The aetiology of the polycystic ovarian syndrome together with new advances in the molecular genetics and possible candidate genes for the inheritance of the syndrome is discussed. The possible role of leptin in the obesity of polycystic ovarian syndrome is reviewed. Hyperinsulinaemia acts not only as the trigger for hyperandrogenaemia and infertility, but also by stimulating plasminogen activator inhibitor type 1; hyperinsulinaemia may also promote atherogenesis in polycystic ovarian syndrome. The long-term effects of the metabolic derangements accompanying hyperinsulinaemia are reviewed. Special emphasis is placed on the use of novel insulin sensitizers such as troglitazone which promise new treatment opportunities in polycystic ovarian syndrome for both fertility and long-term disease prevention.