Glucose tolerance, insulin secretion and insulin sensitivity in polycystic ovary syndrome.

Polycystic ovary syndrome (PCOS) is a disorder affecting approximately 5-10% of reproductive aged women [1]. Initially described by Stein and Leventhal in 1935 [2] as a combination of polycystic ovaries, amenorrhoea, hirsutism and obesity, it has been defined in different ways over the years. Finally, in 1990 the National Institutes of Health (NIH) established the new diagnostic criteria for this disorder, which are based on the presence of hyperandrogenism and chronic oligo-anovulation, with the exclusion of other causes of hyperandrogenism such as non-classical adrenal steroid 21-hydroxylase deficiency, hyperprolactinemia, or androgen-secreting neoplasm [3]. In the past decade it became apparent that the syndrome is also associated with metabolic disturbances. Burghen and colleagues [1] in 1980 first reported that women with PCOS had higher basal and glucose-stimulated insulin levels than weight-matched controls. Subsequently, a number of studies worldwide [4, 5] demonstrated that hyperinsulinemia and insulin-resistance are common features of a large number of patients affected by PCOS. In addition to hyperinsulinemia and insulinresistance, altered first-phase insulin secretion, impaired glucose tolerance, dyslipidemia, hypertension and impaired fibrinolysis have also been described in PCOS [6, 7, 8]. This cluster of metabolic disturbances places women with PCOS at a high risk for the development of cardiovascular disease and diabetes and implies that the PCOS by itself may not be considered just a hyperandrogenic disorder exclusively related to young and fertile-age women, but a syndrome which may have some health implications later in life.