Kathleen A. Page, MD - “Brain, Hormone, and Appetitive Responses to High- Reward Foods: Implications for Obesity and Disease.”
“Brain, Hormone, and Appetitive Responses to High- Reward Foods: Implications for Obesity and Disease.”
Obesity is a worldwide epidemic resulting in part from the ubiquity of high-calorie foods and food images. Our group is interested in the neuroendocrine regulation of appetite and feeding behavior and its sensitivity to environmental food exposure. We are taking a multifaceted approach to examine this problem. One aspect of our research addresses the effects of consumption of two sugars, glucose and fructose, on satiety regulating hormones and brain pathways that regulate food intake. We have found that glucose but not fructose consumption: a) decreases regional cerebral blood flow (a marker of neuronal activity) in the hypothalamus, insula and striatum, brain regions that regulate appetite and reward, b) produces a greater rise in systemic levels of the satiety-signaling hormones, insulin and GLP-1, and c) results in increased ratings of satiety in normal-weight volunteers. These findings offer a potential neuroendocrine mechanism for the association between recent increases in fructose consumption and the obesity epidemic.
In another series of neuroimaging experiments, we investigated how circulating levels of glucose, the primary fuel source for the brain, influence brain regions that regulate the motivation to consume high-calorie foods in obese and normal-weight volunteers. We found that obese individuals exhibited an enhanced sensitivity of the appetite and reward circuitry to high-calorie food cues under mild hypoglycemia, and lacked activation of the prefrontal cortex, the brain’s inhibitory control center, under normal glucose conditions. This imbalance between appetite and reward activation and cortical inhibitory control may make obese people more susceptible to overeating behavior.