Androgen excess in gonads and resultant Anovulation &

 

High insulin and high LH spoils the cyclicity of menstruation & ovulation

Patients with PCOS frequently exhibit insulin resistance and hyperinsulinemia. Insulin resistance and hyperinsulinemia participate in the ovarian steroidogenic dysfunction of PCOS. Insulin alters ovarian steroidogenesis independent of godadotropin secretion in PCOS. Insulin and insulin-like growth factor I (IGF-I) receptors are present I the ovarian stromal cells.

 

 A specific defect in the early steps of insulin receptor-mediated signaling (diminished autophosphorylation) was identified in 50% of women with PCOS .Insulin has direct and indirect roles in the pathogenesis of hyperandrogenism in PCOS.

 

1.  Insulin in collaboration with LH enhances the androgen production of theca cells. Insulin inhibits the hepatic synthesis of sex hormone-binding globulin, the main circulating protein that binds to testosterone, thus increasing the proportion of unbound or bioavailable testosterone.