Metabolic effects of hypothalamic hyperphagia

In order to test the hypothesis that the enhanced gluconeogenesis of hypothalamic obesity remains responsive to changes in food intake, we have measured gluconeogenesis in two models of hypothalamic obesity under both hyperphagic and normophagic conditions. The results show that hyperphagia partially decreases gluconeogenesis and fully restores liver glycogen in both models. The discussion section relates our present findings to the enhanced glucose utilization previously noted after VMH destruction and to the recent hypothesis that hyperphagia is a response to body protein depletion.