| Clinical review: Regulation of food intake, energy balance, and body fat mass: implications for the pathogenesis and treatment of obesity. | |
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MedLine Citation:
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PMID: 22238401 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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CONTEXT: Obesity has emerged as one of the leading medical challenges of the 21st century. The resistance of this disorder to effective, long-term treatment can be traced to the fact that body fat stores are subject to homeostatic regulation in obese individuals, just as in lean individuals. Because the growing obesity epidemic is linked to a substantial increase in daily energy intake, a key priority is to delineate how mechanisms governing food intake and body fat content are altered in an obesogenic environment. EVIDENCE ACQUISITION: We considered all relevant published research and cited references that represented the highest quality evidence available. Where space permitted, primary references were cited. EVIDENCE SYNTHESIS: The increase of energy intake that has fueled the U.S. obesity epidemic is linked to greater availability of highly rewarding/palatable and energy-dense food. Obesity occurs in genetically susceptible individuals and involves the biological defense of an elevated body fat mass, which may result in part from interactions between brain reward and homeostatic circuits. Inflammatory signaling, accumulation of lipid metabolites, or other mechanisms that impair hypothalamic neurons may also contribute to the development of obesity and offer a plausible mechanism to explain the biological defense of elevated body fat mass. CONCLUSIONS: Despite steady research progress, mechanisms underlying the resistance to fat loss once obesity is established remain incompletely understood. Breakthroughs in this area may be required for the development of effective new obesity prevention and treatment strategies. |
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Authors:
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Stephan J Guyenet; Michael W Schwartz |
Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Review Date: 2012-01-11 |
Journal Detail:
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Title: The Journal of clinical endocrinology and metabolism Volume: 97 ISSN: 1945-7197 ISO Abbreviation: J. Clin. Endocrinol. Metab. Publication Date: 2012 Mar |
Date Detail:
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Created Date: 2012-03-06 Completed Date: 2012-07-06 Revised Date: 2013-04-15 |
Medline Journal Info:
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Nlm Unique ID: 0375362 Medline TA: J Clin Endocrinol Metab Country: United States |
Other Details:
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Languages: eng Pagination: 745-55 Citation Subset: AIM; IM |
Affiliation:
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Diabetes and Obesity Center of Excellence, Department of Medicine, University of Washington School of Medicine, South Lake Union, 815 Mercer Street, N334, Box 358055, Seattle, Washington 98109, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adipose Tissue
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physiology* Body Mass Index Eating / physiology* Energy Metabolism / physiology* Homeostasis / physiology Humans Obesity / etiology*, physiopathology |
| Grant Support | |
ID/Acronym/Agency:
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DK052989/DK/NIDDK NIH HHS; DK068384/DK/NIDDK NIH HHS; DK083042/DK/NIDDK NIH HHS; F32DK091989/DK/NIDDK NIH HHS; R01 DK083042/DK/NIDDK NIH HHS; R01 DK090320/DK/NIDDK NIH HHS; T32DK007247/DK/NIDDK NIH HHS |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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