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Insulin Resistance in Nonobese Patients with Polycystic Ovarian Disease^*

Departments of Obstetrics and Gynecology and Pediatrics, University of California Los Angeles, Los Angeles, California 90024
Departments of Obstetrics and Gynecology, University of Southern California School of Medicine, Women's Hospital, LAC/USC Medical Center Los Angeles, California 90033

Address requests for reprints to: R. Jeffrey Chang, M.D., Department of Obstetrics and Gynecology, Division of Reproductive Endocrinology, University of California, Los Angeles, Los Angeles, California 90024.

To determine whether insulin resistance occurs in polycystic ovarian disease (PCO) in the absence of obesity and acanthosis nigricans, circulating levels of insulin in response to oral glucose administration were measured in 10 nonobese PCO patients without acanthosis nigricans and in 10 normal women matched for weight and height. Mean serum testosterone (T), androstenedione (A), dehydroepiandrosterone (D), D sulfate, and LH levels were significantly elevated in the PCO patients compared to those in control subjects. In PCO patients, the mean ± SE basal insulin level (18.7 ± 2.9 µU/ml) and the sum of the insulin levels in response to glucose (674 ±119 µU/ml) were significantly greater than those in the control group (11.0 ± 0.8 µU/ml and 248 ± 29 µU/ml, respectively). In all subjects, serum levels of T and A, but not D and D sulfate, were significantly correlated to basal insulin levels and insulin sums. Serum cortisol, GH, and PRL levels were similar in both groups.

These results indicate that in PCO, a significant degree of insulin resistance exists, which clearly is not related to obesity. The positive correlation of serum T and A levels to circulating insulin levels in this study suggests that the insulin resistance in PCO may be, in part, a consequence of hyperandrogenism.

^* This work was supported by USPHS Research Grants CA-23093, AG-01512, RR-5354, and RR-865.

Received November 5, 1982.

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