Dissociation of epinephrine's hyperglycemic and anorectic effect

The contribution of α- and β-adrenergic receptor mechanisms to epinephrine-induced hyperglycemia, to prandial hepatic glycogenolysis, and to epinephrine-induced inhibition of feeding were investigated in rats, because epinephrine's hyperglycemic and anorectic effect might be related to each other. Intraperitoneal injection of the selective α-adrenergic receptor antagonist phentolamine (0.5 mg/kg body weight) but not of the selective β-adrenergic receptor antagonist propranolol (0.5 mg/kg body weight) reduced the hyperglycemic effect of a subsequent epinephrine injection (0.05 mg/kg body weight). In addition, injection of phentolamine (0.5 mg/kg b.w.) or injection of phentolamine plus propranolol (0.5 mg/kg b.w. each) similarly inhibited epinephrine-induced hepatic glycogenolysis. In contrast, phentolamine injection did not affect prandial hepatic glycogenolysis. Neither phentolamine nor propranolol i injection was sufficient to affect the inhibition of feeding induced by subsequent epinephrine injection, but the combination of both receptor blockers completely abolished epinephrine's effect on food intake. These findings are not consistent with the idea that epinephrine-induced hypophagia is related to epinephrine's effect on hepatic carbohydrate metabolism. In addition, the data suggest that catecholamines are not the main contributors to prandial hepatic glycogenolysis in rats.