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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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Published August 1, 1987 - More info

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