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[Interactions between the central nervous system, the endocrine pancreas and metabolism].

1. The importance of nervous circuits including neural afferences, their integration by the central nervous system and the resulting efferents is illustrated by comparing glucose tolerance following the spontaneous ingestion or the intragastric administration of a glucose load. When these circuits are by-passed (intragastric glucose administration), glucose tolerance is impaired and accompanied by an increased insulin output compared to the situation of normal glucose ingestion. This is due to a decreased glucose utilization in the absence of the numerous reflexes that are elicited by the presence of glucose in the oropharynx. 2. In normal animals, insulin secretion by the B cell of the endocrine pancreas is under an inhibitory tonus by the sympathetic nervous system while the parasympathetic system has no stimulatory tonus. After acute bilateral destruction of the ventromedial hypothalamic nuclei (VMH), such a situation is reversed and there is an activation of the parasympathetic outflow leading to hyperinsulinemia. This hyperinsulinemia is partly responsible for the development of the obesity of VMH-lesioned animals and is accompanied by a decreased activity of some sympathetic efferents amongst which those innervating brown adipose tissue. Analogous data have been obtained when studying genetically obese fa/fa rats. 3. A peptide of around 1'000 daltons extracted from the rat hypothalamus and having insulin secretion promoting activity could possibly be an insulin-releasing factor since it is present not only in the hypothalamus but also in the plasma.