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The link between polycystic ovarian syndrome and type 2 diabetes: preventive and therapeutic approach in Israel.

P olycystic ovarian syndrome is the most common endocrinopathy, affecting 6%–10% of women of reproductive age [1]. It is the major cause of female anovulatory infertility and affects women across their lifespan. It is characterized by disturbed ovarian function, usually manifests as oligomenorrhea or amenorrhea, infertility and enlarged polycystic ovaries, and is associated with clinical and/or biochemical evidence of hyperandrogenism [2]. Endocrine abnormalities may include increased free testosterone levels, low sex hormone binding globulin, and high luteinizing hormone/ follicle-stimulating hormone ratio [2,3]. PCOS1 was originally thought to affect solely women of child-bearing age because of the presence of infertility. However, current evidence has shown that insulin resistance and the compensatory hyperinsulinemia is a central feature of PCOS [4,5]. Women with PCOS have a high incidence of insulin resistance [4], which is accompanied by compensatory hyperinsulinemia and therefore presents an increased risk for type 2 diabetes [4-6]. In vitro and in vivo studies have shown that in women with PCOS the sensitivity of glucose metabolism to insulin is subnormal and modest hyperinsulinemia prevails [3]. Insulin resistance affects approximately 65–80% of women with PCOS and appears to play an important pathogenic role in the hyperandrogenism of both obese and lean women with PCOS [5]. The recognition that the disorder is associated with insulin resistance has provided insight not only into the pathogenesis of PCOS but also into its related short and long-term complications, with significant risk for the development of obesity, metabolic syndrome, impaired glucose tolerance, type 2 diabetes, dyslipidemia, hypertension and atherosclerosis [3,5,6].