Régulation de la prise alimentaire par les protéines

The worlwide development of obesity makes crucial the discovery of new mechanisms to control the sensations of hunger and satiety. The interrelationships between glucose metabolism and energy homeostasis have long been known, especially regarding the curbing effect of portal glucose on hunger. In this context, we demonstrated the existence of the gluconeogenic function in the intestine of rat and human. The genes that regulate intestinal gluconeogenesis are induced strongly during fasting, but also in a particular nutritional situation: High protein diet in rats. In both cases, the induction results in the release of glucose into the portal vein, which lasts after the postprandial period for the high protein diet. Glucose infusion in the portal vein equivalent to intestinal gluconeogenesis decreases food intake and activates the regions of the hypothalamus involved in the control of food intake. The mechanism of induction of intestinal genes involves oligopeptides released into the portal vein during protein assimilation. They inhibit μ-opioid receptors located in the nervous system of the wall of the vein. The signal sent to the brain initiates a reflex arc, which induces the expression of intestinal gluconeogenesis genes. These results provide the mechanistic explanation of the satiety effect of dietary protein, known in animals and humans, but remaining unexplained up to date.