Hypoglycemia during adrenergic beta-blockade: evidence against mediation via a deficiency of lactate for gluconeogenesis.
Acute hypoglycemia was induced using intravenous inulin in three groups of normal volunteers: (1) seventeen control subjects, (2) six subjects under beta-adrenergic blockade with propranolol, and (3) eight subjects given propranolol plus sodium lactate as an exogenous substrate for gluconeogenesis. Under propranolol blockade the recovery from hypoglycemia was significantly impaired. This impairment was not prevented by the infusion of sodium lactate despite the production of an adequate elevation of blood lactate concentrations. These findings suggest that the impaired recovery from hypoglycemia during beta-adrenergic blockade is not mediated via a deficiency of lactate as substrate for hepatic gluconeogenesis.
D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D005934:Glucagon / Q000097:blood; D005943:Gluconeogenesis; D013006:Growth Hormone / Q000097:blood; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007003:Hypoglycemia / Q000097:blood / Q000139:chemically induced*; D007773:Lactates / Q000097:blood* / Q000172:deficiency; D008297:Male; D011433:Propranolol / Q000494:pharmacology*
D001786:Blood Glucose; D007773:Lactates; D013006:Growth Hormone; D005934:Glucagon; D011433:Propranolol; D006854:Hydrocortisone