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Am J Physiol Endocrinol Metab 281: E392-E399, 2001;
0193-1849/01 $5.00
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Vol. 281, Issue 2, E392-E399, August 2001

Defects in insulin receptor signaling in vivo in the polycystic ovary syndrome (PCOS)

Andrea Dunaif1,2, Xinqi Wu1, Anna Lee1, and Evanthia Diamanti-Kandarakis2

1 Division of Women's Health, Departments of Medicine and of Obstetrics and Gynecology, Brigham and Women's Hospital, Boston, Massachusetts 02115; and 2 Section of Diabetes and Metabolism, Department of Medicine, Pennsylvania State University College of Medicine, Hershey, Pennsylvania 17033

Women with polycystic ovary syndrome (PCOS) are insulin resistant secondary to a postbinding defect in insulin signaling. Sequential euglycemic glucose clamp studies at 40 and 400 mU · m-2 · min-1 insulin doses with serial skeletal muscle biopsies were performed in PCOS and age-, weight-, and ethnicity-matched control women. Steady-state insulin levels did not differ, but insulin-mediated glucose disposal was significantly decreased in PCOS women (P < 0.05). Insulin receptor substrate (IRS)-1-associated phosphatidylinositol 3-kinase (PI 3K) activity was significantly decreased in PCOS (n = 12) compared with control skeletal muscle (n = 8; P < 0.05). There was no significant difference in the abundance of IR, IRS-1, or the p85 regulatory subunit of PI 3K in PCOS (n = 14) compared with control (n = 12) muscle. The abundance of IRS-2 was significantly increased (P < 0.05) in PCOS skeletal muscle, suggesting a compensatory change. We conclude that there is a physiologically relevant defect in insulin receptor signaling in PCOS that is independent of obesity and type 2 diabetes mellitus.

insulin resistance; signal transduction; phosphatidylinositol 3-kinase; insulin receptor substrate-1; insulin receptor substrate-2


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