Effects of Metformin on Insulin Secretion, Insulin Action, and Ovarian Steroidogenesis in Women with Polycystic Ovary Syndrome

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Abstract
Hyperinsulinemia contributes to the ovarian androgen overpro- duction and glucose intolerance of polycystic ovary syndrome (PCOS). We sought to determine whether metformin would reduce insulin levels in obese, nondiabetic women with PCOS during a period of weight maintenance and thus attenuate the ovarian steroidogenic response to the GnRH agonist leuprolide. All subjects (n 5 14) had an oral glucose tolerance test, a GnRH agonist (leuprolide) test, a fre- quently sampled iv glucose tolerance test, graded and oscillatory glucose infusions, and a dual energy x-ray absorptiometry scan before and after treatment with metformin (850 mg, orally, three times daily for 12 weeks). With weight maintenance (body mass index: pretreatment, 39.0 6 7.7 kg/m2; posttreatment, 39.1 6 7.9 kg/m2), oral glucose tolerance, insulin sensitivity (Si; 0.87 6 0.82 vs. 0.74 6 0.63 3 1025 min21/ pmolzL), and the relationship between Si and first phase insulin secretion (AIRg vs. Si) were not improved by metformin. The insulin secretory response to glucose, administered in both graded and os- cillatory fashions, was likewise unaltered in response to metformin. Free testosterone levels remained about 2-fold elevated (pretreat- ment, 26.6 6 12.7 pg/mL; posttreatment, 22.4 6 9.8 pg/mL). Both basal and stimulated LH and FSH levels were unaffected by met- formin. The mean responses to leuprolide of 17-hydroxyprogesterone (pretreatment, 387 6 158 ng/dL; posttreatment, 329 6 116 ng/dL) as well as those of the other ovarian secretory products (androstenedi- one, dehydroepiandrosterone, progesterone, and estradiol) were not attenuated by metformin. We conclude that hyperinsulinemia and androgen excess in obese nondiabetic women with PCOS are not improved by the administra- tion of metformin. (J Clin Endocrinol Metab 82: 524 -530, 1997)

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