Inhibitory action of somatostatin on pancreatic alpha and beta cell function

In normal men, the administration of somatostatin almost completely abolished the glucose stimulated insulin-release seen during control studies (without somatostatin), and caused a further reduction in glucagon secretion beyond that induced by hyperglycemia. Following the infusion, there was a rapid and marked rebound for insulin but not glucagon secretion. These events were attended by a marked retardation of the glucose disappearance rate (K) which exhibited two clearly separable components; the initial slow component (mean K equals 0.64) coincided with the period of insulin suppression and was followed by a faster component (mean K equals 1.37) temporally related to the marked rebound increase in insulin release after discontinuation of the somatostatin infusion. Similarly, the addition of somatostatin infusion completely blocked the release of insulin and growth hormone and delayed the release of glucagon stimulated by arginine infusion. Following the somatostatin infusion there was a small rise in GH and a marked rebound for insulin and this was associated with a higher level of plasma glucose than that found following arginine infusion alone. These data establish that the administration of somatostatin can effectively block the release of insulin stimulated by arginine and glucose, can attenuate the release of glucagon induced by arginine and can enhance the glucose-mediated glucagon suppression. The attendance of a relative hyperglycemia during these events is probably the net result of an impediment in peripheral glucose disposition due to acute insulin lack and a decreased hepatic glucose output secondary to glucagon suppression.