Insulin, leptin and reward

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


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.

Publication types

  • Review

MeSH terms

  • Animals
  • Appetite Regulation / drug effects
  • Appetite Regulation / physiology
  • Central Nervous System / drug effects
  • Central Nervous System / physiology
  • Feeding Behavior / drug effects
  • Feeding Behavior / physiology
  • Homeostasis / drug effects
  • Homeostasis / physiology
  • Humans
  • Insulin / pharmacology
  • Insulin / physiology*
  • Leptin / pharmacology
  • Leptin / physiology*
  • Limbic System / drug effects
  • Limbic System / physiology
  • Models, Biological
  • Reward*


  • Insulin
  • Leptin