INSULIN RESISTANCE IN CIRRHOSIS: EVIDENCE FOR A POST‐RECEPTOR DEFECT
- 1 December 1984
- journal article
- research article
- Published by Wiley in Clinical Endocrinology
- Vol. 21 (6), 677-688
- https://doi.org/10.1111/j.1365-2265.1984.tb01410.x
Abstract
Receptor and post-receptor abnormalities of insulin action and their possible role in the insulin resistance of cirrhosis were examined in eight biopsy-proven cirrhotic subjects and eight age-weight matched healthy volunteers. To this end, oral glucose tolerance tests (OGTT), insulin dose response curves and insulin binding to circulating monocytes were determined for each subject. The dose-response curves for the cirrhotic subjects were significantly shifted to the right compared to the control subjects, indicating the presence of insulin insensitivity (ED50 223 ± 30 versus 64 ± 8 mU/l respectively; P2/min; P<0.05). Insulin binding to circulating monocytes was normal in the cirrhotic subjects. It is concluded that the insulin resistance of cirrhosis is due to a post-receptor defect in insulin action which reduces insulin sensitivity but not insulin responsiveness.This publication has 26 references indexed in Scilit:
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