Suppression of Hyperandrogenism Does not Improve Peripheral or Hepatic Insulin Resistance in the Polycystic Ovary Syndrome*

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Abstract
Women with the polycystic ovary syndrome (PCO) have significant insulin resistnce are at risk to develop noninsulin-dependent diabetes mellitus. It remains controversial, however, whether hyperandrogenism directly decreases insulin ation. Hence, we performed 2-h euglycemic glucose (.apprx. 772 pmol/L steady state insulin levels) clamps in nine PCO women with insulin resistance basally and after the 12th week of therapy with a superagonist GnRH analog (40 .mu.g every 8 h, sc). Diet, activity, and weight were kept constant. Despite significant decreases in plasma testosterone and androstenedione levels (both P < 0.05), there was no significant change in insulin-mediated glucose disposal, plasma insulin levels, or hepatic glucose production. The sample size was adequate to detect a clinically significant change in insulin-stimulated glucose disposal (i.e. .apprx. 3.3 .mu.mol/kg.cntdot.min; P .ltoreq. 0.05). We conclude that suppressing androgen levels into the normal range did not range did not result in sigificant changes in insulin resistnce in PCO. Thus, controlling hyperandrogenemia is not a clinically effective modality to improve insulin action and thereby decrease the risk of noninsulin-dependent diabetes in PCO.