Homeostatic and hedonic signals interact in the regulation of food intake

Abstract

Food intake is regulated by 2 complementary drives: the homeostatic and hedonic pathways. The homeostatic pathway controls energy balance by increasing the motivation to eat following depletion of energy stores. In contrast, hedonic or reward-based regulation can override the homeostatic pathway during periods of relative energy abundance by increasing the desire to consume foods that are highly palatable. In contrast to the consumption of food, the motivation to use drugs of abuse is mediated only by the reward pathway. In this article we review the extensive research that has identified several mechanisms by which repeated exposure to drugs of abuse alters neuronal function and increases the motivational incentive to obtain and use these substances. We then compare our current understanding of drug-induced changes in neuronal reward circuitry with what is known about the consequences of repeated consumption of highly palatable foods such as high-fat and high-sugar diets. Next, we discuss the normal homeostatic regulation of food intake, which is a unique aspect of food addiction. Finally, we discuss the clinical implications of these neuronal adaptations in the context of obesity and neuropsychiatric syndromes such as bulimia nervosa and Prader-Willi syndrome.

FIGURE 1

Schematic representation of neural circuits that regulate feeding. Dopaminergic neurons originating in the VTA project to neurons within the nucleus accumbens of the ventral striatum. The lateral hypothalamus receives input from GABAergic projections from the nucleus accumbens as well as melanocortinergic neurons from the Arc of the hypothalamus. In addition, melanocortin receptors are also found on neurons in the VTA and the nucleus accumbens.