Vagal insulin secretion stimulation

Introduction. It is well-known that the hypothalamus participates in the regulation of carbohydrate metabolism via the autonomic nervous system. As far as the secretion of insulin is concerned, vagal stimulation causes release of insulin whereas adrenergic stimulation is inhibitory. Moreover, in addition to the classical neurotransmitters, neuropeptides present in the efferent autonomic nerves (GRP, VIP, peptide histidine-isoleucinamide (PHI), neuropeptide Y (NPY), CCK, galanin) are also of importance. The subject has previously been reviewed by Holst (1992). The existence of a cephalic phase of insulin secretion, i.e. reflex-stimulated secretion, has been well established in rats (Strubbe and Steffens, 1975), and there is also evidence for a cephalic-phase insulin response in humans (Bruce et al., 1987 Loud et al., 1988). 

Glucose, the principal stimulus to insulin secretion, is permissive for the action of many other secretogogues. Glucose provokes insulin secretion more effectively when taken orally than when administered intravenously because the oral route induces the release of GI hormones and stimulates vagal activity. Several GI hormones promote insulin secretion, the most potent of which are glucose-dependent insulinotropic peptide (GIP, also known as gastrointestinal inhibitory peptide) and glucagon-like peptide-1 (GLP-1). 

It is believed that insulin hypoglycemia brings about gastrin secretion by stimulation of the long vagal reflexes. Distension of the stomach is likely to release... 

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