Profound peripheral insulin resistance, independent of obesity, in polycystic ovary syndrome
- 1 September 1989
- journal article
- research article
- Published by American Diabetes Association in Diabetes
- Vol. 38 (9), 1165-1174
- https://doi.org/10.2337/diabetes.38.9.1165
Abstract
Hyperinsulinemia secondary to a poorly characterized disorder of insulin action is a feature of the polycystic ovary syndrome (PCO). However, controversy exists as to whether insulin resistance results from PCO or the obesity that is frequently associated with it. Thus, we determined in vivo insulin action on peripheral glucose utilization (M) and hepatic glucose production (HGP) with the euglycemic glucose-clamp technique in obese (n = 19) and nonobese (n = 10) PCO women and age- and body-composition-matched normal ovulatory women (n = 11 obese and n = 8 nonobese women). None had fasting hyperglycemia. Two obese PCO women had diabetes mellitus, established with an oral glucose tolerance test; no other women had impairment of glucose tolerance. However, the obese PCO women had significantly increased fasting and 2-h glucose levels after an oral glucose load and increased basal HGP compared with their body-composition-matched control group. There were statistically significant interactions between obesity and PCO in fasting glucose levels and basal HGP (P < .05). Steady-state insulin levels of .apprx. 100 .mu.U/ml were achieved during the clamp. Insulin-stimulated glucose utilization was significantly decreased in both PCO groups whether expressed per kilogram total weight (P < .001) or per kilogram fat free mass (P < .001) or when divided by the steady-state plasma insulin (I) level (M/I, P < .001). There was residual HGP in 4 of 15 obese PCO, 0 of 11 obese normal, 2 of 10 nonobese PCO, and 0 of 8 nonobese normal women. The metabolic clearance rate of insulin did not differ in the four groups. We conclude that 1) PCO women have significant insulin resistance that is independent of obesity, changes in body composition, and impairment of glucose tolerance, 2) PCO and obesity have a synergistic deleterious effect on glucose tolerance, 3) hyperinsulinemia in PCO is not the result of decreased insulin clearance, and 4) PCO is associated with a unique disorder of insulin action.This publication has 7 references indexed in Scilit:
- Inhibition of Sex Hormone-Binding Globulin Production in the Human Hepatoma (Hep G2) Cell Line by Insulin and Prolactin*Journal of Clinical Endocrinology & Metabolism, 1988
- Characterization of Groups of Hyperaiidrogenic Women with Acanthosis Nigricans, Impaired Glucose Tolerance, and/or Hyperinsulinemia*Journal of Clinical Endocrinology & Metabolism, 1987
- Acanthosis nigricans and obesity: Acquired and intrinsic defects in insulin actionMetabolism, 1986
- Persistence of insulin resistance in polycystic ovarian disease after inhibition of ovarian steroid secretionFertility and Sterility, 1986
- CLINICAL, BIOCHEMICAL, AND OVARIAN MORPHOLOGIC FEATURES IN WOMEN WITH ACANTHOSIS NIGRICANS AND MASCULINIZATION1985
- Ovarian hyperandrogenism with normal and abnormal histologic findings of the ovariesAmerican Journal of Obstetrics and Gynecology, 1979
- The Polycystic Ovary. I. Clinical and Histologic FeaturesJournal of Clinical Endocrinology & Metabolism, 1962