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Trends Endocrinol Metab. 2010 Feb;21(2):68-74. doi: 10.1016/j.tem.2009.08.004. Epub 2009 Oct 7.

Insulin, leptin and reward.

Author information

1
Department of Psychiatry North, E, Lab 334, University of Cincinnati, 2170 East Galbraith Road, Cincinnati, OH 45237, USA. Jon.Davis@uc.edu

Abstract

Feeding for pleasure, or "non-homeostatic feeding", potentially contributes to the rapid development of obesity worldwide. Obesity is associated with an imbalance of regulatory hormones which normally act to maintain stable energy balance and body weight. The adiposity hormones insulin and leptin are two such signals elevated in obesity with the capacity to dampen feeding behavior through their action on hypothalamic circuits which regulate appetite and metabolism. Recent evidence suggests that both hormones achieve this degree of regulation by inhibiting the rewarding aspects of feeding behavior, perhaps by signaling within midbrain reward circuits. This review describes the capacity of both insulin and leptin to regulate reward-related behavior.

PMID:
19818643
PMCID:
PMC2822063
DOI:
10.1016/j.tem.2009.08.004
[Indexed for MEDLINE]
Free PMC Article

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