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Brain regulation of energy balance and body weight.
MedLine Citation:
PMID:  23990408     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
Body weight is determined by a balance between food intake and energy expenditure. Multiple neural circuits in the brain have evolved to process information about food, food-related cues and food consumption to control feeding behavior. Numerous gastrointestinal endocrine cells produce and secrete satiety hormones in response to food consumption and digestion. These hormones suppress hunger and promote satiation and satiety mainly through hindbrain circuits, thus governing meal-by-meal eating behavior. In contrast, the hypothalamus integrates adiposity signals to regulate long-term energy balance and body weight. Distinct hypothalamic areas and various orexigenic and anorexigenic neurons have been identified to homeostatically regulate food intake. The hypothalamic circuits regulate food intake in part by modulating the sensitivity of the hindbrain to short-term satiety hormones. The hedonic and incentive properties of foods and food-related cues are processed by the corticolimbic reward circuits. The mesolimbic dopamine system encodes subjective "liking" and "wanting" of palatable foods, which is subjected to modulation by the hindbrain and the hypothalamic homeostatic circuits and by satiety and adiposity hormones. Satiety and adiposity hormones also promote energy expenditure by stimulating brown adipose tissue (BAT) activity. They stimulate BAT thermogenesis mainly by increasing the sympathetic outflow to BAT. Many defects in satiety and/or adiposity hormone signaling and in the hindbrain and the hypothalamic circuits have been described and are believed to contribute to the pathogenesis of energy imbalance and obesity.
Authors:
Liangyou Rui
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2013-8-30
Journal Detail:
Title:  Reviews in endocrine & metabolic disorders     Volume:  -     ISSN:  1573-2606     ISO Abbreviation:  Rev Endocr Metab Disord     Publication Date:  2013 Aug 
Date Detail:
Created Date:  2013-8-30     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100940588     Medline TA:  Rev Endocr Metab Disord     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Affiliation:
Department of Molecular & Integrative Physiology, University of Michigan Medical School, Ann Arbor, MI, 48109-0622, USA, ruily@umich.edu.
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