, metabolic syndrome, diabetes, and vascular and renal disorders. More particularly, the present invention relates to the use of estradiol metabolites with little estrogenic activity such as 2-hydroxyestradiol, 4hydroxyestradiol, 2-methoxyestradiol and 4-methoxyestradiol, all of which may be delivered in a controlled release formulation for the prevention or treatment of such disorders.... Obesity is pandemic and worsening in developed countries (see e.g., Mokdad, A. H., et al., J. Am. Medical Assoc. 284:1650 (2000), the disclosure of which is incorporated herein by reference). Obesity contributes importantly to the metabolic syndrome (see e.g., Grundy, S. M., Endocrine 13:155 (2000) (hereinafter, "Grundy, 2000"); Bergman, R. N., et al., Journal of Investigative Medicine 49:119 (2001) (hereinafter, "Bergman, 2001"), the disclosures of which are incorporated herein by reference), a disorder characterized by hypertension, insulin resistance and hyperlipidemia (Grundy, 2000; Bergman, 2001). The metabolic syndrome in turn contributes to heart and vascular disease (see e.g., Colditz, G. A., Medicine & Science in Sports & Exercise 31:S663 (1999), the disclosure of which is incorporated herein by reference), and to the accelerating epidemic of end stage renal failure (see e.g., Hall, W. D, et al., American Journal of the Medical Sciences 313:195 (1997); Hall, J. E. et al., Annals of the New York Academy of Sciences 892:91 (1999), the disclosures of which are incorporated herein by reference). Unfortunately, pharmacological management of obesity has caused, rather than attenuated, cardiovascular disease. For example, a popular phentermine/fenfluramine combination produces valvular heart disease (see e.g., Lepor, N. E., et al., American Journal of Cardiology 86:107 (2000), the disclosure of which is incorporated herein by reference), while another popular treatment option, phenylpropanolamine, causes stroke (see e.g., Kernan, W. N., et al., New England J. Med. 343:1826 (2000), the disclosure of which is incorporated herein by reference). Thus, drugs that prevent or
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treat obesity and its metabolic, vascular and renal sequelae, without adversely affecting the heart, are badly needed. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Agents for preventing or ameliorating insulin resistance and/or obesity Inventor(s): Hashimoto, Hiroyuki; (Nagoya-shi, JP), Jomori, Takahito; (Nagoya-shi, JP), Yamashita, Tokuyuki; (Nagoya-shi, JP), Tubamoto, Yoshiharu; (Naguya-shi, JP), Seino, Yutaka; (Amagasaki-shi, JP), Ban, Nobuhiro; (Kyoto-shi, JP), Yamada, Yuichiro; (Hirakata-shi, JP), Miyawaki, Kazumasa; (Kyoto-shi, JP), Takeda, Motohiro; (Hagoyashi, JP) Correspondence: FISH & RICHARDSON, PC; 4350 LA JOLLA VILLAGE DRIVE; SUITE 500; SAN DIEGO; CA; 92122; US Patent Application Number: 20030157107 Date filed: April 9, 2003 Abstract: An object of the present invention is to provide a prophylactic or ameliorative agent for insulin resistance and/or obesity based on a new concept, and a screening method therefor.The present inventors found that GIP causes insulin resistance and obesity by a new mechanism, and obtained a new concept that a GIP function inhibitory compound exhibits the ameliorative effect of insulin resistance and anti-obesity effect, thereby completing the present invention. That is, the present invention is a prophylactic or ameliorative agent for insulin resistance and/or obesity, having a GIP function inhibitory compound as an active ingredient, and a screening method for a prophylactic or ameliorative agent for insulin resistance and/or obesity, characterized by selecting a GIP function inhibitory compound. Excerpt(s): The present invention relates to a prophylactic or ameliorative agent for insulin resistance and/or obesity, and more specifically to a prophylactic or ameliorative agent for insulin resistance and/or obesity, on the basis of a technological concept that a compound inhibiting a function of GIP (gastric inhibitory polypeptide or glucosedependent insulinotropic peptide) serves as a prophylactic or ameliorative agent for insulin resistance and/or obesity, and a screening method therefor.... GIP is one of gastrointestinal hormones belonging to Glucagon-secretin family. GIP, along with glucagon-like peptide 1 (GLP-1), is called incretin, is secreted on feeding from the K cells existing in the small intestine, and regulates the kinetics of nutrients after eating in the body by stimulating an insulin secretion on.beta.-cells of the pancreas in response to glucose. In addition, GIP has been said to inhibit the gastric motor activity and stimulates the secretion of intestinal juice. However, a doubt exists at present as to its inhibitory effect on gastric acid secretion proposed just after its discovery. The GIPreceptor genes are expressed widely in addition to the.beta.-cells in the pancreas and the adipocytes, so it is assumed that GIP has some effects in other tissues though they have not been clear in details. Naturally, its relationship with insulin resistance is unknown.... Examples of GIP-receptor antagonists include GIP (6-30)-NH.sub.2 (Regulatory Peptide, 69: 151-154, 1997) and GIP (7-30)-NH.sub.2 (Am J Physiol, 276: E1049-1054, 1999). However, they have not been studied as insulin resistance ameliorative agents or antiobesity agents. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Anti-obesity 1,2,3,4,10,10-a-hexahydropy razino [1,2-a] indoles Inventor(s): Roever, Stephan; (Inzlingen, DE), Muller, Marc; (Saint-Louis, FR), Hebeisen, Paul; (Basle, CH), Bentley, Jonathan M. (Reading, GB), Richter, Hans; (GrenzachWyhlen, DE) Correspondence: HOFFMANN-LA ROCHE INC. PATENT LAW DEPARTMENT; 340 KINGSLAND STREET; NUTLEY; NJ; 07110 Patent Application Number: 20020035110 Date filed: July 25, 2001 Abstract: The present invention is directed to 1,2,3,4,10,10a,-hexahydropyrazino[1,2- -a] indole derivatives as well as pharmaceutically acceptable salts, solvates and esters thereof, wherein R.sup.1 to R.sup.8 have the significance given in claim 1 be used in the form of pharmaceutical preparations for the treatment or prevention of disorders of the central nervous system, damage to the central nervous system, cardiovascular disorders, gastrointestinal disorders, diabetes insipidus, obesity and sleep apnea. Excerpt(s): It has been recognised that obesity is a disease process influenced by environmental factors in which the traditional weight loss methods of dieting and exercise need to be supplemented by therapeutic products (S. Parker, "Obesity: Trends and Treatments", Scrip Reports, P J B Publications Ltd, 1996).... Whether someone is classified as overweight or obese is generally determined on the basis of their body mass index (BMI) which is calculated by dividing body weight (kg) by height squared (m.sup.2). Thus, the units of BMI are kg/m.sup.2 and it is possible to calculate the BMI range associated with minimum mortality in each decade of life. Overweight is defined as a BMI in the range 25-30 kg/m.sup.2, and obesity as a BMI greater than 30 kg/m.sup.2. There are problems with this definition in that it does not take into account the proportion of body mass that is muscle in relation to fat (adipose tissue). To account for this, obesity can also be defined on the basis of body fat content: greater than 25% and 30% in males and females, respectively.... As the BMI increases there is an increased risk of death from a variety of causes that is independent of other risk factors. The most common diseases with obesity are cardiovascular disease (particularly hypertension), diabetes, including Type I and Type II diabetes, (obesity aggravates the development of diabetes), gall bladder disease (particularly cancer) and diseases of reproduction. Research has shown that even a modest reduction in body weight can correspond to a significant reduction in the risk of developing coronary heart disease. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Aryl boronate functionalized polymers for treating obesity Inventor(s): Polomoscanik, Steven Craig; (Bedford, MA), Huval, Chad Cori; (Somerville, MA), Dhal, Pradeep K. (Westford, MA), Mandeville, W. Harry III; (Lynnfield, MA), Holmes-Farley, Stephen Randall; (Arlington, MA), Li, Xinhua; (Newton, MA) Correspondence: HAMILTON, BROOK, SMITH & REYNOLDS, P.C. 530 VIRGINIA ROAD; P.O. BOX 9133; CONCORD; MA; 01742-9133; US Patent Application Number: 20030059399 Date filed: June 27, 2002 Abstract: Disclosed are polymers comprising one or more phenyl boronate ester, boronamide or boronate thioester groups. The phenyl boronate ester, boronamide and
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boronate thioester groups are represented by one of the following structural formulas: 1Ar in Structural Formulas (I) and (II) is substituted or unsubstituted; and each Z is --O-, --NH-- or --S-- and is independently selected. Pharmaceutically acceptable salts of the polymer are also included. The aryl boronate ester, boronamide or boronate thioester can be cleaved to release the corresponding aryl boronic acid.Also disclosed are pharmaceutical compositions comprising the polymers of the present invention and a pharmaceutically acceptable carrier or diluent; and methods of treating a subject for obesity with the polymers of the present invention. Excerpt(s): This application claims the benefit of U.S. Provisional Application No. 60/302,221, filed Jun. 29, 2001, and U.S. Provisional Application No. 60/359,473, filed Feb. 22, 2002, the entire teachings of which are incorporated herein by reference.... Human obesity is a recognized health problem with approximately ninety-seven million people considered clinically overweight in the United States. Various chemical approaches have been used for treating obesity. In one such approach, a medicament which inhibits lipases is administered to the obese patient. Lipases are key enzymes in the digestive system which break down diglycerides and triglycerides into monoglycerides and fatty acids. Diglycerides and triglycerides have a high caloric content but are not absorbed by the small intestine until broken down by the lipases. Therefore, inhibition of lipases within the digestive system results in a reduction in the absorption of fat and consequently a decrease in caloric uptake. XENICAL is an example of a commercially available lipase inhibitor that is used for treating obesity.... Administration of lipase inhibitors results in stools with a high fat or oil content from the undigested diglycerides and triglycerides. Leakage of oil from the stool is an unpleasant side effect that often occurs when stools have a high fat or oil content. This condition is referred to as "oily stool" or "leaky stool". It has been reported in U.S. application Ser. No. 09/166,453 that fat-binding polymers, when co-administered with lipase inhibitors, can bind with or "stabilize" the oil and thereby reduce or eliminate the leakage of oil from the stool. However, the need to administer two drugs can reduce patient compliance because it is burdensome and inconvenient. The development of new drugs which both inhibit lipases and bind the lipids which cause "leaky stools" would be an advance with respect to managing and treating obesity in patients. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Aryl boronic acids for treating obesity Inventor(s): Dhal, Pradeep K. (Westford, MA), Huval, Chad Cori; (Somerville, MA), Mandeville, W. Harry III; (Lynnfield, MA), Holmes-Farley, Stephen Randall; (Arlington, MA), Li, Xinhua; (Newton, MA) Correspondence: HAMILTON, BROOK, SMITH & REYNOLDS, P.C. 530 VIRGINIA ROAD; P.O. BOX 9133; CONCORD; MA; 01742-9133; US Patent Application Number: 20030064963 Date filed: June 27, 2002 Abstract: Disclosed is a phenyl boronic acid compound represented by Structural Formula (I): 1Ar is a substituted or unsubstituted aryl group.Z and Z' are independently --O--. --NH-- or --S--.X is an electron withdrawing group.R is a substituted or unsubstituted straight chained hydrocarbyl group optionally comprising one or more amine, ammonium, ether, thioether or phenylene linking groups and Y is --H, an amine, --[NH--(CH.sub.2).sub.q]-.sub.r--NH.sub.2, halogen, --CF.sub.3, thiol ammonium, alcohol, --COOH, --SO.sub.3H, --OSO.sub.3H or phosphonium group covalently bonded
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to the terminal position of R. Each --NH-- in --[NH--(CH.sub.2).sub.q].sub.r--NH-.sub.2 is optionally N-alkylated or N,N-dialkylated and --NH.sub.2 in --[NH-(CH.sub.2).sub.q].sub.r--NH.sub.2 is optionally N-alkylated, N,N-dialkylated or N,N,Ntrialkylated.q is an integer from 2 to about 10 and r is an integer from 1 to about 5.R.sub.1 and R.sub.1' are independently --H, an aliphatic group, a substituted aliphatic group, an aryl group or a substituted aryl group, or, taken together, are a C2-C5 substituted or unsubstituted alkylene group optionally comprising an amine linking group [--N.sup.+(R.sup.1a)--]. Each R.sub.1 is Structural Formula (I) is preferably -H.R.sup.1a is --H, alkyl, substituted alkyl, phenyl or substituted phenyl.Also disclosed is a method of treating obesity in a subject by administering an effective amount of a compound represented by Structural Formula (I) and a pharmaceutical composition comprising the compound and a pharmaceutically acceptable carrier or diluent. Excerpt(s): This application claims the benefit of U.S. Provisional Application No. 60/302,081, filed Jun. 29, 2001 and U.S. Provisional Application No. 60/359,467, filed Feb. 22, 2002. The entire teachings of the above application(s) are incorporated herein by reference.... Human obesity is a recognized health problem with approximately ninetyseven million people considered clinically overweight in the United States. Various chemical approaches have been used for treating obesity. In one such approach, a medicament which inhibits lipases is administered to the obese patient. Lipases are key enzymes in the digestive system which break down diglycerides and triglycerides into monoglycerides and fatty acids. Diglycerides and triglycerides have a high caloric content but are not absorbed by the small intestine until broken down by the lipases. Therefore, inhibition of lipases within the digestive system results in a reduction in the absorption of fat and consequently a decrease in caloric uptake. XENICAL is an example of a commercially available lipase inhibitor that is used for treating obesity.... There is still a need, however, for improved lipase inhibitors. For example, administration of lipase inhibitors results in stools with a high fat or oil content from the undigested diglycerides and triglycerides. Leakage of oil from the stool is an unpleasant side effect that often occurs when stools have a high fat or oil content. This condition is referred to as "oily stool" or "leaky stool". It has been reported in U.S. application Ser. No. 09/166,453 that fat-binding polymers, when co-administered with lipase inhibitors, can bind with or "stabilize" the oil and thereby reduce or eliminate the leakage of oil from the stool. It would be desirable to develop a single compound which is both a lipase inhibitor and a fat-binder. In addition, a lipase inhibitor should be minimally absorbed by the intestines to prevent systemic side-effects. Other desirable features include ease and economy of manufacture. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Aza- indolyl derivatives for treating obesity Inventor(s): Taylor, Sven; (Riedisheim, FR), Hebeisen, Paul; (Basle, CH), Bentley, Jonathan Mark; (Reading, GB) Correspondence: HOFFMANN-LA ROCHE INC. PATENT LAW DEPARTMENT; 340 KINGSLAND STREET; NUTLEY; NJ; 07110 Patent Application Number: 20010025039 Date filed: February 27, 2001 Abstract: Novel compounds of formula (I): 1wherein X.sup.1, X.sup.2, X.sup.3 and X.sup.4, n, R.sup.1, R.sup.2 and R.sup.3 are defined in the specification, and pharmaceutically acceptable salts and prodrugs of the compounds of formula (I) have
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therapeutic uses. These compounds are useful for the treatment of disorders of the central nervous system; damage to the central nervous system; cardiovascular disorders; gastrointestinal disorders; diabetes insipidus, and sleep apnea. They are particularly useful for the treatment of obesity. Excerpt(s): The present invention relates to new aza-indolyl derivatives, to processes and intermediates for their preparation, to pharmaceutical compositions containing them and to their medicinal use. The active compounds of the present invention are useful in treating obesity and other disorders.... It has been recognized that obesity is a disease process influenced by environmental factors in which the traditional weight loss methods of dieting and exercise need to be supplemented by therapeutic products (S. Parker, "Obesity: Trends and Treatments", Scrip Reports, PJB Publications Ltd, 1996).... Whether someone is classified as overweight or obese is generally determined on the basis of their body mass index (BMI) which is calculated by dividing body weight (kg) by height squared (m.sup.2). Thus, the units of BMI are kg/m.sup.2 and it is possible to calculate the BMI range associated with minimum mortality in each decade of life. Overweight is defined as a BMI in the range 25-30 kg/m.sup.2, and obesity as a BMI greater than 30 kg/m.sup.2. There are problems with this definition in that it does not take into account the proportion of body mass that is muscle in relation to fat (adipose tissue). To account for this, obesity can also be defined on the basis of body fat content: greater than 25% and 30% in males and females, respectively. Using BMI and/or other conventional diagnosis tools, prescribing doctors are well able to determine which of their patients are in need of treatment for obesity. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Beta-adrenoceptor genetic polymorphisms and obesity Inventor(s): Johnson, Julie A. (Melrose, FL) Correspondence: SALIWANCHIK LLOYD & SALIWANCHIK; A PROFESSIONAL ASSOCIATION; 2421 N.W. 41ST STREET; SUITE A-1; GAINESVILLE; FL; 326066669 Patent Application Number: 20020187491 Date filed: February 12, 2002 Abstract: The present invention provides a method for identifying a subject having a risk of developing obesity, coronary microvascular dysfunction, or hypertension, comprising detection of the presence of a single nucleotide polymorphism (SNP) in a nucleic acid encoding an element of at least one.beta.-adrenergic receptor from the subject. The presence of the SNP is correlated with obesity, coronary microvascular dysfunction, or hypertension, and thereby identifies the subject as having a risk of developing obesity, coronary microvascular dysfunction, or hypertension. The subject invention also provides methods of identifying patients likely to benefit from the prescription of beta blocker hypertension medications. In various embodiments, the nucleic acids detected include those genes encoding ADRB1 (.beta..sub.1AR), ADRB2 (.beta..sub.2AR), ADRB3 (.beta..sub.3AR), GNB3 (G protein.beta.3 subunit), or GNAS1 (G.sub.S protein alpha subunit). Methods of treating identified individuals are also provided. Excerpt(s): The prevalence of obesity has increased dramatically in Westernized societies. It represents a major health problem, because it markedly increases the risk of cardiovascular disease, diabetes, lipid disorders, and some cancers. Obesity clearly has a heritable basis, with estimates that 40% to 70% of the variability in body weight is
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genetically mediated. Thus, understanding the genetic basis of variability in BMI or obesity is important. The range of treatments for obesity reflects the complexity of the processes involved in weight regulation and the current lack of understanding of these processes. Recent reports have even implicated viruses as a possible causative factor in obesity (U.S. News and World Report, Aug. 7, 2000). In addition, human twin studies strongly suggest a substantial genetic basis in the control of body weight, with estimates of heritability of 80% to 90% (Simopoulos, A. P. and Childs, B., eds. [1989] "Genetic Variation and Nutrition in Obesity", World Review of Nutrition and Diabetes, 63, S. Karger, Basel, Switzerland; Boijeson, M. [1976] Acta. Paediatr. Scand. 65:279-287).... The regulation of body weight, and particularly body fat, in animals is a complex process having enormous implications for the health and well being of humans and other animals. Excess body weight and/or an excess of body fat relative to lean body mass has been associated with a wide range of health problems. Obesity is a major health problem in the United States, with estimates that 50% to 60% of Americans over age 30 are overweight and 25% to 30% are clinically obese (Wickelgren, L. [1998] "Obesity: How Big a Problem?"[news], Science 280(5368):1364-7). Obesity is of concern because numerous studies link obesity with increased risk of cardiovascular disease, metabolic disorders (such as Type II diabetes mellitus and lipid abnormalities) and some forms of cancer.... Individuals 20% over ideal weight guidelines are considered obese. Obesity is classified as mild (20-40% overweight), moderate (41-100% overweight), and severe (>100%). Severe obesity is relatively rare, affecting less than 0.5% of all obese individuals and about 0.1% of the total population. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Botanical composition and methods for the treatment or prevention of obesity Inventor(s): Tseng, Albert Peng Sheng; (New South Wales, AU), Lim, Yoland Sim Huat; (VICTORIA, AU), Sun, Hai Ping; (New South Wales, AU) Correspondence: Mark D. Moore; Williams, Morgan & Amerson, P.C. Suite 250; 7676 Hillmont; Houston; TX; 77040; US Patent Application Number: 20020197338 Date filed: June 6, 2001 Abstract: Disclosed are botanical compositions, and more particularly to compositions having particularly beneficial therapeutic or prophylactic properties in a mammal. In particular, the compositions of the present inventions are useful inter alia in the treatment and/or prophylaxis of obesity, overeating, and other eating disorders, as well as an oral supplement in place of, or commensurate with, the consumption of food. The compositions of the present invention may be conveniently formulated for suitable administration, such as, for example, as a dried composition. In particularly preferred embodiments, the compositions of the present invention encompass formulations that comprise, consist essentially of, or consist of, a plurality of at least three herbal plants, horticultural and/or botanical equivalents, and/or extracts thereof, having similar or equivalent medicinal or therapeutic properties. Excerpt(s): The present application claims priority from U.S. Provisional Application Serial No. 60/209,544, filed Jun. 6, 2000, the entire contents of which is specifically incorporated herein by reference in its entirety.... The present invention relates generally to a composition and more particularly to a composition having therapeutic properties. The composition of the present invention is useful inter alia in the treatment and/or prophylaxis of obesity as well as an oral supplement in place of or commensurate with
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the consumption of food. The composition of the present invention is conveniently packaged for consumption as a dried formulation. In a particularly preferred embodiment, the composition of the present invention is a formulation derived from three or more herbal plants or horticultural and/or botanical equivalents thereof having similar or equivalent medicinal or therapeutic properties and/or extracts therefrom.... Obesity is one of the more significant problems frequently associated with affluent societies. Obesity is not confined to middle age and is now an increasing problem with younger children and adolescents. Although medical conditions leading to obesity exist, modem obesity frequently appears as a consequence of less exercise and an increase in the availability of fatty foods and high calorie foods at affordable prices. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Cobalt-porphyrin complexes and use thereof as an anti-obesity agent Inventor(s): Ghosh, Soumitra S. (San Diego, CA), Szabo, Tomas R. (San Diego, CA), Davis, Robert E. (San Diego, CA) Correspondence: SEED INTELLECTUAL PROPERTY LAW GROUP PLLC; 701 FIFTH AVE; SUITE 6300; SEATTLE; WA; 98104-7092; US Patent Application Number: 20020165216 Date filed: December 14, 2001 Abstract: Cobalt-porphyrin (Co-P) complexes for use as anti-obesity agents, and compositions and methods related thereto. The Co-P complexes exhibit reduced redox activity compared to cobalt mesoporphyrin (Co-MP) and cobalt protoporphyrin (CoPP), which alleviates the deleterious effects associated with administration of Co-P associated with oxidative stress, particularly in the context of injection site toxicity. Excerpt(s): The present invention relates generally to cobalt-porphyrin complexes which are useful as anti-obesity agents, as well as to compounds, compositions and methods related to the same.... Cobalt protoporphyrin ("Co-PP") has been reported to regulate food intake and body weight in rats (Galbraith and Kappas, Proc. Natl. Acad Sci. U.S.A. 86:7653-7657, 1989), as well as in other animals such as rats, dogs and monkeys. A single subcutaneous injection of Co-PP produces a prompt dose-dependent decrease in food intake in Sprague Dawley rats. This result is accompanied by a sustained decrease in body weight, that is characterized by decreases in carcass fat content without changes in protein content. Smaller doses of Co-PP delivered by intracerebroventricular administration has also been found to elicit the same effect.... The regulatory effect of Co-PP has also been extended to animals that are genetically destined to become markedly obese. Thus, subcutaneous administration of Co-PP to Zucker rats whose obesity is conferred by homozygosity of the fa gene (fa/fa) produces long-sustained reduction in body weight (Galbraith and Kappas, Pharmacology 41:292-298, 1990). The effect of Co-PP is profound and believed to be caused by the phenotype of gene expression in the fa/fa animal to revert to a phenotype similar to that of the heterozygous lean animal. Whereas cobalt mesoporphyrin ("Co-MP") has a comparable biological profile, the same effect is not found upon administration of inorganic cobalt, or a number of other metal chelates of porphyrins. The mechanism of action of Co-PP for regulation of body weight is unknown, and it has been shown that the weight loss in rats is not mediated by the neuropeptide Y system (Choi et al, Brain Research 729:223227, 1996; Turner et al, Physiology and Behavior 56:10009-1014, 1994). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Combination of a CB1 receptor antagonist and of sibutramine, the pharmaceutical compositions comprising them and their use in the treatment of obesity Inventor(s): Petitet, Francois; (Creteil, FR), Picaut, Philippe; (Fontenay Aux Roses, FR), Piot-Grosjean, Odile; (Choisy Le Roi, FR) Correspondence: Finnegan, Henderson, Farabow,; Garrett & Dunner, L.L.P. 1300 I Street, N.W. Washington; DC; 20005-3315; US Patent Application Number: 20020091114 Date filed: October 3, 2001 Abstract: The present invention relates to the combination of a CB1 receptor antagonist and of sibutramine, to the pharmaceutical compositions comprising them and to their use in the treatment of obesity. Excerpt(s): The present invention relates to the combination of a CB1 receptor antagonist and of sibutramine, to the pharmaceutical compositions comprising them and to their use in the treatment of obesity.... CB1 receptor antagonists are known for their effect on food intake and their use as anorexigenic (G. Colombo et al., Life Sciences, 63 (8), 113117 (1998); J. Siamand et al., Behavioural Pharmacol., 9, 179-181 (1998)).... Sibutramine (BTS 54524; N-{1-[1-(4-chlorophenyl)cyclobutyl]-3-methy- lbutyl}-N,N-dimethylamine; Meridia.sup.R, Reductil.sup.R), its hydrate and its pharmaceutically acceptable salts and in particular its hydrochloride reduces food intake and is of use in the treatment of obesity (WO 90/061110; D. H. Ryan et al., Obesity Research, 3 (4), 553 (1995); H. C. Jackson et al., British Journal of Pharmacology, 121, 1758 (1997); G. Fanghanel et al., Inter. J. Obes., 24 (2), 144 (2000); G. A. Bray et al., Obes. Res., 7 (2), 189 (1999)). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Composition for treating obesity and esthetic treatment process Inventor(s): Rombi, Max; (Bordighera, IT) Correspondence: BURNS, DOANE, SWECKER & MATHIS, L.L.P. P.O. Box 1404; Alexandria; VA; 22313-1404; US Patent Application Number: 20030104081 Date filed: October 22, 2002 Abstract: The invention relates to a composition for the curative and prophylactic treatment of obesity, comprising a catechol-rich extract of green tea, in particular containing from 20% to 50% by mass of catechols expressed as epigallocatechol gallate (EGCG). Excerpt(s): The therapeutic objective as regards obesity is well defined: it is a matter either of allowing the individual to lose a significant amount of weight, or of helping the individual to maintain a weight level which is as low as desired.... Several types of approach have been envisaged to date.... Nutritional approaches are directed toward reducing the supply of energy in the form of foods. This can be achieved either by drastically reducing the energy supplies or by replacing high-energy nutrients with others which are lower in energy: such as indigestible substitute fats, structured triglycerides which are difficult to assimilate or dietary fibers which cannot be assimilated. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
Patents 347
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Compositions and methods for the diagnosis and treatment of body weight disorders, including obesity Inventor(s): Nagle, Deborah Lynn; (Watertown, MA), Moore, Karen; (Maynard, MA) Correspondence: PENNIE AND EDMONDS; 1155 AVENUE OF THE AMERICAS; NEW YORK; NY; 100362711 Patent Application Number: 20020150973 Date filed: June 27, 2001 Abstract: The present invention relates to mammalian mahogany genes, including the human mahogany gene, which are novel genes involved in the control of mammalian body weight. The invention encompasses nucleotide sequences of the mahogany gene, host cell expression systems of the mahogany gene, and hosts which have been transformed by these expression systems, including transgenic animals. The invention also encompasses novel mahogany gene products, including mahogany proteins, polypeptides and peptides containing amino acid sequences mahogany proteins, fusion proteins of mahogany proteins polypeptides and peptides, and antibodies directed against such mahogany gene products. The present invention also relates to methods and compositions for the diagnosis and treatment of mammalian body weight disorders, including obesity, cachexia, and anorexia, and for the identification of subjects susceptible to such disorders. Further, the invention relates to methods of using the mahogany gene and gene products of the invention for the identification of compounds which modulate the expression of the mahogany gene and/or the activity of the mahogany gene product. Such compounds can be useful as therapeutic agents in the treatment of mammalian body weight disorders, including obesity, cachexia, and anorexia. Excerpt(s): Obesity represents the most prevalent of body weight disorders, and it is the most important nutritional disorder in the western world, with estimates of its prevalence ranging from 30% to 50% within the middle-aged population. Other body weight disorders, such as anorexia nervosa and bulimia nervosa, which together affect approximately 0.2% of the female population of the western world, also pose serious health threats. Further, such disorders as anorexia and cachexia (wasting) are also prominent features of other diseases such as cancer, cystic fibrosis, and AIDS.... Obesity, defined as an excess of body fat relative to lean body mass, also contributes to other diseases. For example, this disorder is responsible for increased incidence of diseases such as coronary artery disease, hypertension, stroke, diabetes, hyperlipidemia, and some cancers (See, e.g., Nishina, P. M. et al., 1994, Metab. 43: 554-558; Grundy, S. M. & Barnett, J. P., 1990, Dis. Mon. 36: 641-731). Obesity is not merely a behavioral problem, i.e., the result of voluntary hyperphagia. Rather, the differential body composition observed between obese and normal subjects results from differences in both metabolism and neurologic/metabolic interactions. These differences seem to be, to some extent, due to differences in gene expression, and/or level of gene products or activity (Friedman, J. M. et al., 1991, Mammalian Gene 1: 130-144).... The epidemiology of obesity strongly shows that the disorder exhibits inherited characteristics (Stunkard, 1990, N. Eng. J. Med. 322: 1438). Moll et al. have reported that, in many populations, obesity seems to be controlled by a few genetic loci (Moll et al., 1991, Am. J. Hum. Gen. 49: 1243). In addition, human twin studies strongly suggest a substantial genetic basis in the control of body weight, with estimates of heritability of 80-90% (Simopoulos, A. P. & Childs, B., eds., 1989, in "Genetic Variation and Nutrition in Obesity", World Review of Nutrition and Diabetes 63, S. Karger, Basel, Switzerland; Borjeson, M., 1976, Acta. Paediatr. Scand. 65: 279-287).
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Compounds for the treatment of obesity Inventor(s): Hank, Richard F. (No. Stonington, CT), Elliott, Richard L. (East Lyme, CT), Hammond, Marlys; (Salem, CT) Correspondence: Gregg C. Benson; Pfizer Inc. Patent Department, MS 4159; Eastern Point Road; Groton; CT; 06340; US Patent Application Number: 20010039277 Date filed: January 4, 2001 Abstract: NPY antagonists, methods of using such NPY antagonists and pharmaceutical compositions containing such NPY antagonists. The NPY antagonists are useful for the treatment of NPY mediated disease/conditions including obesity. Excerpt(s): This application claims priority from provisional application U.S. Ser. No. 60/132,029 filed Apr. 30, 1999, the benefit of which is hereby claimed under 37 C.F.R..sctn.1.78(a)(3).... This invention relates to NPY antagonists, particularly NPY-5 antagonists, and pharmaceutical compositions containing such antagonists and the use of such antagonists to treat, for example, obesity, feeding disorders, as well as other NPY mediated diseases/conditions in mammals, including humans, dogs, cats and horses.... Neuropeptide Y (NPY), a 36 amino acid peptide neurotransmitter, is a member of the pancreatic polypeptide class of neurotransmitters/neuroho- rmones which has been shown to be present in both the periphery and central nervous system. NPY is one of the most potent orexogenic agents known and has been shown to play a major role in the regulation of food intake in animals. At least 6 NPY receptor subclasses have been identified and cloned to date, with two of these subclasses, NPY-1 and NPY-5, thought to be the most important receptor subtypes modulating food intake and energy expenditure. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Comprehensive pharmacologic therapy for treatment of obesity Inventor(s): Hinz, Martin C. (Duluth, MN) Correspondence: VIDAS, ARRETT & STEINKRAUS, P.A. 6109 BLUE CIRCLE DRIVE; SUITE 2000; MINNETONKA; MN; 55343-9185; US Patent Application Number: 20020040054 Date filed: August 29, 2001 Abstract: The comprehensive pharmacologic therapy for treatment of obesity is a procedure which involves the administration of a desired therapeutic range of Diethylpropion and/or Phentermine in combination with a SSRI medication and nutritional supplementation for brief and long durations which may be 12 months or more. The preferred procedure involves the administration of drugs in combination which are identified as: Citalopram (Celexa) and Phentermine; Citalopram (Celexa) and Diethylpropion; Citalopram (Celexa), Phentermine, and Diethylpropion. In addition nutritional supplementation such as a multivitamin, 5-Hydroxytryptophan, vitamin B6, vitamin C, Tyrosine, Calcium, and Lysine may be used to enhance the performance of the weight loss treatment program.
Patents 349
Excerpt(s): Safer than Phen-Fen (copyright 1997), Written by Michael Anchors, MD Ph.D. Pulmonary Vascular Disease, Medical Clinics of North America Nov. 6, 1997, Written by Donald Heath, MD Ph.D.... The "Phen-pro" Diet Drug Combination Is Not Associated with Valvular Heart Disease. Jan. 12, 1998 Archives of Internal Medicine. Written by: Len Griffen, MD and Michael Anchors, MD Ph.D.... Fluoxetine (Prozac) and Other Drugs for Treatment of Obesity, Nov. 25, 1994 The Medical Letter. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Comprehensive pharmacologic therapy for treatment of obesity Inventor(s): Hinz, Martin C. (Duluth, MN) Correspondence: VIDAS, ARRETT & STEINKRAUS, P.A. 6109 BLUE CIRCLE DRIVE; SUITE 2000; MINNETONKA; MN; 55343-9185; US Patent Application Number: 20020065311 Date filed: August 30, 2001 Abstract: The comprehensive pharmacologic therapy for treatment of obesity is a procedure which involves the administration of a desired therapeutic range of Diethylpropion and/or Phentermine in combination with a SSRI medication and nutritional supplementation for brief and long durations which may be 12 months or more. The preferred procedure involves the administration of drugs in combination which are identified as: Citalopram (Celexa) and Phentermine; Citalopram (Celexa) and Diethylpropion; Citalopram (Celexa), Phentermine, and Diethylpropion. In addition nutritional supplementation such as a multivitamin, 5-Hydroxytryptophan, vitamin B6, vitamin C, Tyrosine, Calcium, and Lysine may be used to enhance the performance of the weight loss treatment program. Excerpt(s): Safer than Phen-Fen (copyright 1997), Written by Michael Anchors, MD Ph.D. Pulmonary Vascular Disease, Medical Clinics of North America November 6, 1997, Written by Donald Heath, MD Ph.D.... The "Phen-pro" Diet Drug Combination Is Not Associated with Valvular Heart Disease. Jan. 12, 1998 Archives of Internal Medicine. Written by: Len Griffen, MD and Michael Anchors, MD Ph.D.... Fluoxetine (Prozac) and Other Drugs for Treatment of Obesity, Nov. 25, 1994 The Medical Letter. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Comprehensive pharmacologic therapy for treatment of obesity Inventor(s): Hinz, Martin C. (Duluth, MN) Correspondence: VIDAS, ARRETT & STEINKRAUS, P.A. 6109 BLUE CIRCLE DRIVE; SUITE 2000; MINNETONKA; MN; 55343-9185; US Patent Application Number: 20020072537 Date filed: August 29, 2001 Abstract: The comprehensive pharmacologic therapy for treatment of obesity is a procedure which involves the administration of a desired therapeutic range of Diethylpropion and/or Phentermine in combination with a SSRI medication and nutritional supplementation for brief and long durations which may be 12 months or more. The preferred procedure involves the administration of drugs in combination which are identified as: Citalopram (Celexa) and Phentermine; Citalopram (Celexa) and
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Diethylpropion; Citalopram (Celexa), Phentermine, and Diethylpropion. In addition nutritional supplementation such as a multivitamin, 5-Hydroxytryptophan, vitamin B6, vitamin C, Tyrosine, Calcium, and Lysine may be used to enhance the performance of the weight loss treatment program. Excerpt(s): The medications stop working during therapy where at least 40% to 50% of patients quit losing weight (plateau) on an average of 3.3 months into therapy; and 5% to 8 % of patients who receive drug therapy for weight problems experience the complication where the medications fail to assist in appetite suppression where the patient therefore does not lose significant weight.... In the past long term treatment, defined as treatment longer than 3 months to many years, with drugs has been a problem due to long term safety issues including, medication intolerability by the patient, medication side effects and most important ineffectiveness of the drugs or the cessation of benefit of the drugs which in turn causes the patient to fall out of appetite suppression and terminate weight loss.... A weight loss procedure using SSRI medication is disclosed in U.S. Pat. No. 5,795,895. The potential for patients to obtain goal weight loss under the process of U.S. Pat. No. 5,795,895 is low, and the failure of the drugs to provide a desired level of performance is at the heart of the problem. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Comprehensive pharmacologic therapy for treatment of obesity including cysteine Inventor(s): Hinz, Martin C. (Duluth, MN) Correspondence: VIDAS, ARRETT & STEINKRAUS, P.A. 6109 BLUE CIRCLE DRIVE; SUITE 2000; MINNETONKA; MN; 55343-9185; US Patent Application Number: 20020094969 Date filed: September 6, 2001 Abstract: The comprehensive pharmacologic therapy for treatment of obesity including Cysteine is a procedure which involves the administration of a desired therapeutic range of Diethylpropion and/or Phentermine in combination with a SSRI medication and nutritional supplementation for brief and long durations which may be 12 months or more. The preferred procedure involves the administration of drugs in combination which are identified as: Citalopram (Celexa) and Phentermine; Citalopram (Celexa) and Diethylpropion; Citalopram (Celexa), Phentermine, and Diethylpropion. In addition nutritional supplementation such as a multivitamin, 5-Hydroxytryptophan, Cysteine, vitamin B6, vitamin C, Tyrosine, Calcium, and Lysine may be used to enhance the performance of the weight loss treatment program. Excerpt(s): This application is a continuation-in-part application from Ser. No. 09/412,701 filed Oct. 5, 1999, the entire contents of which are hereby incorporated by reference.... The medications stop working during therapy where at least 40% to 50% of patients quit losing weight (plateau) on an average of 3.3 months into therapy; and 5% to 8% of patients who receive drug therapy for weight problems experience the complication where the medications fail to assist in appetite suppression where the patient therefore does not lose significant weight.... In the past long term treatment, defined as treatment longer than 3 months to many years, with medications, has raised safety issues including, medication intolerability by the patient, medication side effects and most important ineffectiveness of the drugs or the cessation of benefit of the drugs which in turn causes the patient to fall out of appetite suppression and terminate weight loss.
Patents 351
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Derivatives of C2-substituted indan-1 ol systems for the prophylaxis or treatment of obesity Inventor(s): Bickel, Martin; (Bad Homburg, DE), Krone, Volker; (Hofheim, DE), Jaehne, Gerhard; (Frankfurt, DE), Gossel, Matthias; (Hofheim, DE) Correspondence: HELLER EHRMAN WHITE & MCAULIFFE LLP; 1666 K STREET,NW; SUITE 300; WASHINGTON; DC; 20006; US Patent Application Number: 20030134881 Date filed: August 29, 2002 Abstract: Derivatives of C2-substituted indan-1-ol compounds of the formula I: 1its physiologically acceptable salts, and its physiologically functional derivatives for the prophylaxis or treatment of obesity are disclosed herein. Compositions comprising the same, methods for preparing the instant compounds, and methods for reducing weight in mammals and for the prophylaxis or treatment of obesity are also described. Excerpt(s): The instant application takes priority from DE 10142660.7 filed Aug. 31, 2001 which is incorporated herein by reference in its entirety.... The invention relates to C2substituted indan-1-ol systems and their physiologically acceptable salts and physiologically functional derivatives for the prophylaxis or treatment of obesity.... EP 0009554 discloses indan-1-one and -1-ol derivatives as herbicides and analgesics. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Diet food formula for overweight people and diabetics Inventor(s): Li, Rui; (Arcadia, CA), Liu, Tian Xiao; (Arcadia, CA), Liu, Xue Wu; (Arcadia, CA), Liu, Xuewen; (Arcadia, CA) Correspondence: Joe Nieh; Suite 411; 17800 Castleton Street; City of Industry; CA; 91748; US Patent Application Number: 20020068110 Date filed: December 4, 2000 Abstract: A diet food formula for overweight people and diabetics, comprising of agar, carrageenans, alginate, chlorella, spirulina, and water. The diet food formula comprises of all natural materials. The diet food formula cannot be metabolized by the human body after ingestion and will supply the human body with proper nutrients that it requires. Excerpt(s): The present invention relates to a diet food formula for overweight people and diabetics.... People with overweight problems and/or diabetes have extremely limited choices of food that both satisfies their desire to eat and satisfies the body's nutrient requirements.... People with overweight problems are often instructed by their physicians to limit their intake of food while attempting to also maintain a healthy diet by including food with nutrients that the body needs or by taking dietary supplements such as vitamins. However, limiting the intake of food is extremely difficult to do since the body craves for food to fulfill the hunger sensation. Furthermore, the more one tries to limit the intake of food, the more the body craves for them. Therefore attempting to limit food intake to the body often becomes a self-defeating process.
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Fibroblast growth factor-19 (FGF-19) nucleic acids and polypeptides and methods of use for the treatment of obesity and related disorders Inventor(s): Yu, Xing Xian; (Carlsbad, CA), Stewart, Timothy A. (San Francisco, CA), Gurney, Austin L. (Belmont, CA), Goddard, Audrey; (San Francisco, CA), Adams, Sean; (Randolph Township, NJ), Tomlinson, Elizabeth; (Griswold, CT) Correspondence: GENENTECH, INC. 1 DNA WAY; SOUTH SAN FRANCISCO; CA; 94080; US Patent Application Number: 20020155543 Date filed: August 7, 2001 Abstract: The present invention is directed to novel polypeptides belonging to the fibroblast growth factor family and to nucleic acid molecules encoding those polypeptides. Also provided herein are vectors and host cells comprising those nucleic acid sequences, chimeric polypeptide molecules comprising the polypeptides of the present invention fused to heterologous polypeptide sequences, antibodies which bind to the polypeptides of the present invention and to methods for producing the polypeptides of the present invention. Furthermore, methods of treating obesity are provided. Excerpt(s): The present invention relates generally to the identification and isolation of novel DNA and to the recombinant production of novel polypeptides designated herein as fibroblast growth factor-19 (FGF-19) polypeptides, and to methods, compositions and assays utilizing such polypeptides for the therapeutic treatment of obesity and related disorders and for producing pharmaceutically active materials having therapeutic and pharmacologic properties including those associated with the treatment of obesity and related disorders.... Obesity is a chronic disease that is highly prevalent in modem society and is associated not only with a social stigma, but also with decreased life span and numerous medical problems, including adverse psychological development, reproductive disorders such as polycystic ovarian disease, dermatological disorders such as infections, varicose veins, Acanthosis nigricans, and eczema, exercise intolerance, diabetes mellitus, insulin resistance, hypertension, hypercholesterolemia, cholelithiasis, osteoarthritis, orthopedic injury, thromboembolic disease, cancer, and coronary heart disease. Rissanen et al., British Medical Journal, 301: 835-837 (1990).... Existing therapies for obesity include standard diets and exercise, very low calorie diets, behavioral therapy, pharmacotherapy involving appetite suppressants, thermogenic drugs, food absorption inhibitors, mechanical devices such as jaw wiring, waist cords and balloons, and surgery. Jung and Chong, Clinical Endocrinology, 35: 11-20 (1991); Bray, Am. J. Clin. Nutr., 55: 538S-544S (1992). Protein-sparing modified fasting has been reported to be effective in weight reduction in adolescents. Lee et al., Clin. Pediatr., 31: 234-236 (April 1992). Caloric restriction as a treatment for obesity causes catabolism of body protein stores and produces negative nitrogen balance. Protein-supplemented diets, therefore, have gained popularity as a means of lessening nitrogen loss during caloric restriction. Because such diets produce only modest nitrogen sparing, a more effective way to preserve lean body mass and protein stores is needed. In addition, treatment of obesity would be improved if such a regimen also resulted in accelerated loss of body fat. Various approaches to such treatment include those discussed by Weintraub and Bray, Med. Clinics N. Amer., 73: 237 (1989); Bray, Nutrition Reviews, 49: 33 (1991).
Patents 353
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Ginseng berry extracts and pharmaceutical compositions from ginseng berry for the treatment of type 2 diabetes and obesity Inventor(s): Yuan, Chun-Su; (Chicago, IL) Correspondence: MARK B WILSON; FULBRIGHT & JAWORSKI LLP; 600 CONGRESS AVENUE; SUITE 2400; AUSTIN; TX; 78701; US Patent Application Number: 20020136785 Date filed: October 9, 2001 Abstract: The present invention relates to methods and compositions for the use in treating type 2 diabetes and obesity. More specifically, the invention relates to the methods of screening for the active compound from berries from plants of the Panax genus that decreases blood glucose and decreases body weight. It is contemplated that the active compound may comprise a ginsenoside or a combination thereof. Excerpt(s): This application claims priority to U.S. Provisional Application No. 60/246,628, filed Nov. 7, 2000.... The present invention relates generally to the fields of physiology and medicine. More particularly, it relates to pharmaceutical compositions and the methods of screening for constituents that are anti-hyperglycemic or antiobesity agents. Such constituents can be extracted from ginseng berry.... Diabetes mellitus is a major health problem, affecting approximately 5% of the total population in the U.S., and 3% of the population world-wide. Diabetes mellitus is a chronic metabolic disease that can cause blindness, kidney failure, or nerve damage. In addition, diabetes mellitus confers an increased risk of ischemic heart disease, stroke and peripheral vascular disease. Over 90% of diabetics are classified as type 2, or non-insulindependent diabetes mellitus (NIDDM); the rest fall into the category of type 1, or insulin-dependent diabetes mellitus (IDDM). Although the two types of diabetes have distinct pathogeneses, hyperglycemia and various life-threatening complications resulting from long-term hyperglycemia are the most common features. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Health food and preparation having an anti-obesity effect Inventor(s): Ueda, Ryohei; (Yokohama, JP), Hirayama, Shin; (Yokohama, JP) Correspondence: OBLON SPIVAK MCCLELLAND MAIER & NEUSTADT PC; FOURTH FLOOR; 1755 JEFFERSON DAVIS HIGHWAY; ARLINGTON; VA; 22202; US Patent Application Number: 20030026811 Date filed: July 2, 2002 Abstract: The present invention discloses an anti-obesity agent comprising:D-cysteinolic acid represented by Formula I, as an active ingredient: 1 Excerpt(s): This application is based upon and claims the benefit of priority from prior Japanese Patent Applications No. 2001-226298 filed Jul. 26, 2001; and No. 2001-353609 filed Nov. 19, 2001, the entire contents of both of which are incorporated herein by reference.... The present invention relates to an anti-obesity agent, food and pharmaceutical product containing a component suppressing adipogenesis, which is used as a raw material for pharmaceutical products, and pharmaceutical compositions
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as well as an additive for health foods and health beverages.... D-cysteinolic acid (C.sub.3H.sub.9NO4S: molecular weight: 155) was first isolated from red algae and identified by B. Wickberg in 1957 (Acta Chem Scand 11, 506 (1957)). In 1963, Itoh (University of Hiroshima) found that D-cysteinolic acid is also present in green algae and brown algae of seaweed (Bull. Jpn. Scient. Fish., 29, 771 (1963)). Recently, it was found that sardine contain D-cysteinolic acid. Since D-cysteinolic acid has an anticlotting effect, its use as a raw material for pharmaceutical products has been expected. Indeed, an invention directed to thrombosis treatment and a preventive drug for thrombosis using D-cysteinolic acid from sardine has already been filed under Japanese Patent Application Publication No. 61-47880. Also, an invention directed to a cholesterol-reducing drug using D-cysteinolic acid or a cysteinolic acid/bile acid conjugate has been filed under Japanese Patent Application Publication No. 3-49113. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
HMGI PROTEINS IN CANCER AND OBESITY Inventor(s): ZHOU, XIANJIN; (PISCATAWAY, NJ), TKACHENKO, ALEX; (NEW BRUNSWICK, NJ), ASHAR, HENA; (EDISON, NJ), CHADA, KIRAN K. (NORTH BRUNSWICK, NJ) Correspondence: LYON & LYON LLP; 633 WEST FIFTH STREET; SUITE 4700; LOS ANGELES; CA; 90071; US Patent Application Number: 20030051260 Date filed: January 6, 1999 Abstract: The present invention pertains to a method for treating obesity in a mammal which comprises reducing the biological activity of HMGI genes in the mammal. In another embodiment, the invention pertains to a method for treating a tumor in a patient by reducing the biological activity of normal HMGI genes which comprises administering to the patient a therapeutically effective amount of an inhibitor compound active against normal HMGI-C or HMGI(Y) genes. In another embodiment, the invention pertains to a method of producing a transgenic non-human mammal, the germ cells and somatic cells of which contain an inactivated HMGI gene sequence introduced into the mammal at an embryonic stage. In another embodiment, the invention pertains to a method for screening candidate compounds capable of inhibiting the biological activity of normal HMGI proteins. In another embodiment, the invention pertains to a method for screening candidate compounds capable of inhibiting the biological activity of normal HMGI genes. In another embodiment, the invention pertains to a method for detecting normal HMGI proteins as a diagnostic marker for a tumor using a probe. that recognizes normal HMGI proteins, which comprises the steps of (a) contacting normal HMGI proteins from a sample from a patient with a probe which binds to HMGI proteins; and (b) analyzing for normal HMGI proteins by detecting levels of the probe bound to the normal HMGI proteins, wherein the presence of normal HMGI proteins in the sample is positive for a tumor. In another embodiment, the invention pertains to a method for detecting antibodies to normal HMGI proteins using a probe that recognizes antibodies to HMGI normal proteins, which comprises the steps of (a) treating a sample from a patient with a probe which binds to antibodies to normal HMGI proteins; and (b) analyzing for antibodies to HMGI proteins by detecting levels of the probe bound to the antibodies to HMGI proteins, wherein the presence of antibodies to normal HMGI proteins in the sample is positive for a tumor. In another
Patents 355
embodiment, the invention pertains to HMGI genes and proteins for use as a starting point to isolate downstream target genes regulated by the HMGI genes and proteins. Excerpt(s): This application is a continuation-in-part of U.S. patent application Ser. No. 08/852,666, filed May 7, 1997, which application is a continuation-in-part of U.S. patent application Ser. No. 08/679,529, filed Jul. 12, 1996.... The present invention pertains to a method for treating obesity in a mammal which comprises reducing the biological activity of HMGI genes in the mammal. In another embodiment, the invention pertains to a method for treating a tumor in a patient by reducing the biological activity of normal HMGI genes which comprises administering to the patient a therapeutically effective amount of an inhibitor compound active against normal HMGI-C or HMGI(Y) genes. In another embodiment, the invention pertains to a method of producing a transgenic non-human mammal, the germ cells and somatic cells of which contain an inactivated HMGI gene sequence introduced into the mammal, or an ancestor of the mammal, at an embryonic stage. In another embodiment, the invention pertains to a method for screening candidate compounds capable of inhibiting the biological activity of normal HMGI proteins, or a fragment thereof, which comprises the steps of (a) incubating a HMGI protein, or a fragment thereof, with a candidate compound under conditions which promote optimal interaction; and (b) measuring the binding affinity of the candidate compound to the HMGI protein, or a fragment thereof; and (c) determining from the binding affinity which candidate compounds inhibit the biological activity of HMGI proteins, or a fragment thereof. In another embodiment, the invention pertains to a method for screening candidate compounds capable of inhibiting the biological activity of normal HMGI genes which comprises the steps of (a) transfecting into a cell a DNA construct which contains a reporter gene under control of a normal HMGI protein-regulated promoter; (b) administering to the cell a candidate compound; (c) measuring the levels of reporter gene expression; and (d) determining from the levels of reporter gene expression which candidate compounds inhibit the HMGI biological activity. In another embodiment, the invention pertains to a method for detecting normal HMGI proteins as a diagnostic marker for a tumor using a probe that recognizes normal HMGI proteins, which comprises the steps of (a) contacting normal HMGI proteins from a sample from a patient with a probe which binds to HMGI proteins; and (b) analyzing for normal HMGI proteins by detecting levels of the probe bound to the normal HMGI proteins, wherein the presence of normal HMGI proteins in the sample is positive for a tumor. In another embodiment, the invention pertains to a method for detecting antibodies to normal HMGI proteins using a probe that recognizes antibodies to HMGI normal proteins, which comprises the steps of (a) treating a sample from a patient with a probe which binds to antibodies to normal HMGI proteins; and (b) analyzing for antibodies to HMGI proteins by detecting levels of the probe bound to the antibodies to HMGI proteins, wherein the presence of antibodies to normal HMGI proteins in the sample is positive for a tumor. In another embodiment, the invention pertains to HMGI genes and proteins for use as a starting point to isolate downstream target genes regulated by the HMGI genes and proteins.... The disclosures referred to herein to illustrate the background of the invention and to provide additional detail with respect to its practice are incorporated herein by reference and, for convenience, are referenced in the following text and respectively grouped in the appended bibliography. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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INDOLINE DERIVATIVES AND METHOD OF TREATING OBESITY Inventor(s): Mansell, Howard Langham; (Winnersh, GB), Monck, Nathaniel Julius Thomas; (Winnersh, GB), Davidson, James Edward Paul; (Winnersh, GB), Bentley, Jonathan Mark; (Winnersh, GB) Correspondence: HOFFMANN-LA ROCHE INC. PATENT LAW DEPARTMENT; 340 KINGSLAND STREET; NUTLEY; NJ; 07110 Patent Application Number: 20020183349 Date filed: October 15, 2001 Abstract: The present invention relates to indoline derivatives. These compounds are especially useful for the prevention and treatment of disorders of the central nervous system; damage to the central nervous system; cardiovascular disorders; gastrointestinal disorders; diabetes, sleep apnea, and especially for the treatment and prevention of obesity. Excerpt(s): The present invention relates to indoline derivatives, to processes and intermediates for their preparation, to pharmaceutical compositions comprising them and to their medicinal use. The active compounds of the present invention are useful in treating obesity, diabetes and other disorders.... It has been recognised that obesity is a disease process influenced by environmental factors in which the traditional weight loss methods of dieting and exercise need to be supplemented by therapeutic products (S. Parker, "Obesity: Trends and Treatments", Scrip Reports, PJB Publications Ltd, 1996).... Whether someone is classified as overweight or obese is generally determined on the basis of their body mass index (BMI) which is calculated by dividing body weight (kg) by height squared (m.sup.2). Thus, the units of BMI are kg/m.sup.2 and it is possible to calculate the BMI range associated with minimum mortality in each decade of life. Overweight is defined as a BMI in the range 25-30 kg/m.sup.2, and obesity as a BMI greater than 30 kg/m.sup.2. There are problems with this definition in that it does not take into account the proportion of body mass that is muscle in relation to fat (adipose tissue). To account for this, obesity can also be defined on the basis of body fat content: greater than 25% and 30% in males and females, respectively. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Intragastric device for treating obesity Inventor(s): Surti, Vihar C. (Winston-Salem, NC), Hashiba, Kiyoshi; (Sao Paulo, BR) Correspondence: BRINKS HOFER GILSON & LIONE; P.O. BOX 10395; CHICAGO; IL; 60611; US Patent Application Number: 20030078611 Date filed: May 17, 2002 Abstract: An apparatus and method comprising at least one intragastric member or artificial bezoar made of a digestive-resistant or substantially indigestible material that is introduced into a gastric lumen of a mammal for the treatment of obesity. The intragastric member or artificial bezoar is typically at inserted into the gastric lumen in a partially compacted configuration, whereby it is then manipulated into, or allowed to assume, a second expanded configuration sufficiently large to remain within the reservoir of the stomach during normal activities and not be passed through the pylorus into the intestines. In animals, the present invention has been found to be effective in
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achieving weight loss over a several month period, while being easy to place and retrieve. Excerpt(s): This application claims the benefit of U.S. Provisional Application No. 60/291,790 filed May 17, 2001, and U.S. Provisional Application No. 60/360,353 filed Feb. 27, 2002, both entitled "Intragastric Device For Treating Obesity".... This invention relates to medical devices, and more particularly to obesity treatment devices that can be placed in the stomach of a patient to reduce the size of the stomach reservoir.... It is well known that obesity is a very difficult condition to treat. Methods of treatment are varied, and include drugs, behavior therapy, and physical exercise, or often a combinational approach involving two or more of these methods. Unfortunately, results are seldom long term, with many patients eventually returning to their original weight over time. For that reason, obesity, particularly morbid obesity, is often considered an incurable condition. More invasive approaches have been available which have yielded good results in many patients. These include surgical options such as bypass operations or gastroplasty. However, these procedures carry high risks, and are therefore not appropriate for most patients. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
MCH antagonists and their use in the treatment of obesity Inventor(s): Chan, Tin Yau; (Edison, NJ), Palani, Anandan; (Bridgewater, NJ), Josien, Hubert B. (Hoboken, NJ), Clader, John W. (Cranford, NJ) Correspondence: SCHERING-PLOUGH CORPORATION; PATENT DEPARTMENT (K6-1, 1990); 2000 GALLOPING HILL ROAD; KENILWORTH; NJ; 07033-0530; US Patent Application Number: 20030105094 Date filed: March 19, 2002 Abstract: The present invention discloses compounds which, are novel antagonists for melanin-concentrating hormone (MCH), as well as methods for preparing such compounds. In another embodiment, the invention discloses pharmaceutical compositions comprising such MCH antagonists as well as methods of using them to treat obesity, metabolic disorders, eating disorders such as hyperphagia, and diabetes. Excerpt(s): This application claims the benefit of U.S. Provisional Application No. 60/277,584, filed Mar. 21, 2001.... This invention relates to antagonists for melaninconcentrating hormone (MCH) and their use in the treatment of metabolic and eating disorders.... MCH, a cyclic peptide, was first identified over a decade ago in teleost fish where it appears to regulate color change. More recently, MCH has been the subject of investigation for its possible role as a regulator of eating behavior in mammals. As reported by Shimada et al., Nature, Vol. 396 (Dec. 17, 1998), pp. 670-673, MCH-deficient mice have reduced body weight and leanness due to hypophagia (reduced feeding). In view of their findings, it was suggested that antagonists of MCH action may be effective for the treatment of obesity. U.S. Pat. No. 5,908,830 discloses a combination therapy for the treatment of diabetes or obesity involving the administration of a metabolic rate increasing agent and a feeding behavior modifying agent, an example of the latter being an MCH antagonist. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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MCH antagonists for the treatment of obesity Inventor(s): McBriar, Mark D. (Stewartsville, NJ), Shapiro, Sherry A. (Belford, NJ), Palani, Anandan; (Bridgewater, NJ), Su, Jing; (Scotch Plains, NJ) Correspondence: SCHERING-PLOUGH CORPORATION; PATENT DEPARTMENT (K6-1, 1990); 2000 GALLOPING HILL ROAD; KENILWORTH; NJ; 07033-0530; US Patent Application Number: 20030144261 Date filed: October 23, 2002 Abstract: The present invention discloses compounds, which are novel antagonists for melanin-concentrating hormone (MCH), as well as methods for preparing such compounds. In another embodiment, the invention discloses pharmaceutical compositions comprising such MCH antagonists as well as methods of using them to treat obesity, metabolic disorders, eating disorders such as hyperphagia, and diabetes. Excerpt(s): This application claims the benefit of U.S. Provisional Application No. 60/343,065 filed on Oct. 25, 2001.... This invention relates to antagonists of melaninconcentrating hormone (MCH) and their use in the treatment of obesity, eating disorders and diabetes, pharmaceutical compositions containing the compounds, and methods of treatment using the compounds.... MCH, a cyclic peptide, was first identified over a decade ago in teleost fish where it appears to regulate color change. More recently, MCH has been the subject of investigation for its possible role as a regulator of eating behavior in mammals. As reported by Shimada et al., Nature, Vol. 396 (17 Dec. 1998), pp. 670-673, MCH-deficient mice have reduced body weight and leanness due to hypophagia (reduced feeding). In view of their findings, it was suggested that antagonists of MCH action may be effective for the treatment of obesity. U.S. Pat. No. 5,908,830 discloses a combination therapy for the treatment of diabetes or obesity involving the administration of a metabolic rate increasing agent and a feeding behavior modifying agent, an example of the latter being an MCH antagonist. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Medicament for treating obesity and improving lipid metabolism Inventor(s): Nakata, Tadashi; (Saitama, JP), Shimizu, Takeshi; (Saitama, JP), Suzuki, Kunio; (Saitama, JP) Correspondence: GREENBLUM & BERNSTEIN, P.L.C. 1941 ROLAND CLARKE PLACE; RESTON; VA; 20191; US Patent Application Number: 20020086855 Date filed: January 7, 2002 Abstract: A medicament for preventive and therapeutic treatment of obesity and a disease with abnormal lipid metabolism which comprises a 24-alkylcholest-5-en-3-one as an active ingredient. Excerpt(s): This application is a divisional of application Ser. No. 09/480,892, filed Jan. 11, 2000, which is a continuation-in-part of application Ser. No. 09/186,153, filed Nov. 5, 1998. The entire disclosures of application Ser. Nos. 09/480,892 and 09/186,158 are expressly incorporated by reference herein in their entireties.... The present invention relates to medicaments useful for preventive and/or therapeutic treatment of obesity, and to medicaments of improving lipid metabolism.... Obesity is caused by insufficient exercise of habitual hyperphagia, or by metabolic disturbance due to genetic causes or
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endocrine diseases and other. Obesity may be a risk factor that causes various adult diseases such as myocardial infarct or arterial sclerosis, and it may also be a cause for deteriorating these diseases. Therefore, early therapeutic and preventive treatment of obesity is very important. Diet therapies or exercise therapies have been applied heretofore as the treatment of mild obesity, and drug therapies are sometimes used for serious obesity in combination with these therapies. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Method and apparatus for treating obesity and for delivering time-released medicaments Inventor(s): Lloyd, Greg A. (Spokane, WA) Correspondence: WELLS ST. JOHN ROBERTS GREGORY & MATKIN P.S. 601 W. FIRST AVENUE; SUITE 1300; SPOKANE; WA; 99201-3828; US Patent Application Number: 20030021822 Date filed: July 25, 2001 Abstract: An apparatus and method for treating obesity and for delivering time-released medicaments is described and which includes a plurality of space-filling portions which are sized to be received within a human patient's body and which come together in a patient's body to form a structure which provides therapeutic benefit to the patient. In the method of the present invention, the method includes providing a plurality of spacefilling portions which are sized to be received within the patient's body; and inserting the space-filling portions into the body of the patient and wherein the respective spacefilling portions come together following insertion into the body to form a structure providing therapeutic benefit to the patient. Excerpt(s): The present invention relates to a method and apparatus for treating obesity in humans and for delivering time-release medicaments into a patient's stomach and more particularly to a therapeutic structure which includes a plurality of space-filling portions which are sized to be received within the human patient's body and which come together in the patient's body to form a structure which provides therapeutic benefits.... The adverse health consequences of obesity are well known and established. It is clear that many interrelated behavioral and/or metabolic factors are at work. Consequently, it is extremely difficult for many obese people to lose weight on there own volition.... For obese patients at high risk of weight-related illness, and for the morbidly obese, there are a variety of available bariatric treatments. The most aggressive procedures are the various bariatric surgeries for reducing the stomach lumen. These surgeries include gastroplasty, gastric banding, intragastric balloons and gastric stapling. These methods can be highly effective because they severely limit the amount of food a person can ingest at one sitting, and depending upon the procedure, may induce a continual sense of satiety. Unfortunately, these surgical procedures are quite expensive. Further, the general poor health of this class of patient in combination with a major surgical procedure results in a high incidence of complications and mortality. In another approach utilizing minor surgery, an intragastric balloon can be positioned by way of permanently placed, percutaneous endoscopic gastrostomy tube. However, as with any permanent aperture made through the skin, special hygienic practices are required of the patient and complications often arise. Non-surgical bariatric procedures such as the placement of intragastric inflatable balloons via the esophagus, for example, require what is viewed to be an uncomfortable endoscopic procedure. Yet another nonsurgical bariatric procedure entails wiring a patient's jaw shut to limit food intake.
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However, besides being quite embarrassing and physically uncomfortable, this procedure carries an attendant risk of aspiration of vomit so patients must carry scissors or wire cutters at all times. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Method for the treatment and prevention of overweight in mammals Inventor(s): Verlaan, George; (Wageningen, NL), Raggers, Rene John; (Amsterdam, NL) Correspondence: YOUNG & THOMPSON; 745 SOUTH 23RD STREET 2ND FLOOR; ARLINGTON; VA; 22202 Patent Application Number: 20030175368 Date filed: March 11, 2003 Abstract: The present invention relates to a method for the prevention and/or treatment of overweight in mammals. More particularly the invention is concerned with such a method comprising the enteral administration to a mammal of a preparation comprising an effective amount of a combination of dill or an isolate thereof and one or more components capable of stimulating in vivo lipolysis. Suitable examples of components capable of stimulating in vivo lipolysis include methylxanthines, adrenergic amines, Paullinia cupana or an isolate thereof, Zingziber officinale or an isolate thereof, Camellia sinensis or an isolate thereof, Ilex paraguayiensis or an isolate thereof.Another aspect of the invention relates to a solid or semi-solid unit dosage, preferably selected from the group consisting of tablets, pills, microparticles, microspheres, suppositories, capsules, caplets and the like, that is suitable for enteral unitary administration to human subjects and other mammals comprising:a. dill or an isolate thereof in an amount equivalent to between 5 mg and 20 g dill andb. a component capable of stimulating in vivo lipolysis. Excerpt(s): The present invention relates to a method for the prevention and/or treatment of overweight comprising the enteral administration of a component capable of stimulating in vivo lipolysis. Additionally the present invention provides unit dosages, which can suitably be used for the prophylactic and curative treatment of overweight.... Obesity is very common in nowadays society. Approximately 25% to 35% of the population of the Western world is overweight. Overweight is associated with considerable morbidity and mortality. Obesity is the second preventable death cause in de US and a major risk factor for coronary heart disease, hypertension and diabetes mellitus type II. A reduction of body weight with 10% has shown to decrease the risk for coronary heart disease with 20%. Besides this, overweight and/or excess body fat is generally considered a problem, influencing social satisfaction and perception of health.... Attempts to combat overweight are often focussed on alteration of the diet or manipulation of the appetite in order to reduce caloric intake. However, there is accumulating evidence that low energy output predisposes individuals to weight gain and obesity, whether the low energy output is caused by low metabolic rate, physical inactivity or both. Increased energy metabolism therefore is an attractive target for treating overweight. Additionally, it allows people to maintain food intake at socially acceptable levels. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Method for the treatment of obesity, overweight and fluctuations in blood insuline and/or glucose levels Inventor(s): Nieuwenhuizen, Arie Gijsbert; (Utrecht, NL), Van Laere, Katrien Maria Jozefa; (Heteren, NL) Correspondence: YOUNG & THOMPSON; 745 SOUTH 23RD STREET 2ND FLOOR; ARLINGTON; VA; 22202 Patent Application Number: 20030113310 Date filed: December 17, 2001 Abstract: The present invention relates to a method of treating or preventing obesity, overweight, fluctuations in blood insulin levels and/or fluctuations in blood glucose levels in mammals. The method acording to the invention comprises the enteral administration to a mammal of an effective amount of a preparation containing an enzyme capable of converting an ingested carbohydrate or digestion product thereof into one or more absorbable components, wherein the total metabolic caloric value of the absorbable component(s) is less than the metabolic caloric value of the ingested carbohydrate or digestion product thereof. Thus the present invention effectively provides a method that allows complete digestion of ingested digestible carbohydrates whilst at the same time reducing the actual metabolic caloric value of said ingested carbohydrates.Another aspect of the invention relates to a pill for oral administration provided with an enteric coating and containing 25 to 10.000 IU glucose isomerase per gram. Excerpt(s): The present invention relates to method for the prevention or treatment of overweight, obesity or fluctuations in blood insuline and/or glucose levels in mammals, the method comprising the administration to a mammal of an enzyme capable of converting an ingested carbohydrate or a digestion product thereof into one or more absorbable components, wherein the total metabolic caloric value of the absorbable component(s) is less than the metabolic caloric value of the ingested carbohydrate or digestion product thereof. The invention also provides a preparation useful for such treatment.... Methods for treatment or prevention of obesity, overweight and fluctuations in blood glucose and/or blood insulin levels known in the art often make use of foodstuffs with reduced caloric value; compositions stimulating metabolism, e.g. by inducing in vivo thermogenisis; or compositions providing in vivo inhibition of digestive enzyme activity. Many drawbacks are attached to the methods as described above. Especially low caloric diets are particularly undesirable due to the required change in consumption pattern and the adverse taste of many low caloric foodstuffs. The inhibition of digestive enzyme activity has the disadvantage that it often causes flatulence and that its efficacy is seriously influenced by dietary factors.... Like obese individuals, also subjects who desire to reduce blood glucose and/or blood insulin fluctuations have to carefully control their diet, e.g. by consuming limited amounts of carbohydrates or by consuming foodstuffs with a low carbohydrate content. The downsides are significant as, for example, low carbohydrate compositions often have a bad taste. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Method for treating morbid obesity Inventor(s): Stein, Alan; (Moss Beach, CA), Silverman, David E. (Palo Alto, CA) Correspondence: DORSEY & WHITNEY LLP; INTELLECTUAL PROPERTY DEPARTMENT; 4 EMBARCADERO CENTER; SUITE 3400; SAN FRANCISCO; CA; 94111; US Patent Application Number: 20030158601 Date filed: March 10, 2003 Abstract: A method for treating morbid obesity in a body of a mammal having a gastrointestinal tract extending through a stomach and a pyloric sphincter and a wall forming the stomach and pyloric sphincter. At least one implant is formed in the wall in the vicinity of the pyloric sphincter to inhibit emptying of the stomach. Excerpt(s): This application claims priority to U.S. provisional patent application Serial No. 60/212,072, filed Jun. 15, 2000, the entire contents of which are hereby incorporated herein by reference.... This invention pertains to the treatment of morbid obesity.... Numerous modalities are purported to treat morbid obesity. These include patientspecific dietary restrictions and nutritional supplementation, abdominoplasty or panniculectomy, gastric banding and/or stapling and the more invasive and surgically aggressive gastric bypass. There is a need for a method which is less invasive and more clinically efficacious in treating morbid obesity. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Method for treatment of insulin resistance in obesity and diabetes Inventor(s): Hochgeschwender, Ute; (Oklahoma City, OK), Brennan, Miles B. (Denver, CO) Correspondence: SHERIDAN ROSS PC; 1560 BROADWAY; SUITE 1200; DENVER; CO; 80202 Patent Application Number: 20020099014 Date filed: September 13, 2001 Abstract: Disclosed is a method to identify compounds useful for reducing insulin resistance in a patient, and particularly a patient that has insulin resistance associated with obesity and/or type II diabetes. Also disclosed is a method of reducing insulin resistance in a patient by administering a compound identified using the method of the invention, and particularly, by administering an antagonist of melanocortin stimulating hormone (MSH) biological activity. Excerpt(s): This invention claims priority under 35 U.S.C..sctn.119(e) from U.S. Provisional Application Serial No. 60/232,292, filed Sep. 13, 2000, entitled, "Method for Investigating and Treating Diabetes". The entire disclosure of U.S. Provisional Application Serial No. 60/232,292 is incorporated herein by reference.... The present invention relates to a non-human animal model for obesity and uses of such an animal for studying and developing methods for identifying compounds for use in the regulation of insulin resistance in obesity and type II diabetes, as well as a method of treating insulin resistance in obesity and type II diabetes by administration of such compounds.... Diabetes, and conditions related thereto, are major health concerns throughout the world, and, particularly in the United States, contribute to morbidity and mortality. Non-insulin dependent diabetes mellitus (NIDDM), also known as type II
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diabetes, is the major form of diabetes in developed countries. While a large number of environmental and genetic factors contribute to the risk of NIDDM in the United States, prolonged obesity is by far the largest risk factor. The molecular basis of this association, however, is not fully understood. As a consequence, efficient means of therapeutical intervention are lacking. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Method of identifying compounds suitable for treatment and/or prophylaxis of obesity Inventor(s): Preuschoff, Ulf; (Lehrte, DE), Weske, Michael; (Burgdorf, DE), David, Samuel; (Hannover, DE), Antel, Jochen; (Bad Muender, DE), Hebebrand, Johannes; (Marburg, DE), Sann, Holger; (Hannover, DE) Correspondence: CROWELL & MORING LLP; INTELLECTUAL PROPERTY GROUP; P.O. BOX 14300; WASHINGTON; DC; 20044-4300; US Patent Application Number: 20020022245 Date filed: July 18, 2001 Abstract: A method for the discovery of compounds suitable for the treatment and/or prophylaxis of obesity, in which the ability of the test compounds to inhibit de novo lipogenesis in mammals and/or man is determined. The use of compounds which are capable of inhibiting de novo lipogenesis in mammals, and which are substantially free of effects directed towards the CNS, for the preparation of pharmaceutical compositions for the treatment and/or prophylaxis of obesity, as well as for the treatment and/or inhibition of obesity, are also described. Excerpt(s): The present invention relates to a method of identifying compounds suitable for the treatment and/or prophylaxis of obesity. The invention further relates to the use of compounds which are capable of inhibiting de novo lipogenesis in mammals, and which are substantially free of effects directed towards the central nervous system (=CNS), for the preparation of drugs for the treatment and/or prophylaxis of obesity.... Today, especially in the developed industrial nations, obesity is an increasingly serious problem for the health of the population, being caused predominantly by unbalanced and excessively high-fat nutrition. The increase in the percentage of overweight people in the population is being accompanied by an increase in the consequences of obesity, which range from personal discontentment to cardiovascular disease or certain forms of diabetes. There are therefore already a number of therapeutic procedures aimed at the treatment or prophylaxis of obesity. One example which may be mentioned is lipaseinhibitory compounds, which reduce lipolysis in the intestinal tract and thereby cut down the energy yield from the food intake. Thus, in this therapeutic procedure, at least part of the alimentary fats is excreted undecomposed. It is however desirable to have other novel therapeutic procedures for the treatment and/or prophylaxis of obesity which can complement the previously known forms of therapy.... It has now been found, surprisingly, that compounds which are capable of inhibiting de novo lipogenesis in mammals, especially man, are advantageously suitable for the effective treatment and/or prophylaxis of obesity. Particularly good results are achieved by administering the above-mentioned compounds over prolonged periods, for example for periods of several weeks. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Method of treating obesity in adult patients exhibiting primary insulin hypersecretion Inventor(s): Lustig, Robert H. (San Francisco, CA) Correspondence: Michael L. Goldman; NIXON PEABODY LLP; Clinton Square; P.O. Box 31051; Rochester; NY; 14603; US Patent Application Number: 20020156010 Date filed: November 8, 2001 Abstract: Methods of treating obesity in adult patients, reducing the caloric intake in an obese adult patient, and inhibiting insulin hypersecretion in an obese adult patient are disclosed. The methods are practiced by administering to an obese adult patient exhibiting primary insulin hypersecretion an effective amount of somatostatin, a somatostatin receptor agonist or its salt, or combinations thereof, under conditions effective to reduce the weight of the obese adult patient, reduce the caloric intake of the obese adult patient, or inhibit insulin hypersecretion by pancreatic.beta.-cells of the obese adult patient. Excerpt(s): This application claims benefit of U.S. Provisional Patent Application Serial No. 60/252,324, filed Nov. 20, 2000, which is hereby incorporated by reference in its entirety.... The present invention generally relates to method of treating obesity, inhibiting insulin hypersecretion, and reducing the caloric intake in obese adult patients exhibiting primary insulin hypersecretion.... Obesity has reached epidemic proportions throughout the world. The prevalence of obesity (BMI>30 kg/m.sup.2) in the U.S. has risen from 12.8% to 22.5% during the last 20 years (Kuczmarski, et al., "Increasing prevalence of overweight in U.S. adults: The National Health and Nutrition Examination Surveys, 1960 to 1991," JAMA, 272:205-211 (1994); Mokdad, et al., "The spread of the obesity epidemic in the United States, 1991-1998," JAMA, 282:1519-1522 (1999); Bray, et al., "Current and potential drugs for treatment of obesity," Endocrine Rev, 20:805-875 (1999)). Diet and exercise alone are frequently unsuccessful in ameliorating the obesity long-term (Luepker, et al., "Outcomes of a field trial to improve children's dietary patterns and physical activity," JAMA, 275:768-776 (1996); Skender, et al., "Comparison of 2-year weight loss trends in behavioral treatments of obesity: diet, exercise, and combination interventions," J Am Diet Assoc, 96:342-346 (1996); Bray, et al., "Treatment of obesity: an overview," Diab Metab Rev, 4:653-679 (1988)), stressing the importance of metabolic and genetic components to this syndrome. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Methods and therapeutic combinations for the treatment of obesity using sterol absorption inhibitors Inventor(s): Veltri, Enrico P. (Princeton, NJ), Strony, John T. (Lebanon, NJ), Ress, Rudyard J. (Flemington, NJ), Davis, Harry R. (Berkeley Heights, NJ) Correspondence: SCHERING-PLOUGH CORPORATION; PATENT DEPARTMENT (K6-1, 1990); 2000 GALLOPING HILL ROAD; KENILWORTH; NJ; 07033-0530; US Patent Application Number: 20030119428 Date filed: September 19, 2002 Abstract: The present invention provides methods for the treatment of obesity using sterol or 5.alpha.-stanol absorption inhibitors and compositions and therapeutic
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combinations including sterol or 5.alpha.-stanol absorption inhibitors and at least one obesity control medication. Excerpt(s): This application claims the benefit of priority from U.S. Provisional Patent Application Serial No. 60/323,840, filed Sep. 21, 2001, and is a continuation-in-part of U.S. patent application Ser. No. 10/166,942, filed Jun. 11, 2002, each incorporated herein by reference.... The present invention relates to compositions and therapeutic combinations for treating obesity in a subject comprising the administration of sterol and/or 5.alpha.-stanol absorption inhibitor(s) or combinations with obesity control medications.... Obesity is one of the most common medical problems in the United States and other developed countries and a risk factor for other illnesses, such as hypertension, diabetes, degenerative arthritis and myocardial infarction. Weight loss medications may be appropriate for use in selected patients who are obese or who are overweight with co-morbid conditions. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Methods for predicting susceptibility to obesity and obesity-associated health problems Inventor(s): Vohl, Marie-Claude; (Cap-Rouge, CA), Williams, Scott M. (Nashville, TN), Gaudet, Daniel; (Chicoutimi, CA), Engert, James C. (Montreal, CA), Hudson, Thomas J. (Montreal, CA), Lepage, Pierre; (Montreal, CA) Correspondence: HAMILTON, BROOK, SMITH & REYNOLDS, P.C. 530 VIRGINIA ROAD; P.O. BOX 9133; CONCORD; MA; 01742-9133; US Patent Application Number: 20030032099 Date filed: April 4, 2002 Abstract: Methods for determining an individual's susceptibility to obesity or to a health disorder associated with obesity, comprising detecting an allele at a polymorphic site genetically linked to the resistin gene locus, wherein the allele is further linked to obesity, and wherein detection of the allele is indicative of the patient's susceptibility to a health disorder associated with obesity are provided. Also included in the present disclosure are nucleic acid molecules containing allelic variants at polymorphic sites. Excerpt(s): This application claims the benefit of U.S. Provisional Application No. 60/281,449, filed Apr. 4, 2001, the entire teachings of which are incorporated herein by reference.... The frequency of obesity is increasing worldwide. Obesity is associated with health disorders such as diabetes mellitus, coronary heart disease, cancer, and sleepbreathing disorders. Indeed, the recent increase in numbers of obese people is cited as a reason for the corresponding rise in the number of cases of Type II diabetes. The documented association of obesity with disorders such as diabetes suggests a need for a better understanding of both the factors that affect obesity and the mechanisms by which obesity is related to other disorders.... Notions of obese individuals as lacking the will power sufficient to curb eating habits are being replaced by theories that obesity has specific genetic and molecular determinants. From genetic evidence, it is becoming clear that factors leading to a predisposition for obesity are heritable, thus implying the existence of one or more genes responsible for causing obesity. Identification of these genes and characterization of their gene products will provide clues to the treatment of obesity and disorders commonly associated with obesity. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Methods for the treatment of metabolic disorders, including obesity and diabetes Inventor(s): Xu, Haiyan; (Weymouth, MA) Correspondence: Jean M. Silveri; Millennium Pharmaceuticals, Inc. 75 Sidney Street; Cambridge; MA; 02139; US Patent Application Number: 20030143610 Date filed: January 8, 2003 Abstract: The invention relates to methods and compositions for the diagnosis and treatment of metabolic disorders, including, but not limited to, obesity, diabetes, overweight, insulin resistance, anorexia, and cachexia. The invention further provides methods for identifying a compound capable of treating a metabolic disorder. The invention also provides methods for identifying a compound capable of modulating a metabolic activity. Yet further, the invention provides a method for modulating a metabolic activity. In addition, the invention provides a method for treating a subject having a metabolic disorder characterized by aberrant SARP3 polypeptide activity or aberrant SARP3 nucleic acid expression. In another aspect, the invention provides methods for modulating lipogenesis in a subject and methods for modulating lipolysis in a subject. Excerpt(s): This application claims the benefit of U.S. Provisional Application No. 60/346,523, filed Jan. 8, 2002, the contents of which are incorporated herein by this reference.... During normal embryonic and adult development of multicellular organisms, cells that are not necessary or deleterious are eliminated by a process referred to as programmed cell death or apoptosis (Ellis R. E. et al. (1991) Annual Rev. Cell Biol. 7:663-698). Programmed cell death occurs in both vertebrate and invertebrate species and is characterized by unique morphological alterations, such as cytoplasmic contraction and chromatin condensation, as well as by specific DNA cleavage into oligonucleosomal fragments. Unlike necrosis, programmed cell death or apoptosis is an irreversible process which in most systems appears to depend on the expression of a specific set of novel "death genes". Deregulation of this process contributes to the pathogenesis of several diseases including cancer, immunodeficiency, autoimmune diseases, and neurodegenerative disorders (Thompson C. B. et al. (1995) Science 267: 1456).... Adipose tissue consists primarily of adipocytes. Vertebrates possess two distinct types of adipose tissue: white adipose tissue (WAT) and brown adipose tissue (BAT). WAT stores and releases fat according to the nutritional needs of the animal. This stored fat is used by the body for (1) heat insulation (e.g., subcutaneous fat), (2) mechanical cushion (e.g., surrounding internal organs), and (3) as a source of energy. BAT burns fat, releasing the energy as heat through thermogenesis. BAT thermogenesis is used both (1) to maintain homeothermy by increasing thermogenesis in response to lower temperatures and (2) to maintain energy balance by increasing energy expenditure in response to increases in caloric intake (Sears, I. B. et al. (1996) Mol. Cell. Biol. 16(7):34103419). BAT is also the major site of thermogenesis in rodents and plays an important role in thermogenesis in human infants. In humans, and to a lesser extend rodents, brown fat diminishes with age, but can be re-activated under certain conditions, such as prolonged exposure to cold, maintenance on a high fat diet and in the presence of noradrenaline producing tumors. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
Patents 367
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Methods for the treatment of metabolic disorders, including obesity and diabetes Inventor(s): An, Wenqian Frank; (Framingham, MA), Chen, Hong; (Newton, MA) Correspondence: Jean M. Silveri; Millennium Pharmaceuticals, Inc. 75 Sidney Street; Cambridge; MA; 02139; US Patent Application Number: 20030157110 Date filed: January 7, 2003 Abstract: The invention relates to methods and compositions for the diagnosis and treatment of metabolic disorders, including, but not limited to, obesity, overweight, diabetes, insulin resistance, anorexia, and cachexia. The invention further provides methods for identifying a compound capable of treating a metabolic disorder. The invention also provides methods for identifying a compound capable of modulating a metabolic activity. Yet further, the invention provides a method for modulating a metabolic activity. In addition, the invention provides a method for treating a subject having a metabolic disorder characterized by aberrant MMP-12 polypeptide activity or aberrant MMP-12 nucleic acid expression. In another aspect, the invention provides methods for modulating lipogenesis in a subject and methods for modulating lipolysis in a subject. Excerpt(s): This application claims the benefit of U.S. Provisional Application No. 60/346,354, filed Jan. 7, 2002, the contents of which are incorporated herein by this reference.... The matrix metalloproteinases (MMPs) are a family of structurally related matrix-degrading enzymes produced by macrophages that play important roles in tissue growth and remodeling during normal embryonic development as well as during tissue repair. These zinc-binding endopeptidases are involved in the degradation of extracellular matrix (ECM) components, such as elastin, and function at neutral pH and require Ca.sup.+2 to be active. MMP activitiy is further regulated by tissue inhibitors of metalloproteinases (TIMPs), also produced by macrophages. The MMPs can be divided into four major subfamilies based on sequence homology and domain structures. One subfamily includes matrilysin (also known as MMP-7). It has been attributed with elastolytic activity and is found in peripheral blood monocytes, but not in alveolar macrophages (Busick, et al., (1992) J. Biol. Chem. 267:9087-9092). A second family includes at least three collagenases (MMP-1, MMP-8, and MMP-13), stromelysin (MMP3, MMP-10, and MMP-11), and metalloelastase (MMP-12). The DNA cloning of stromelysin is described in WO 87/07907. The DNA cloning of MMP-12 is described, e.g., in U.S. Pat. No. 6,204,043; and Shapiro, e al., (1992) J. Biol. Chem. 267:4664-4671. A third family includes two type IV-collagenase/gelatinases (MMP-2 and MMP-9), described, e.g., in U.S. Pat. Nos. 4,772,557, 4,923,818, and 4,992,537, respectively. The fourth family includes five members (MMP-14, MMP-15, MMP-16, MMP-17 or MTI-4MMP, and MT5-MMP) that are known as membrane type MMPs.... Given their role in tissue remodeling and repair, aberrant MMP expression or activity is associated with various diseases, such as tumorigenesis, metastasis, and inflammatory disorders such as rheumatoid arthritis, osteoarthritis, atherosclerosis, and pulmonary emphysema. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
368 Obesity
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METHODS FOR TREATING OBESITY Inventor(s): KOLTERMAN, ORVILLE G. (POWAY, CA), DUFT, BRADFORD J. (SANTE FE, CA) Correspondence: Bradford J Duft Esq; Brobeck Phleger and Harrison LLP; 12390 El Camino Real; San Diego; CA; 92130-2081; US Patent Application Number: 20030026812 Date filed: June 6, 1997 Abstract: Methods for treating obesity are disclosed which comprise administration of a therapeutically effective amount of an amylin or an amylin agonist alone or in conjunction with another obesity relief agent. Excerpt(s): The present invention relates to methods for treating obesity. More particularly, the invention relates to the use of an amylin or agonist of amylin in the treatment of obesity.... The structure and biology of amylin have previously been reviewed. See, for example, Rink et al., Trends in Pharmaceutical Sciences, 14:113-118 (1993); Gaeta and Rink, Med. Chem. Res., 3:483-490 (1994); and, Pittner et al., J. Cell. Biochem., 55S:19-28 (1994). Amylin is a 37 amino acid protein hormone. It was isolated, purified and chemically characterized as the major component of amyloid deposits in the islets of pancreases of deceased human Type 2 diabetics (Cooper et al., Proc. Natl. Acad. Sci. USA, 84:8628-8632 (1987)). The amylin molecule has two important posttranslational modifications: the C-terminus is amidated, and the cysteines in positions 2 and 7 are cross-linked to form an N-terminal loop. The sequence of the open reading frame of the human amylin gene shows the presence of the Lys-Arg dibasic amino acid proteolytic cleavage signal, prior to the N-terminal codon for Lys, and the Gly prior to the Lys-Arg proteolytic signal at the C-terminal position, a typical sequence for amidation by protein amidating enzyme, PAM (Cooper et al., Biochem. Biophys. Acta, 1014:247-258 (1989)). Amylin is the subject of U.S. Pat. No. 5,367,052, issued Nov. 22, 1995.... In Type 1 diabetes, amylin has been shown to be deficient and combined replacement with insulin has been proposed as a preferred treatment over insulin alone in all forms of diabetes. The use of amylin and other amylin agonists for the treatment of diabetes mellitus is the subject of U.S. Pat. No. 5,175,145, issued Dec. 29, 1992. Pharmaceutical compositions containing amylin and amylin plus insulin are described in U.S. Pat. No. 5,124,314, issued Jun. 23, 1992. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Methods for using the obese gene and its gene product to stimulate hematopoietic development Inventor(s): Cioffi, Joseph; (New Albany, OH), Zupancic, Thomas Joel; (Worthington, OH), Snodgrass, H. Ralph; (Powell, OH), Shafer, Alan Wayne; (Lancaster, OH) Correspondence: PENNIE AND EDMONDS; 1155 AVENUE OF THE AMERICAS; NEW YORK; NY; 100362711 Patent Application Number: 20020197232 Date filed: March 12, 2002 Abstract: The present invention relates to methods for using various forms of a novel receptor expressed by hematopoietic and endothelial cells. An additional variant form of this receptor has been detected in brain cells and shown to bind to the obese gene
Patents 369
product, leptin. Therefore, leptin may be used to stimulate the growth and development of receptor-positive hematopoietic and endothelial cells in vitro and in vivo. In addition, this receptor is selectively expressed in hematopoietic progenitor cells with long-term repopulating potential. Thus, agents that specifically bind to this receptor may be used to identify and isolate progenitor cells for a variety of clinical applications. Excerpt(s): The present application is a continuation of co-pending U.S. patent application Ser. No. 08/618,957, filed Mar. 20, 1996, which is a continuation-in-part of U.S. patent application Ser. No. 08/589,915, filed Jan. 23, 1996, (now abandoned) which is a continuation-in-part of U.S. patent application Ser. No. 08/355,888, filed Dec. 14, 1994 (now U.S. Pat. No. 5,763,211), which is a continuation-in-part of U.S. patent application Ser. No. 08/306,231 filed Sep. 14, 1994 (now U.S. Pat. No. 5,643,748), each of which is incorporated by reference herein in its entirety.... The present invention relates to methods for using various forms of a novel receptor expressed by hematopoietic and endothelial cells. An additional variant form of this receptor has been detected in brain cells and shown to bind to the obese gene product, leptin. Therefore, leptin may be used to stimulate the growth and development of receptor-positive hematopoietic and endothelial cells in vitro and in vivo. In addition, this receptor is selectively expressed in hematopoietic progenitor cells with long-term repopulating potential. Thus, agents that specifically bind to this receptor may be used to identify and isolate progenitor cells for a variety of clinical applications.... A variety of diseases, including malignancy and immunodeficiency, are related to malfunction within the lympho-hematopoietic system. Some of these conditions could be alleviated and/or cured by repopulating the hematopoietic system with progenitor cells, which when triggered to differentiate would overcome the patient's deficiency. Therefore, the ability to initiate and regulate hematopoiesis is of great importance (McCune et al., 1988, Science 241:1632). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Methods of treating obesity using a neurotensin receptor ligand Inventor(s): Hadcock, John R. (East Lyme, CT) Correspondence: Gregg C. Benson; Pfizer Inc. Patent Department, MS 4159; Eastern Point Road; Groton; CT; 06340; US Patent Application Number: 20010046956 Date filed: April 24, 2001 Abstract: The present invention relates to methods of treating obesity, diabetes, sexual dysfunction, atherosclerosis, insulin resistance, impaired glucose tolerance, hypercholesterolemia or hypertrigylceridemia using a neurotensin receptor ligand. The present invention also relates to pharmaceutical compositions and kits that comprise a neurotensin receptor ligand. Excerpt(s): This application claims priority of U.S. provisional application No. 60/199,951, filed Apr. 27, 2000.... The present invention relates to methods of treating obesity, diabetes, sexual dysfunction (including erectile dysfunction), atherosclerosis, insulin resistance, impaired glucose tolerance, hypercholesterolemia, or hypertrigylceridemia using a compound that is a neurotensin receptor ligand. The present invention also relates to compositions and kits that comprise a neurotensin receptor ligand.... Obesity is a devastating disease. In addition to harming physical health, obesity can wreak havoc on mental health because obesity affects self-esteem, which ultimately can affect a person's ability to interact socially with others.
370 Obesity
Unfortunately, obesity is not well understood, and societal stereotypes and presumptions regarding obesity only tend to exacerbate the psychological effects of the disease. Because of the impact of obesity on individuals and society, much effort has been expended to find ways to treat obesity, but little success has been achieved in the long-term treatment and/or prevention of obesity. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Novel genes and their use in the modulation of obesity, diabetes and energy imbalance Inventor(s): McMillan, Janine Susan; (Torquay, AU), Walder, Kenneth Russell; (Ocean Grove, AU), Zimmet, Paul Zev; (Toorak, AU), Collier, Gregory; (Ocean Grove, AU), Windmill, Kelly Fiona; (Newtown, AU) Correspondence: Leopold Presser; Scully, Scott, Murphy & Presser; 400 Garden City Plaza; Garden City; NY; 11530; US Patent Application Number: 20020169287 Date filed: December 31, 2001 Abstract: The present invention relates generally to nucleic acid molecules encoding proteins associated with the modulation of obesity, diabetes and/or metabolic energy levels. More particularly, the present invention is directed to nucleic acid molecules and the recombinant and purified proteins encoded thereby and their use in therapeutic and diagnostic protocols for conditions such as obesity, diabetes and energy imbalance. The subject nucleic acid molecules and proteins and their derivatives, homologs, analogs, chemical equivalents and mimetics are proposed as therapeutic and diagnostic agents for obesity, diabetes and energy imbalance. Excerpt(s): This application a continuation of International Application No. PCT/AU00/00786, filed on Jun. 29, 2000.... The present invention relates generally to nucleic acid molecules encoding proteins associated with the modulation of obesity, diabetes and/or metabolic energy levels. More particularly, the present invention is directed to nucleic acid molecules and the recombinant and purified proteins encoded thereby and their use in therapeutic and diagnostic protocols for conditions such as obesity, diabetes and energy imbalance. The subject nucleic acid molecules and proteins and their derivatives, homologs, analogs, chemical equivalents and mimetics are proposed as therapeutic and diagnostic agents for obesity, diabetes and energy imbalance.... Bibliographic details of the publications referred to by author in this specification are collected at the end of the description. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Novel genes expressed in obese rat hypothalamus Inventor(s): Wu, Linda H. (Woodbridge, CT) Correspondence: BANNER & WITCOFF; 1001 G STREET N W; SUITE 1100; WASHINGTON; DC; 20001; US Patent Application Number: 20020041870 Date filed: July 26, 2001
Patents 371
Abstract: Novel genes expressed in obese rat hypothalamus can be used to provide therapeutic reagents for treating obesity and related disorders. Excerpt(s): This application claims the benefit of and incorporates by reference copending provisional application Ser. No. 60/220,878 filed Jul. 26, 2000.... The invention relates to methods and compositions for the modulation of processes related to mammalian body weight regulation, including treatment of body weight disorders such as obesity and cachexia, and modulation of thermogenesis.... The regulation of body fat in mammals is a complex process involving the regulation of not only appetite but also energy expenditure. See U.S. Pat. No. 6,057,109. An important component of energy expenditure is non-shivering thermogenesis (NST). In rodents, the majority of NST appears to occur in brown adipose tissue (BAT) via the uncoupling protein (UCP) (Cannon & Nedergaard, Essays in Biochem. 20, 110-65, 1985; Himms-Hagen, Prog. Lipid Res. 28, 67-115, 1989). UCP is a proton channel located exclusively in the inner mitochondrial membrane of adipocytes of the BAT (Nicholls & Locke, Physiol. Rev. 64, 1-64, 1984). By allowing protons to equilibrate across the inner mitochondrial membrane, UCP uncouples oxidative phosphorylation from ATP production and thus converts stored energy into heat rather than work (Klingenberg, Trends Biochem. Sci. 15, 108-12, 1990; Klaus et al., Int. J. Biochem. 23, 791-801, 1991). UCP-mediated uncoupling is not only capable of increasing body temperature in cold-acclimatized rodents and hibernating animals, but can also dissipate surplus caloric energy (Rothwell & Stock, In BROWN ADIPOSE TISSUE, Trayhurn et al., eds., London, Arnold, p. 269298, 1986; Spiegelman & Flier, Cell 87, 377-89, 1996; Hamann & Flier, Endocrinology 137:2129, 1996). A number of studies have now implicated UCP and brown adipose tissue as important regulators of body weight in rodents (Hamann & Flier, Endocrinology 137, 2129, 1996; Lowell et al., Nature 366, 740-42, 1993; Kopecky et al., J. Clin. Invest. 96, 2914-23, 1995; Cunmnings et al., Nature 382, 622-26, 1996). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Ob receptor and methods for the diagnosis and treatment of body weight disorders, including obesity and cachexia Inventor(s): Tepper, Robert I. (Weston, MA), Tartaglia, Louis A. (Watertown, MA), Culpepper, Janice A. (Brookline, MA), White, David W. (Holbrook, MA) Correspondence: ANITA L. MEIKLEJOHN, PH.D. Fish & Richardson P.C. 225 Franklin Street; Boston; MA; 02110-2804; US Patent Application Number: 20020182676 Date filed: February 19, 2002 Abstract: The present invention relates to the discovery, identification and characterization of nucleotides that encode Ob receptor (ObR), a receptor protein that participates in mammalian body weight regulation. The invention encompasses obR nucleotides, host cell expression systems, ObR proteins, fusion proteins, polypeptides and peptides, antibodies to the receptor, transgenic animals that express an obR transgene, or recombinant knock-out animals that do not express the ObR, antagonists and agonists of the receptor, and other compounds that modulate obR gene expression or ObR activity that can be used for diagnosis, drug screening, clinical trial monitoring, and/or the treatment of body weight disorders, including but not limited to obesity, cachexia and anorexia.
372 Obesity
Excerpt(s): This application is a continuation-in-part of application Ser. No. 08/708,123 filed Sep. 3, 1996, which is a continuation-in-part of application Ser. No. 08/638,524 filed Apr. 26, 1996, which is a continuation-in-part of application Ser. No. 08/599,455, filed Jan. 22, 1996, which is a continuation-in-part of application Ser. No. 08/583,153, filed Dec. 28, 1995, which is a continuation-in-part of application Ser. No. 08/570,142, filed Dec. 11, 1995, which is a continuation-in-part of application Ser. No. 08/569,485, filed Dec. 8, 1995, which is a continuation-in-part of application Ser. No. 08/566,622, filed Dec. 4, 1995, which is a continuation-in-part of application Ser. No. 08/562,663, filed Nov. 27, 1995.... The present invention relates to the discovery, identification and characterization of nucleotides that encode Ob receptor (ObR), a receptor protein that participates in mammalian body weight regulation. The invention encompasses obR nucleotides, host cell expression systems, ObR proteins, fusion proteins, polypeptides and peptides, antibodies to the receptor, transgenic animals that express an obR transgene, or recombinant knock-out animals that do not express the ObR, antagonists and agonists of the receptor, and other compounds that modulate obR gene expression or ObR activity that can be used for diagnosis, drug screening, clinical trial monitoring, and/or the treatment of body weight disorders, including but not limited to obesity, cachexia and anorexia.... Obesity represents the most prevalent of body weight disorders, and it is the most important nutritional disorder in the western world, with estimates of its prevalence ranging from 30% to 50% within the middle-aged population. Other body weight disorders, such as anorexia nervosa and bulimia nervosa which together affect approximately 0.2% of the female population of the western world, also pose serious health threats. Further, such disorders as anorexia and cachexia (wasting) are also prominent features of other diseases such as cancer, cystic fibrosis, and AIDS. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Obesity inhibitory materials Inventor(s): Takebe, Minoru; (Tokyo, JP) Correspondence: Koda & Androlia; Suite 3850; 2029 Century Park East; Los Angeles; CA; 90067-3024; US Patent Application Number: 20030082247 Date filed: March 6, 2002 Abstract: Anti-obesity material of the present invention is absorbed in vivo by oral ingestion, drops, etc. so as to act against the causes of overeating and control food consumption, and it can thereby promote fat metabolism and control accumulation of body fat while at the same time can inhibit elevation of blood pressure, all without compromising immune system function, thus safely controlling an increase in body weight (obesity). There have previously been no anti-obesity materials like that of the present invention whatsoever. The main characteristic of the present invention is that an anti-obesity material having the above-described excellent effects is obtained since the anti-obesity material has isoflavone aglycone and/or isoflavone glycoside. Excerpt(s): The present invention relates to an anti-obesity material capable of controlling obesity (weight increase) and in particular to an anti-obesity material capable of effectively controlling obesity by controlling an increase in body weight while controlling food consumption and enhancing in vivo immune function as a result of being absorbed in vivo.... Obesity is a cause of development of lifestyle-related disease, including hypertension, diabetes, hyperlipidemia, etc. Moreover, it is reported that, according to epidemiological research, when obese persons lose weight, their average
Patents 373
remaining years are improved. However, it is also a fact that even though obese persons recognize the fact that they are at high risk for lifestyle-related disease, they do not lose weight because it is extremely difficult for them to keep weight off by dietary, etc. methods.... Postmenopausal women in particular develop so-called climacteric symptoms due to a reduction in female hormone (estrogen) secretion. In addition to the climacteric disturbances represented by hot flashes, these symptoms are said to have an effect on general functions of bone metabolism, the cardiovascular system, fat metabolism, the urogenital system, the digestive system, the neurological system, etc. Consequently, hormone-replacement therapy (HRT) whereby female hormones are artificially replenished is being examined as a treatment for the symptoms caused by this loss of estrogen activity. Nevertheless, HRT also poses many problems in that adverse reactions such as uterine bleeding and breast tenderness, etc. readily develop. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Obesity treatment tools and methods Inventor(s): Andreas, Bernard H. (Redwood City, CA), Gifford, Hanson S. III; (Woodside, CA), Deem, Mark E. (Mountain View, CA), Sutton, Douglas S. (Pacifica, CA), French, Ronald G. (Santa Clara, CA) Correspondence: Johney U. Han; Morrison & Foerster LLP; 755 Page Mill Road; Palo Alto; CA; 94304-1018; US Patent Application Number: 20030109892 Date filed: January 14, 2003 Abstract: Various obesity treatment tools and methods are described herein, as well as treatments for other gastric-related diseases, e.g., GERD. Treatment includes reducing the size of the stomach pouch to limit the caloric intake as well as to provide an earlier feeling of satiety. This may be done by creating a smaller gastric pouch within the stomach directly from the interior of the stomach itself. The smaller pouches may be made through the use of individual anchoring devices, rotating probes, or volume reduction devices. A pyloroplasty procedure may also be performed to render the pyloric sphincter incompetent. A gastric bypass procedure may additionally be performed using atraumatic magnetic anastomoses devices so that sugars and fats are passed directly to the bowel while bypassing the stomach. Many of these procedures may be done in a variety of combinations. Treatment may create enforced behavioral modifications by discouraging the ingestion of high-caloric foods. Excerpt(s): This is a continuation of U.S. patent application Ser. No. 09/871,297, filed May 30, 2001, which is incorporated herein by reference in its entirety.... The present invention relates generally to tools and methods for the treatment of obesity. More particularly, the present invention relates to tools and methods for performing less traumatic gastroplasty procedures.... Obesity is considered a major health problem with annual associated costs reaching $100 billion in the U.S. alone. Morbid obesity is a condition of obesity with the presence of a secondary debilitating progressive disease and is generally associated with a body mass index (BMI).gtoreq.40 kg/m.sup.2. While the basic mechanism of obesity is simply an imbalance between caloric intake and burn rate, the underlying factors are varied and complex and conservative attempts at sustained weight loss with this population are almost always unsuccessful. Often, there are genetic and other biological influences that may override environmental causes. Consequently, obesity is a disease that eludes a simple treatment, with a recurrence rate above 90% for those who attempt to lose weight. Moreover, long-term results using
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conservative treatments for morbid obesity are generally unsuccessful and are typically associated with further loss of self-esteem with the regaining of weight. Hypertension, cardiovascular disease, diabetes, along with a host of other comorbidities all make morbid obesity second only to smoking as a preventable cause of death. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Obesity treatment tools and methods Inventor(s): Andreas, Bernard H. (Redwood City, CA), Gifford, Hanson S. III; (Woodside, CA), Sutton, Douglas S. (Pacifica, CA), Deem, Mark E. (Mountain View, CA), French, Ronald G. (Santa Clara, CA) Correspondence: Johney U. Han; Morrison & Foerster LLP; 755 Page Mill Road; Palo Alto; CA; 94304-1018; US Patent Application Number: 20030120265 Date filed: December 5, 2002 Abstract: Various obesity treatment tools and methods are described herein, as well as treatments for other gastric-related diseases, e.g., GERD. Treatment includes reducing the size of the stomach pouch to limit the caloric intake as well as to provide an earlier feeling of satiety. This may be done by creating a smaller gastric pouch within the stomach directly from the interior of the stomach itself. The smaller pouches may be made through the use of individual anchoring devices, rotating probes, or volume reduction devices. A pyloroplasty procedure may also be performed to render the pyloric sphincter incompetent. A gastric bypass procedure may additionally be performed using atraumatic magnetic anastomoses devices so that sugars and fats are passed directly to the bowel while bypassing the stomach. Many of these procedures may be done in a variety of combinations. Treatment may create enforced behavioral modifications by discouraging the ingestion of high-caloric foods. Excerpt(s): This is a divisional of U.S. patent application Ser. No. 09/871,297, filed May 30, 2001, which is incorporated herein by reference in its entirety.... The present invention relates generally to tools and methods for the treatment of obesity. More particularly, the present invention relates to tools and methods for performing less traumatic gastroplasty procedures.... Obesity is considered a major health problem with annual associated costs reaching $100 billion in the U.S. alone. Morbid obesity is a condition of obesity with the presence of a secondary debilitating progressive disease and is generally associated with a body mass index (BMI).gtoreq.40 kg/m.sup.2. While the basic mechanism of obesity is simply an imbalance between caloric intake and bum rate, the underlying factors are varied and complex and conservative attempts at sustained weight loss with this population are almost always unsuccessful. Often, there are genetic and other biological influences that may override environmental causes. Consequently, obesity is a disease that eludes a simple treatment, with a recurrence rate above 90% for those who attempt to lose weight. Moreover, long-term results using conservative treatments for morbid obesity are generally unsuccessful and are typically associated with further loss of self-esteem with the regaining of weight. Hypertension, cardiovascular disease, diabetes, along with a host of other comorbidities all make morbid obesity second only to smoking as a preventable cause of death. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
Patents 375
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Obesity-specific G protein coupled receptors Inventor(s): Wu, Linda H. (Woodbridge, CT) Correspondence: BANNER & WITCOFF; 1001 G STREET N W; SUITE 1100; WASHINGTON; DC; 20001; US Patent Application Number: 20020068306 Date filed: October 17, 2001 Abstract: Novel obesity-specific G protein-coupled receptors can be used to provide therapeutic reagents for treating obesity and related disorders. Excerpt(s): This application incorporates by reference and claims the benefit of copending provisional application Ser. No. 60/240,835 filed Oct. 17, 2000.... The invention relates to methods and compositions for the modulation of processes related to mammalian body weight regulation, including treatment of body weight disorders such as obesity and cachexia, and modulation of thermogenesis.... The regulation of body fat in mammals is a complex process involving the regulation of not only appetite but also energy expenditure. See U.S. Pat. No. 6,057,109. An important component of energy expenditure is non-shivering thermogenesis (NST). In rodents, the majority of NST appears to occur in brown adipose tissue (BAT) via the uncoupling protein (UCP) (Cannon & Nedergaard, Essays in Biochem. 20, 110-65, 1985; Himms-Hagen, Prog. Lipid Res. 28, 67-115, 1989). UCP is a proton channel located exclusively in the inner mitochondrial membrane of adipocytes of the BAT (Nicholls & Locke, Physiol. Rev. 64, 1-64, 1984). By allowing protons to equilibrate across the inner mitochondrial membrane, UCP uncouples oxidative phosphorylation from ATP production and thus converts stored energy into heat rather than work (Klingenberg, Trends Biochem. Sci. 15, 108-12, 1990; Klaus et al, Int. J. Biochem. 23, 791-801, 1991). UCP-mediated uncoupling is not only capable of increasing body temperature in cold-acclimatized rodents and hibernating animals, but can also dissipate surplus caloric energy (Rothwell & Stock, In BROWN ADIPOSE TISSUE, Trayhum et al., eds., London, Arnold, p. 269298, 1986; Spiegelman & Flier, Cell 87, 377-89, 1996; Hamann & Flier, Endocrinology 137:2129, 1996). A number of studies have now implicated UCP and brown adipose tissue as important regulators of body weight in rodents (Hamann & Flier, Endocrinology 137, 2129, 1996; Lowell et al., Nature 366, 740-42, 1993; Kopecky et al., J. Clin. Invest 96, 2914-23, 1995; Cummings et al., Nature 382, 622-26, 1996). Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html
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Percutaneous intragastric balloon catheter for the treatment of obesity Inventor(s): De Hoyos Garza, Andres; (Mexico City, MX) Correspondence: Paul J. Ethington; REISING ,ETHINGTON , BARNES, KISSELLE,; LEARMAN & McCULLOCH, P.C. Post Office Box 4390; Troy; MI; 48099; US Patent Application Number: 20010037127 Date filed: February 23, 2001 Abstract: The present invention relates to a percutaneous intragastric balloon catheter for the treatment of obesity. The invention occupies a portion of the gastric cavity causing a feeling of satiety and decreasing the consumption of food by an obese patient. This invention consists in a percutaneous intragastric balloon that is placed in a nonsurgically form. The percutaneous intragastric balloon catheter is collocated by
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percutaneous endoscopic gastrotomy (PEG). The invention comprises an affixed valve for regulating the amount of fluid introduced or evacuated from the percutaneous intragastric balloon. Excerpt(s): This invention relates to gastrostomy devices for use in the treatment of obesity. More particularly, the invention relates to percutaneous balloon catheters positioned in the stomach for medical treatment of morbid obesity in humans.... Morbid obesity is a chronic medical illness defined as overweight of 50 to 100 percent above the ideal body weight. Obesity is a major medical problem affecting millions of people worldwide. In addition to the phychosocial stigmas associated with the condition or disease, many serious health ramifications may develop. Hypertension, hyperlipidemia, exacerbation of diabetes mellitus, heart disease, degenerative arthritis, and Pickwickian syndrome. Certain types of cancer, gallstones, varicose veins, thromboembolism and hernias are more common among overweight individuals. In addition, morbid obesity can lead to psychosocial difficulties such as depression, loss of self-esteem and decreased employability.... To date, numerous attempts have been made to cause weight loss in morbidly obese patients. None of them have been entirely successful. The weight loss methods can be broadly divided into behavioral modification, vigorous exercise, use of pharmaceuticals, medical diets, surgical procedures and devices. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Pharmaceutical composition for the treatment of obesity or to facilitate or promote weight loss Inventor(s): Dow, Robert L. (Waterford, CT), O'Neill, Brian Thomas; (Old Saybrook, CT), Harrigan, Edmund Patrick; (Old Lyme, CT), Sands, Steven Bradley; (Stonington, CT), Coe, Jotham Wadsworth; (Niantic, CT), Watsky, Eric Jacob; (Stonington, CT) Correspondence: PFIZER INC; 150 EAST 42ND STREET; 5TH FLOOR - STOP 49; NEW YORK; NY; 10017-5612; US Patent Application Number: 20030176457 Date filed: February 13, 2003 Abstract: Pharmaceutical compositions are disclosed for the treatment of obesity, an overweight condition and compulsive overeating. The pharmaceutical compositions are comprised of a therapeutically effective combination of a nicotine receptor partial agonist and an anti-obesity agent or weight loss facilitator or promoter and a pharmaceutically acceptable carrier. The method of using these compounds is also disclosed. Excerpt(s): The present invention relates to pharmaceutical compositions for the treatment of obesity, compulsive overeating; or to facilitate or promote weight loss in a mammal (e.g. human) comprising a nicotine receptor partial agonist (NRPA) and an anti-obesity or weight loss promoting agent. The term NRPA refers to all chemical compounds which bind at neuronal nicotinic acetylcholine specific receptor sites in mammalian tissue and elicit a partial agonist response. A partial agonist response is defined here to mean a partial, or incomplete functional effect in a given functional assay. Additionally, a partial agonist will also exhibit some degree of antagonist activity by its ability to block the action of a full agonist (Feldman, R. S., Meyer, J. S. & Quenzer, L. F. Principles of Neuropsychopharmacology, 1997; Sinauer Assoc. Inc.). The present invention may be used to treat mammals (e.g. humans) for obesity, an overweight condition or compulsive overeating with a decrease in the severity of unwanted side
Patents 377
effects such as causing nausea and/or stomach upset.... Obesity is a major health risk that leads to increased mortality and incidence of Type 2 diabetes mellitus, hypertension and dyslipidemia. It is the second leading cause of preventable death in the United States, and contributes to>300,000 deaths per year. The estimated direct annual health cost associated with obesity is $70 billion, while the total overall cost to the U.S. economy has been estimated to be over $140 billion. In the U.S., more than 50% of the adult population is overweight, and almost 1/4 of the population is considered to be obese (BMI greater than or equal to 30). Furthermore, the prevalence of obesity in the United States has increased by about 50% in the past 10 years. While the vast majority of obesity occurs in the industrialized world, particularly in U.S. and Europe, the prevalence of obesity is also increasing in Japan. The prevalence of obesity in adults is 10%-25% in most countries of Western Europe. The rise in the incidence of obesity has promoted the WHO to recognize obesity as a significant disease. What is needed are orally active agents that induce sustained weight loss of 10-15% of initial body weight, due to selective loss of body fat in moderately obese patients. These orally active agents should increase energy expenditure, decrease food intake and partition energy away from adipose tissue. This degree of sustained weight loss would then improve comorbidities including hyperglycemia, hypertension and hyperlipidemia, all of which are exacerbated by obesity.... However, even though weight loss agents have therapeutic utility in the treatment of obesity, there are significant liabilities to the use of weight loss compounds. Specifically, many of these compounds that have been tested in humans can cause potentially serious side effects such as gastrointestinal complications including nausea, emesis, ulcers, constipation, flatulence, diarrhea, hypertension, respiratory depression, and psychological and physical dependence. Web site: http://appft1.uspto.gov/netahtml/PTO/search-bool.html •
Pharmaceuticals for treating obesity Inventor(s): Zhang, Bei B. (Edison, NJ), Zhou, Gaochao; (Scotch Plains, NJ), Moller, David E. (Bedminster, NJ), Mosley, Ralph T. (Roselle, NJ), Tolman, Richard L. (Menlo Park, CA), Leibowitz, Mark D. (San Diego, CA), Doebber, Thomas W. (Scotch Plains, NJ), Berger, Joel P. (Hoboken, NJ), Ventre, John; (Nutley, NJ) Correspondence: Merck & Co., Inc. Patent Department; P.O. Box 2000 - RY60-30; Rahway; NJ; 07065-0907; US Patent Application Number: 20030032581 Date filed: September 11, 2002 Abstract: Compounds which are antagonists of strong PPAR-gamma agonists, such as rosiglitazone, and are also partial agonists of the PPAR-gamma receptor, are active agents for correcting or reducing obesity. For example, 1-(p-chlorobenzyl)-5-chloro-3thiophenylindole-2-carboxylic acid, is characterized as being a potent and selective ligand for PPAR-gamma which has partial agonist (