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Research Article Free access | 10.1172/JCI113091

Early posthypoglycemic insulin resistance in man is mainly an effect of beta-adrenergic stimulation.

S Attvall, B M Eriksson, J Fowelin, H von Schenck, I Lager, and U Smith

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First published August 1, 1987 - More info

Published in Volume 80, Issue 2 (August 1, 1987)
J Clin Invest. 1987;80(2):437–442. doi:10.1172/JCI113091.
Copyright © 1987, The American Society for Clinical Investigation.

Published August 1, 1987
Abstract

The insulin effect following hypoglycemia was studied with the euglycemic clamp technique in seven healthy subjects. Following an initial euglycemic clamp hypoglycemia was induced and after glucose recovery a second clamp was performed. Glucose production (Ra) and utilization (Rd) were studied with [3-3H]glucose. Each subject was studied four times; during infusion of placebo, propranolol, somatostatin, and a control study where hypoglycemia was prevented. Hypoglycemia induced an insulin resistance with a lower steady state glucose infusion rate following the hypoglycemia during placebo as compared to the control study (2.5 +/- 0.5 and 4.8 +/- 1.0 mg/kg min, respectively, P less than 0.05). The insulin resistance was due to an attenuated insulin effect on both inhibition of Ra (impaired by 37%) and stimulation of Rd (impaired by 61%). The insulin-antagonistic effect was completely prevented by propranolol but only partly by somatostatin. Thus, early posthypoglycemic insulin resistance (2.5-3.5 h after hypoglycemia) is a sustained effect mainly due to beta-adrenergic stimulation.

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