Document Detail

Obesity and leptin resistance: distinguishing cause from effect.
MedLine Citation:
PMID:  20846876     Owner:  NLM     Status:  MEDLINE    
Because leptin reduces food intake and body weight, the coexistence of elevated leptin levels with obesity is widely interpreted as evidence of 'leptin resistance.' Indeed, obesity promotes a number of cellular processes that attenuate leptin signaling (referred to here as 'cellular leptin resistance') and amplify the extent of weight gain induced by genetic and environmental factors. As commonly used, however, the term 'leptin resistance' embraces a range of phenomena that are distinct in underlying mechanisms and pathophysiological implications. Moreover, the induction of cellular leptin resistance by obesity complicates efforts to distinguish the mechanisms that predispose to weight gain from those that result from it. We suggest a framework for approaching these issues and important avenues for future investigation.
Martin G Myers; Rudolph L Leibel; Randy J Seeley; Michael W Schwartz
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review     Date:  2010-09-16
Journal Detail:
Title:  Trends in endocrinology and metabolism: TEM     Volume:  21     ISSN:  1879-3061     ISO Abbreviation:  Trends Endocrinol. Metab.     Publication Date:  2010 Nov 
Date Detail:
Created Date:  2010-11-01     Completed Date:  2011-02-02     Revised Date:  2013-05-27    
Medline Journal Info:
Nlm Unique ID:  9001516     Medline TA:  Trends Endocrinol Metab     Country:  United States    
Other Details:
Languages:  eng     Pagination:  643-51     Citation Subset:  IM    
Copyright Information:
Copyright © 2010 Elsevier Ltd. All rights reserved.
Division of Metabolism, Endocrinology and Diabetes, Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, USA.
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MeSH Terms
Animals, Genetically Modified
Disease Models, Animal
Drug Resistance / genetics,  physiology*
Leptin / genetics,  metabolism*,  physiology*
Models, Biological
Obesity / complications*,  etiology*,  genetics,  metabolism
Receptors, Leptin / metabolism,  physiology
Signal Transduction / genetics,  physiology
Grant Support
DK052989/DK/NIDDK NIH HHS; DK056731/DK/NIDDK NIH HHS; DK057768/DK/NIDDK NIH HHS; DK078056/DK/NIDDK NIH HHS; DK083042/DK/NIDDK NIH HHS; DK52431/DK/NIDDK NIH HHS; R01 DK052431-17/DK/NIDDK NIH HHS; R01 DK052431-18/DK/NIDDK NIH HHS; R01 DK052431-19/DK/NIDDK NIH HHS; R01 DK052989-14/DK/NIDDK NIH HHS; R01 DK057768-11/DK/NIDDK NIH HHS; R01 DK078056-03/DK/NIDDK NIH HHS; R01 DK078056-04/DK/NIDDK NIH HHS; R01 DK083042-17/DK/NIDDK NIH HHS; R01 DK090320-02/DK/NIDDK NIH HHS; R37 DK056731-12/DK/NIDDK NIH HHS; R37 DK056731-13/DK/NIDDK NIH HHS
Reg. No./Substance:
0/Leptin; 0/Receptors, Leptin

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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