The
polycystic ovary syndrome (PCOS) is a condition characterized by
hyperandrogenism and chronic oligo-
anovulation. However, many features of the
metabolic syndrome are inconsistently present in the majority of women with PCOS. Approximately 50% of PCOS women are
overweight or obese and most of them have the abdominal phenotype.
Obesity may play a pathogenetic role in the development of the syndrome in susceptible individuals. In fact,
insulin possesses true gonadotrophic function and an increased
insulin availability at the level of ovarian tissue may favour excess
androgen synthesis.
Obesity, particularly the abdominal phenotype, may be partly responsible for
insulin resistance and associated
hyperinsulinemia in women with PCOS. Therefore,
obesity-related
hyperinsulinemia may play a key role in favouring
hyperandrogenism in these women. Other factors such as increased
estrogen production rate, increased activity of the
opioid system and of the hypothalamic-pituitary-adrenal axis, decreased
sex hormone binding globulin synthesis and, possibly, high dietary
lipid intake, may be additional mechanisms by which
obesity favours the development of
hyperandrogenism in PCOS. Irrespective of the pathogenetic mechanism involved, obese PCOS women have more severe
hyperandrogenism and related clinical features (such as
hirsutism, menstrual abnormalities and
anovulation) than normal-weight PCOS women. This picture tends to be more pronounced in obese PCOS women with the abdominal phenotype.
Body weight loss is associated with beneficial effects on
hormones, metabolism and clinical features. A further clinical and endocrinological improvement can also be achieved by adding
insulin-sensitizing agents and/or
antiandrogens to
weight reduction programmes. These obviously emphasize the role of
obesity in the pathophysiology of PCOS.