Insulin, leptin and reward

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. The prevalence of obesity has reached epidemic proportion, and the development of pharmacological treatments continues to challenge current thinking. Over the past several years, key insights have broadened our understanding of how organisms sense and respond to peripheral and central signals to regulate energy homeostasis. However, this increased understanding has not yet led to successful therapies to reduce body weight. Importantly, feeding for pleasure or “non-homeostatic feeding ” is presumed in part to underlie the rapi