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Rev Endocr Metab Disord. 2013 Dec;14(4):387-407. doi: 10.1007/s11154-013-9261-9.

Brain regulation of energy balance and body weight.

Author information

1
Department of Molecular & Integrative Physiology, University of Michigan Medical School, Ann Arbor, MI, 48109-0622, USA, ruily@umich.edu.

Abstract

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.

PMID:
23990408
PMCID:
PMC3817823
DOI:
10.1007/s11154-013-9261-9
[Indexed for MEDLINE]
Free PMC Article

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