PubMed2004
The motivation to eat in humans is a complex process influenced by intrinsic mechanisms relating to the hunger and satiety cascade, and extrinsic mechanisms based on the appetitive incentive value of individual foods, which can themselves induce desire. This study was designed to investigate the neural basis of these two factors contributing to the control of motivation to eat within the same experimental design using positron emission tomography. Using a novel counterbalanced approach, participants were scanned in two separate sessions, once after fasting and once after food intake, in which they imagined themselves in a restaurant and considered a number of items on a menu, and were asked to choose their most preferred. All items were tailored to each individual and varied in their incentive value. No actual foods were presented. In response to a hungry state, increased activation was shown in the hypothalamus, amygdala and insula cortex as predicted, as well as the medulla, striatum and anterior cingulate cortex. Satiety, in contrast, was associated with increased activation in the lateral orbitofrontal and temporal cortex. Only activity in the vicinity of the amygdala and orbitofrontal cortex was observed in response to the processing of extrinsic appetitive incentive information. These results suggest that the contributions of intrinsic homeostatic influences, and extrinsic incentive factors to the motivation to eat, are somewhat dissociable neurally, with areas of convergence in the amygdala and orbitofrontal cortex. The findings of this study have implications for research into the underlying mechanisms of eating disorders.