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ß-Cell Function: A Key Pathological Determinant in Polycystic Ovary Syndrome

Division of Endocrinology, Diabetes, and Hypertension (M.O.G., S.G.K.), Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, California 90095; Division of Endocrinology, Diabetes, and Metabolism and Department of Obstetrics and Gynecology (M.O.G.), Cedars-Sinai Medical Center, Los Angeles, California 90048; and Department of Statistics (S.E., S.C.P., R.I.J.), University of California, Los Angeles, Los Angeles, California 90095

Address all correspondence and requests for reprints to: Mark O. Goodarzi, M.D., Ph.D., Cedars-Sinai Medical Center, Division of Endocrinology, Diabetes, and Metabolism, 8700 Beverly Boulevard, Becker B-128, Los Angeles, California 90048. E-mail: mark.goodarzi{at}cshs.org.

We report data from 60 patients with polycystic ovary syndrome (PCOS) who had undergone assessment of insulin resistance, pancreatic ß-cell function, obesity, and androgen levels to elucidate the complex relationships among these traits. Homeostasis model assessment was used to quantify insulin resistance and ß-cell function. A reference population was derived from the National Health and Nutrition Examination Study (NHANES III, 1988–1994). Indices of insulin resistance, insulin secretion, bioavailable testosterone, and body mass index all exhibited significant pairwise correlations. Multiple regression analysis clarified the phenotypic relationships, demonstrating that insulin resistance and bioavailable testosterone were independent predictors of ß-cell function; ß-cell function and obesity were independent predictors of insulin resistance; and ß-cell function was an independent predictor of bioavailable testosterone. Of note, comparison with normal women from NHANES revealed a significantly stronger relationship between ß-cell function and insulin resistance in PCOS, raising the possibility of an intrinsic defect in ß-cell function whereby increasing insulin resistance leads to a greater insulin response in PCOS than normal. The altered relationship of ß-cell function and insulin resistance coupled with the fact that ß-cell function, not insulin resistance, was a predictor of hyperandrogenemia suggests that ß-cell dysfunction may be a key pathogenic determinant in PCOS.

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