Polycystic Ovary Syndrome: A Syndrome of Ovarian Hypersensitivity to Insulin?
Abstract
Polycystic ovary syndrome (PCOS) affects 6–10% of women of child-bearing age (1). It is defined by hyperandrogenism, chronic anovulation, and/or polycystic ovaries (two of three criteria); after exclusion of secondary causes (2). However, it has become apparent that insulin resistance and hyperinsulinemia play a critical role in the syndrome’s pathogenesis (1). Despite advances over the past decade, many questions remain regarding both the nature of insulin resistance in PCOS and the mechanism by which insulin resistance or insulin produces hyperandrogenemia. During the past 15 yr, several studies demonstrated that insulin stimulates ovarian steroidogenesis in vitro. At physiological concentrations, insulin increases androgen production by cultured ovarian cells from women with PCOS (3), an increase significantly greater than that after stimulation of cells from normal women. Moreover, combined stimulation with LH and insulin at physiological concentrations have been shown to synergistically increase androgen biosynthesis by ovarian tissues from normal and PCOS women (4). LH enhances theca cell steroidogenesis mostly through the cAMP-protein kinase A pathway. The molecular mechanism by which insulin regulates steroidogenesis is less well understood, but it has clearly been shown that insulin acts through its own receptor (3). In classical insulin-responsive tissues, insulin’s actions are mediated via three major pathways: the phosphatidyl-inositol 3-kinase (PI-3K) pathway,…
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