Since beta-adrenergic blockade dampens the rebound of plasma glucose after insulin-induced hypoglycemia in man but does not affect epinephrine-stimulated hepatic glycogenolysis, studies were undertaken to define further the metabolic role of beta-adrenergic stimulation, particularly its participation in the induction of peripheral insulin resistance by epinephrine. In in vitro studies, propranolol, a specific beta-adrenergic blocker, was shown to prevent both epinephrine and isoproterenol from inducing inhibition of insulin-stimulated glucose uptake by rat hemidiaphragm. Methoxamine, an alpha-adrenergic stimulator, did not alter insulin-stimulated glucose uptake. In man, propranolol blocked the late rise of blood lactate levels which occurs during insulin tolerance tests, indicating that muscle glycogenolysis was prevented and suggesting that propranolol prevents epinephrine from inducing peripheral insulin resistance. This might in part account for the prolonged hypoglycemia observed in propranolol-insulin tolerance tests.

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