Effect of bilateral lesions of the suprachiasmatic nucleus on hyperglycemia caused by 2-deoxy- d-glucose and vasoactive intestinal peptide in rats

In mammals, the brain usually uses glucose as a sole energy source. Thus, under a central glucopenic condition after intracranial injection of 2-deoxy- d-glucose (2DG), an inhibitor of glucose utilization, it has been shown that rats elevate their blood glucose level through excitation of the sympathetic nerves. Experiments were conducted with rats to examine the role of the hypothalamic suprachiasmatic nucleus (SCN) in the hyperglycemic response to intracerebroventricular injection of either 2DG or vasoactive intestinal peptide (VIP). It was observed that, (1) intracerebroventricular injection of a VIP-antagonist inhibited the hyperglycemic and hyperglucagonemic responses to the intracranial injection of 2DG; (2) bilateral electrolytic lesioning of the SCN suppressed the hyperglycemic and hyperglucagonemic responses to intracranial injection of 2DG, and intracerebroventricular injection of VIP restored these responses to 2DG; and (3) bilateral electrolytic lesioning of the SCN also suppressed the hyperglycemic and hyperglucagonemic responses to the VIP injection, and additional intracerebroventricular injection of 2DG caused hyperglycemia. These findings indicate that in rats with bilateral lesions of the SCN intracranial injection of 2DG is able to elicit hyperglycemia when VIP was administered intracranially, and suggest that neurons containing VIP-like immunoreactive substance (VIP-neurons) in the SCN have an important role in the mechanism of hyperglycemia elicitation following intracranial injection of 2DG. Moreover, these findings show that 2DG and VIP are able to realize their functions through acting on the brain sites outside the SCN.