The ventromedial hypothalamic area and the vagus are neural substrates for anticipatory insulin release.
It has been clearly demonstrated in a number of animal species including man, that insulin secretion can occur in response to sensory stimuli associated with meal taking and in advance of any ingestional rise in blood nutrients. The neural basis of this anticipatory insulin rise is poorly delineated and was therefore investigated in two experiments. In the first, rats with electrolytic lesions of the ventromedial hypothalamic area (VMH), or sham lesions were assessed and in the second experiment rats with bilateral subdiaphragmatic vagotomies or sham vagotomies were studied. In both experiments rats with jugular cannulae were conditioned to expect a meal 5 min following the beginning of a complex (light, tone and odor) stimulus. On the test trial the stimulus was given but no meal was forthcoming. Blood was sampled via the jugular catheter before and during the stimulus presentation. In both experiments the control rats showed a significant insulin rise during the stimulus presentation. However, neither the VMH-lesioned nor the vagotomized rats showed any significant change in insulin levels. The results clearly demonstrate an insulin rise to a complex sensory stimulus which has been paired with food and further show the dependence of that response on the integrity of the hypothalamic-vagal-visceral neural pathway. It is suggested that the VMH receives meal-associated sensory input and employs that information to prepare the animal metabolically for incoming nutrients. One aspect of this anticipatory mechanism is a vagally mediated insulin secretion.
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D003463:Cues; D004435:Eating; D007328:Insulin / Q000097:blood*; D051381:Rats; D011919:Rats, Inbred Strains; D014630:Vagus Nerve / Q000502:physiology*; D014697:Ventromedial Hypothalamic Nucleus / Q000502:physiology*
D001786:Blood Glucose; D007328:Insulin