Insulin action in the normal and polycystic ovary

Insulin stimulates steroidogenesis by granulosa cells of normal and polycystic ovaries and interacts with gonadotropins in an additive or, as in the case of LH, a synergistic manner. These actions appear to be mediated specifically by the insulin receptor rather than by cross-reaction with the type-I IGF receptor, even in tissue obtained from PCOS women with biochemical evidence of insulin resistance. This article suggests that hyperinsulinemia makes a significant contribution to premature arrest of follicle growth, which is characteristic of anovulation in women with PCOS, and that the interaction of insulin with LH is a key element in this process. Insulin also may have a role in amplifying LH-induced androgen production by theca cells, which may help to explain the prominence of symptoms of hyperandrogenism in obese patients with PCOS.