Adrenergic receptor and epinephrine-induced hyperglycemia and glucose tolerance.
Intravenous glucose tolerance in fasting rats was improved by phentolamine, an alpha-adrenergic blocking agent, and diminished by propranolol, a beta-adrenergic blocking agent. These effects of adrenergic blockers were dependent on the action of insulin, secretion of which is controlled by an adrenergic mechanism. Epinephrine caused by hyperglycemia and impaired glucose tolerance. Both actions of epinephrine were partly inhibited by either an alpha or beta blocker and completely abolished by combination of both blockers in normal rats. However, in rats treated with anti-insulin serum or 5-methoxyindole-2-carboxylic acid, a potent inhibitor of gluconeogenesis, both actions of epinephrine were blocked by propranolol alone, but not by phentolamine. It is concluded that beta-receptor-mediated inhibiton of peripheral glucose utilization is primarily responsible for epinephrine-induced hyperglycemia and impairment of glucose tolerance. Furthermore, the reduction of glycemic action of epinephrine observed after alpha blockade is due to the hypoglycemic action of insulin secreted by the stimulation of beta receptors in pancreatic beta cells.
D000818:Animals; D001639:Bicarbonates / Q000378:metabolism; D001786:Blood Glucose / Q000378:metabolism; D002250:Carbon Radioisotopes; D004837:Epinephrine / Q000494:pharmacology*; D005947:Glucose / Q000378:metabolism*; D006943:Hyperglycemia / Q000139:chemically induced / Q000503:physiopathology*; D007211:Indoles / Q000494:pharmacology; D007328:Insulin / Q000378:metabolism; D000078790:Insulin Secretion; D008297:Male; D010646:Phentolamine / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D051381:Rats; D011941:Receptors, Adrenergic
D001639:Bicarbonates; D001786:Blood Glucose; D002250:Carbon Radioisotopes; D007211:Indoles; D007328:Insulin; D011941:Receptors, Adrenergic; C008400:5-methoxyindole-2-carboxylic acid; D011433:Propranolol; D005947:Glucose; D004837:Epinephrine; D010646:Phentolamine