Insulin Hypoglycemia and Epinephrine Output from the Adrenal Glands

Abstract

It has been shown that the severity of experimental pancreatic diabetes is not modified by reduction or suppression of the epinephrine output from the adrenal glands. 1 The insulin requirement under these conditions is not different from that of diabetic animals whose epinephrine secretion is not interfered with. Furthermore, it was found that depancreatized dogs, not subjected to interference with the adrenals, sooner or later develop reduced or suppressed secretion of epinephrine, which appears to be due primarily to the diabetic state. 2

Our experimental investigations in progress have yielded results which indicate that epinephrine, when introduced intravenously at a constant rate in amounts corresponding to the ordinary rate of liberation from the adrenals in normal dogs, can elevate the level of blood sugar. The influence of similar amounts of epinephrine in animals previously subjected to operations for reduction or suppression of secretion from the adrenals is under investigation.

Although epinephrine secretion is not concerned primarily with the cause or progress of experimental pancreatic diabetes, it might, nevertheless, play a rôle, perhaps not indispensable, in normal carbohydrate metabolism. Cannon, Mclver and Bliss 3 have suggested that epinephrine secretion from the adrenals constitutes a mechanism for mobilizing sugar in hypoglycemia. Their experimental evidence is in support of the view that as the level of blood-sugar declines to a “critical point” (between 110 and 70 mg % in cats, under chloralose anesthesia), an increased discharge of epinephrine from the adrenals is produced. They employed the Folin-Wu method for estimating blood sugar.