Hypoglycemia during adrenergic beta-blockade: Evidence against mediation via a deficiency of lactate for gluconeogenesis

B. M. Frier, R. J.M. Corrall, I. A.D. O'Brien, I. G. Lewin, I. D. Hay, J. Roland

Research output: Contribution to journalArticle

4 Scopus citations

Abstract

Acute hypoglycemia was induced using intravenous insulin 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.

Original languageEnglish (US)
Pages (from-to)1039-1043
Number of pages5
JournalMetabolism
Volume34
Issue number11
DOIs
StatePublished - Nov 1985

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

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