PCOS is mostly ahyperandrogenic disorder and is possibly the most common endocrinopathy of premenopausal women. The primary defect in PCOS appears to be an exaggerated androgen synthesis and secretion by the ovaries and the adrenal glands. In a substantial proportion of PCOS patients, the primary defect in androgen secretion is triggered by factors such as the hyperinsulinism resulting from insulin resistance and/or the secretion of metabolically active substances by visceral adipose tissue. The prevalence of obesity in PCOS patients is increased when compared to the general female population and conversely, the prevalence of PCOS is increased in overweight and obese women when compared to their lean counterparts. Almost 50% of women with PCOS are obese. Obesity exerts a major impact on the PCOS phenotype, particularly on the metabolic association and complications of the syndrome. Women with PCOS are at significantly increased risk of developing type 2 DM. Studies in isolated adipocytes and cultured skin fibroblasts from PCOS women have demonstrated intrinsic post binding defect in insulin mediated glucose metabolism. In fibroblasts, the mitogenic pathway of insulin action is intact, consistent with a selective defect in insulin signaling. While PCOS skeletal muscle is resistant to insulin in vivo, cultured muscle cells have normal insulin sensitivity, consistent with a major role of extrinsic factors in producing insulin resistance in this tissue. Excessive serine phosphorylation of insulin receptor or downstream signaling protein may be involved in the pathogenesis of insulin resistance in PCOS. The explanations for tissue specific and signaling pathway- specific differences in insulin action in PCOS may involve differential roles of insulin receptor substrate (IRS)-1 and IRS – 2 in insulin signal transduction. Obesity without PCOS is associated with suppressed levels of SHBG, leading to higher free androgen levels which prolong follicular phase without affecting ovulation, leading to longer menstrual cycles..