| Leptin and the regulation of body weigh. | |
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MedLine Citation:
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PMID: 21460597 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The cloning of the ob gene and its gene product, leptin, has led to the elucidation of a robust physiologic system that maintains fat stores at a relatively constant level. Leptin is a peptide hormone secreted by adipose tissue in proportion to its mass. Recessive mutations in the leptin gene are associated with massive obesity in mice and humans, establishing a genetic basis for obesity. Leptin circulates in blood and acts on the brain to regulate food intake and energy expenditure. When fat mass falls, plasma leptin levels fall, stimulating appetite and suppressing energy expenditure until fat mass is restored. When fat mass increases, leptin levels increase, suppressing appetite until weight is lost. This system maintains homeostatic control of adipose tissue mass. The discovery of leptin has advanced our understanding of metabolic disease in a number of respects. Its identification has revealed a new endocrine system regulating body weight. This system provides a means by which changes in nutritional state regulate other physiologic systems. A number of leptin deficiency syndromes that are treatable with leptin replacement have been identified. The majority of obese subjects are leptin resistant, which establishes that obesity is the result of hormone resistance. Leptin treatment results in weight loss in a subset of obese patients and can also synergize with other anti-obesity agents to reduce weight in the general population. Leptin provides an entry point for studying a complex human behavior. Finally, this research has established that there is a powerful biological basis for obesity, a fact that is (correctly) changing public perception about the pathogenesis of this medical condition. |
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Authors:
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Jeffrey M Friedman |
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Publication Detail:
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Type: Lectures |
Journal Detail:
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Title: The Keio journal of medicine Volume: 60 ISSN: 1880-1293 ISO Abbreviation: Keio J Med Publication Date: 2011 |
Date Detail:
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Created Date: 2011-04-04 Completed Date: 2011-07-29 Revised Date: 2011-11-04 |
Medline Journal Info:
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Nlm Unique ID: 0376354 Medline TA: Keio J Med Country: Japan |
Other Details:
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Languages: eng Pagination: 1-9 Citation Subset: IM |
Affiliation:
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Rockefeller University, 1230 York avenue, New York, NY 10065, USA. friedj@mail.rockefeller.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adipose Tissue
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physiology* Animals Anti-Obesity Agents / therapeutic use Appetite Body Weight / physiology Energy Metabolism Feeding Behavior / physiology Female Homeostasis Hormone Replacement Therapy Humans Leptin* / genetics, metabolism Mice Mutation Nutritional Status Obesity / genetics, metabolism*, therapy Rats Signal Transduction / physiology Weight Loss |
| Chemical | |
Reg. No./Substance:
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0/Anti-Obesity Agents; 0/Leptin |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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