Role of the Sympathoadrenal System in Exercise-Induced Inhibition of Insulin Secretion: Effects of Islet Transplantation

The present study was designed to investigate the mechanism leading to inhibition of insulin release during exercise. To investigate the influence of circulating epinephrine and norepinephrine, these catecholamines were infused intravenously in resting islet-transplanted and control rats. The role of neural influences on insulin release was investigated by a swimming exercise study in islet-transplanted and control rats, before and after adrenodemedullation. Streptozotocin-induced diabetic Albino Oxford rats received 5 μl islet tissue into the portal vein, resulting in return of normal basal glucose and insulin levels. Transplanted and control animals were provided with two permanent heart catheters to sample blood and to give infusions. Infusion of epinephrine and norepinephrine did not result in inhibition of plasma insulin levels. Blood glucose levels, as well as nonesterified fatty acids and insulin levels in plasma, were similar in both groups. After the infusion study, the animals were subjected to strenuous swimming. During exercise, plasma insulin levels decreased not only in controls, but also in the islet-transplanted group. Blood glucose and plasma catecholamine responses were identical in both groups. After adrenodemedullation, epinephrine was not detectable and the exercise-induced decrease of insulin was not affected. These results indicate that circulating epinephrine and norepinephrine in physiological concentrations do not cause inhibition of insulin secretion. Since the exercise-induced inhibition of insulin secretion is still present in rats with islet grafts, it seems reasonable to suggest that sympathetic neural influences are responsible for the inhibition of insulin release during exercise and that transplanted islets are sympathetically reinnervated.