Hormonal mechanisms of recovery from insulin-induced hypoglycemia in man.

Abstract

Mechanisms for recovery of plasma glucose from acute insulin-induced hypoglycemia were investigated in normal and adrenalectomized human subjects with somatostatin used to inhibit glucagon and growth hormone [GH] secretion. In normal subjects with glucagon and GH deficiency, infusion of somatostatin enhanced insulin-induced plasma glucose decrements and attenuated restitution of normoglycemia despite augmented plasma cortisol, epinephrine and norepinephrine responses; these effects were prevented by simultaneous infusion of somatostatin with glucagon (subjects with GH deficiency) but not with GH (subjects with glucagon deficiency). In adrenalectomized subjects receiving glucocorticoid replacement (epinephrine deficiency), plasma glucose responses after insulin administration were not significantly different from those of normal subjects; however, somatostatin infusion (epinephrine, glucagon and GH deficiency) enhanced insulin-induced hypoglycemia more in these subjects than in the normal subjects and completely abolished restitution of normoglycemia. Glucagon plays a primary role and epinephrine a secondary role in recovery of plasma glucose from acute insulin-induced hypoglycemia in man. The immediate contributions of growth hormone, cortisol or neurally released norepinephrine were not indicated.