Current concepts in the polycystic ovary syndrome

Over the past 20 years, it has been clearly documented that the polycystic ovary syndrome (PCOS) has major metabolic sequelae related to insulin resis tance and that insulin resistance plays an important role in the pathogenes is of the reproductive disturbances of the disorder. Family studies have in dicated a genetic susceptibility to PCOS. Polycystic ovaries and hyperandro genemia are present in similar to 50% of sisters of affected women. Increas ed androgen secretion and insulin resistance persist in cultured theca cell s and skin fibroblasts, respectively, from women with PCOS; this finding su ggests that these are intrinsic, presumably genetic, defects. Insulin resis tance and elevated low-density lipoprotein (LDL) levels also cluster in the sisters of women with PCOS, consistent with genetic traits. Moreover, the brothers of women with PCOS have insulin resistance and elevated dehydroepi androsterone sulfate (DHEAS) levels, which supports a genetic basis for the se findings. Family-based studies of linkage and association have implicate d several genes in the pathogenesis of PCOS. The strongest evidence to date points to a gene in the region of the insulin receptor. Insulin-sensitizin g therapy mitigates the reproductive disturbances of PCOS.