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Review
. 2008 Dec;37(4):811-23.
doi: 10.1016/j.ecl.2008.08.005.

Brain regulation of appetite and satiety

Rexford S Ahima  1 , Daniel A Antwi
Affiliations
Review

Brain regulation of appetite and satiety

Rexford S Ahima et al. Endocrinol Metab Clin North Am. 2008 Dec.

Abstract

Interest in the control of feeding has increased as a result of the obesity epidemic and rising incidence of metabolic diseases. The brain detects alterations in energy stores and triggers metabolic and behavioral responses designed to maintain energy balance. Energy homeostasis is controlled mainly by neuronal circuits in the hypothalamus and brainstem, whereas reward and motivation aspects of eating behavior are controlled by neurons in limbic regions and the cerebral cortex. This article provides an integrated perspective on how metabolic signals emanating from the gastrointestinal tract, adipose tissue, and other peripheral organs target the brain to regulate feeding, energy expenditure, and hormones. The pathogenesis and treatment of obesity and abnormalities of glucose and lipid metabolism are discussed.

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Figures

Figure 1
Figure 1
Hypothalamic leptin signal transduction. Leptin inhibits NPY/AGRP and stimulates POMC/CART, resulting in an increase in anorexigenic input to the paraventricular nucleus. These changes in neuropeptide expression culminate in satiety, stimulation of energy expenditure and weight loss.
Figure 2
Figure 2
Cross-talk between insulin and leptin signaling in the hypothalamus. Insulin inhibits NPY/AGRP and induces POMC/CART through activation of IRS and PI3 kinase. Leptin activates JAK2, which interacts with insulin via IRS.
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