Insulin stimulates steroidogenesis by granulosa cells of normal and polycys
tic ovaries and interacts with gonadotropins in an additive or, as in the c
ase of LH, a synergistic manner. These actions appear to be mediated specif
ically by the insulin receptor rather than by cross-reaction with the type-
I IGF receptor, even in tissue obtained from PCOS women with biochemical ev
idence of insulin resistance. This article suggests that hyperinsulinemia m
akes a significant contribution to premature arrest of follicle growth, whi
ch is characteristic of anovulation in women with PCOS, and that the intera
ction 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, w
hich may help to explain the prominence of symptoms of hyperandrogenism in
obese patients with PCOS.