The metabolic signal of hunger and satiety, and its pharmacological manipulation.
Hunger is elicited by the depletion of available macronutrients to the cells. The question is how the depletion is sensed and transduced into a biologically meaningful signal of hunger. Accumulating data show that the signal comes not from depletion of carbohydrates alone or from one of the other major macronutrients. Instead, the signal is generated by the overall cellular power production that induces hunger when it decreases and satiety when it increases. As for satiation, i.e. the state that causes the termination of a meal before nutrients cross the intestinal barrier, it is induced by early metabolic events elicited reflexly from orogastric afferences and tuning the preprandial metabolism towards the level of the postprandial metabolism. Neuronal responses from the medial hypothalamus suggest that they may integrate information on the degree of utilization of glucose and of lipids. Some of the pharmacological agents that reduce feeding seem to operate by increasing the metabolic rate in a way similar to that induced by a meal. These pharmacological agents are active because they mobilize endogenous metabolites, such as lipids, so inducing a sort of 'autocanibalic' meal.
Nicolaidis
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Laboratoire de Neurobiologie des Régulations, UA 637, CNRS, Institut de Biologie du Collège de France, Paris.
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D000818:Animals; D004435:Eating / Q000502:physiology; D004734:Energy Metabolism; D006801:Humans; D006815:Hunger / Q000502:physiology*; D007031:Hypothalamus / Q000502:physiology; D008954:Models, Biological; D009474:Neurons / Q000502:physiology; D012527:Satiation / Q000502:physiology*