Insulin Action in Polycystic Ovary Syndrome: In Vivo and In Vitro

Polycystic ovary syndrome, insulin, signaling pathways, hyperandrogenemia, theca cells, granulosa cells Polycystic ovary syndrome (PCOS) is a common disorder affecting 6–10% of women of childbearing age [1–3]. It is the most frequent endocrine disorder among young women and the principal medical cause of female infertility in North America. It is defined by the presence of hyperandrogenism, chronic anovulation, and/or polycystic ovaries (see Chap. 1 for a fuller discussion of the definition of PCOS), after exclusion of all secondary causes. However, most experts in the field agree that hyperandrogenemia is the central feature of PCOS and probably results from the same ovarian dysfunction that causes oligoanovulation and infertility. Therefore, in this chapter, we will focus on the mechanisms of hyperandrogenemia in PCOS, as this was the most studied characteristic of PCOS in the literature, particularly with respect to insulin actions.