[Modulation by the central nervous system (CNS) of the activity of the endocrine pancreas]

Electrical stimulation of Nucleus Ambiguus (NA) and of Lateral Hypothalamus (LH) produces a sympathetic response that partly inhibits insulin secretion in anesthetized rats in vivo. This inhibitory component is accompanied by a stimulatory one that can, in both cases, be revealed by the infusion of an alpha-blocker to the rats. The analogy between the stimulatory effect on insulin secretion due to NA or LH electrical stimulation is only partial. Indeed the NA-induced insulin secretion is abolished by vagotomy, while that induced by LH stimulation appears to be mediated by possible release of humoral factor(s). Acute bilateral lesions of the ventromedial hypothalamus (VMH) in anesthetized rats produce, within minutes, an hyperinsulinemia that is abolished by superimposed vagotomy. Semi-chronic (7 d.) lesions of the VMH in rats result in changes in the activity of their subsequently isolated perfused pancreases. Indeed, and compared to controls, pancreases from VMH-lesioned rats oversecrete insulin and glucagon while undersecreting somatostatin. Such alterations due to lesions of the VMH appear to be the result of increased vagal activity and (possibly via a trophic effect of the nerve) of increased cholinergic (muscarinic) receptors. CNS organisation of genetically obese (ob/ob) mice is abnormal when compared to controls. Abnormalities are mainly a relative increase of the size of neurons of the LH and the dorsomotor nucleus of the vagus (DMX), compared to that of other CNS neurons. These abnormalities could conceivably play a role in the genesis of hyperinsulinemia of these animals.