The endometrium in polycystic ovary syndrome
Abstract
Polycystic ovary syndrome (PCOS) is a common endocrinopathy and cause of anovulation, with abnormally elevated circulating androgens and insulin levels being common components of PCOS. The potential effects of the metabolic and endocrinologic changes seen in PCOS on the human endometrium are likely to be complex and comprise an important area of research. Androgen receptors and steroid receptor co-activators are overexpressed in the endometrium of women with PCOS. In addition, molecular markers of endometrial receptivity including αvβ3 integrin and glycodelin are decreased in endometrial biopsy specimens from patients with PCOS. Clinically, reproductive performance of women with PCOS is improved by insulin-lowering agents such as metformin, primarily by restoring ovulation; however, the effects of insulin-lowering agents on endometrium are unknown. In vitro studies on the effects of insulin on endometrial stromal cells demonstrate that insulin inhibits the normal process of decidualization. Insulin-like growth factors (IGFs) and their binding proteins (IGFBPs) are important in the maternal–fetal interface and in the circulation. Hyperinsulinemia results in decreased circulating IGFBP-1 and increased free IGF-1. Thus, a combination of elevated unopposed estrogen, hyperinsulinemia, elevated free IGF-1, elevated androgens, and obesity likely contribute to the endometrial dysfunction, infertility, increased miscarriage rate and endometrial hyperplasia seen in PCOS.
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