Polycystic ovary syndrome (PCOS) is a major risk factor for impaired glucose tolerance (IGT) and type 2 diabetes mellitus (T2D). Several studies have examined possible mechanisms related to glucose metabolism and insulin secretion that may be responsible for the high prevalence of disorders of glucose metabolism in women with PCOS. The actual pathogenic mechanisms appear to be complex and multifactorial, possibly characterized by the lack of uniformity between patients, thus reflecting the heterogeneity of PCOS. Impaired insulin action and/or beta-cell dysfunction and/or decreased hepatic clearance of insulin have been implicated so far. This article focuses on the role of beta-cell function in the increased predisposition to GDM and T2D in PCOS and the possible genetic basis of defects in insulin secretion. Conditions, like pregnancy and exogenous glucocorticoid administration, aggravate insulin resistance ,thereby placing additional strains upon beta-cells, which may be inherently prone to dysfunction in women with PCOS. The aggravation of insulin resistance amplifies the demands for insulin secretion by beta-cells. The resultant unfavourable state unmasks potential latent defects of beta-cell function, thereby possibly precipitating the development of T2D or of gestational diabetes (GDM) in pregnant women with PCOS. In addition to metabolic sequelae, insulin resistance and compensatory hyperinsulinemia contribute to ovarian dysfunction,manifested by hyperandrogenemia and anovulation, characterizing PCOS. The role of ovarian androgen excess in metabolic aberrations,specifically insulin action and secretion remains unclears.