The pathophysiology of polycystic ovary syndrome: trying to understand PCOS and its endocrinology.
The pathophysiology of the polycystic ovary syndrome (PCOS) encompasses inherent ovarian dysfunction that is strongly influenced by external factors, such as disturbances of the hypothalamic-pituitary-ovarian axis and hyperinsulinaemia. Exaggerated gonadotrophin releasing hormone (GnRH) pulsatility results in hypersecretion of luteinising hormone (LH), which has effects both on ovarian androgen production and oocyte development. Disturbed ovarian-pituitary and hypothalamic feedback accentuates the 0gonadotrophin abnormalities. Hyperinsulinaemia is secondary both to insulin resistance at the periphery and to abnormal pancreatic beta cell function. PCOS runs in families and a number of genetic abnormalities appear to result in features of the syndrome and account for the heterogeneity of the symptoms. Environmental influences, such as nutrition and lifestyle, further influence expression of the syndrome.
Balen
Adam
A
Department of Reproductive Medicine, The General Infirmary, Belmont Grove, West Yorkshire, Leeds LS2 9NS, UK. adam.balen@leedsth.nhs.uk
D005260:Female; D006801:Humans; D017588:Hyperandrogenism / Q000503:physiopathology; D006946:Hyperinsulinism / Q000503:physiopathology; D007030:Hypothalamo-Hypophyseal System / Q000503:physiopathology; D007333:Insulin Resistance; D007986:Luteinizing Hormone / Q000502:physiology; D010053:Ovary / Q000503:physiopathology; D011085:Polycystic Ovary Syndrome / Q000503:physiopathology*
D007986:Luteinizing Hormone