Factors modifying plasma insulin and glucose responses to ventromedial hypothalamic stimulation

Experiments were performed to evaluate the role of the pituitary, adrenal medulla, and sympathetic nervous system in the plasma glucose, insulin, and glucagon responses to brief electric stimulation of the ventromedial hypothalamic nucleus (VMN) of rats. Hypophysectomy resulted in decreased base-line insulin and glucose levels. The hyperglycemic response to VMN stimulation was only slightly impaired by hypophysectomy, while the insulin rebound following the end of stimulation was completely blocked. Starvation also partially inhibited the hyperglycemic response and blocked the insulin rebound. Following adrenal autotransplantation, the hyperglycemic response was preserved but of shortened duration, while the suppression of insulin secretion seen in normal animals was eliminated. Neither centrally administered 6-hydroxydopamine nor propranolol altered the glucose or insulin responses to VMN stimulation. Injection of phentolamine increased both prestimulatory insulin levels and the poststimulatory rebound but failed to block the inhibition of insulin secretion during stimulation. In animals stimulated for longer periods of time, the continuous suppression of insulin secretion was relieved by an infusion of phentolamine, and the hyperglycemia was attenuated. No significant inhibition of the glucagon response to stimulation was produced by either phentolamine or propranolol. The results indicate that in the rat the glucose and insulin responses to VMN stimulation are independent of the pituitary, and that inhibition of insulin secretion is mediated by alpha receptor stimulation provided by circulating catecholamines of adrenal origin.