The polycystic ovary syndrome: what does insulin resistance have to do with it?

About half of infertility cases are attributable to female factors, of which anovulation is the leading cause. Most cases of anovulation are due to the polycystic ovarian syndrome (PCOS). Clinically PCOS, present in 5% of all women, consists of anovulation, acne, hirsutism, reversed LH-to-FSH ratio and often resistance to insulin. In some cases PCOS appears in familial clusters but its genetic cause is unknown. Several genes were suggested as possible culprits for PCOS but their involvement has not been proven. The central paradox regarding the role of insulin in PCOS is the high responsiveness to insulin by the ovary, as opposed to the resistance of the whole body. On the backdrop of knowledge of several paralogous genes for each of the participating proteins in the insulin signal transduction pathways, it is possible that different paralogues propagate the intracellular signal in the ovary as opposed to peripheral tissues. Studies by microarray techniques of the different gene expression profiles in the two ovarian cells and peripheral cells such as adipocytes could clarify whether the ovarian defect in PCOS is identical to the peripheral defect in insulin signal transduction, or whether serum insulin concentrations simply serve to reveal the ovarian defect.