Food intake regulation by diet-induced thermogenesis

Diet-induced thermogenesis represents energy wasted in the assimilation of food. Since this source of energy loss is variable, it has long been linked to obesity in people who assimilate food at high efficiency, the saved energy converting to adipose tissue. In this report we provide evidence to dispel that notion and, instead, show that the variability in DIT may be linked to the amount of food one consumes during the course of a meal. We call upon the well known temperature sensitive neurons in the hypothalamus acting in concert with the ventromedial nuclei to present a new version of an old 'thermostatic hypothesis' of food intake regulation.