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The Journal of Clinical Endocrinology & Metabolism Vol. 82, No. 9 3074-3077
Copyright © 1997 by The Endocrine Society

Special Articles

The Effect of a Desogestrel-Containing Oral Contraceptive on Glucose Tolerance and Leptin Concentrations in Hyperandrogenic Women1

Shahla Nader, Maggy G. Riad-Gabriel and Mohammed F. Saad

Department of Obstetrics, Gynecology, and Reproductive Sciences, University of Texas Medical School (S.N.), Houston, Texas 77030; and the Department of Medicine, University of Southern California Medical School (M.G.R.-G., M.F.S.), Los Angeles, California 90033

Address all correspondence and requests for reprints to: Shahla Nader, M.D., Division of Reproductive Endocrinology, University of Texas Medical School, 6431 Fannin, Suite 3.036, Houston, Texas 77030.

Ovarian hyperandrogenism can be associated with insulin resistance, hyperinsulinemia, glucose intolerance, and obesity. High levels of the lipostatic hormone, leptin, have also been reported in this condition. The purpose of the present study was to examine the effect of an oral contraceptive (OC) of low androgenicity containing desogestrel on glucose tolerance in hyperandrogenic women and the impact of changes in androgenic/estrogenic status on leptin concentrations. Sixteen nondiabetic hyperandrogenic women, aged 29 ± 1 yr with a body mass index (BMI) of 36.8 ± 1.8 kg/m2, underwent an oral glucose tolerance test before and after 6 months of therapy with the OC. Free testosterone decreased and sex hormone-binding globulin increased after therapy (P < 0.001). Glucose tolerance deteriorated significantly, and two women developed diabetes. Body weight, BMI, and leptin did not change significantly. Leptin correlated with BMI before (r = 0.56; P = 0.02) and after (r = 0.51; P = 0.04) treatment, but not with glucose, insulin, total and free testosterone, or sex hormone-binding globulin before or after treatment. In conclusion, 1) glucose tolerance should be monitored in hyperandrogenic women using OC, even those of low androgenicity; and 2) changes in androgenic/estrogenic status had no effect on the leptin concentration, suggesting that its sexual dimorphism is not related to sex steroids.




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