Insulin resistance in polycystic ovary syndrome.
Hyperinsulinaemia is found in 30% of slim and 75% of obese women with polycystic ovary syndrome. Despite resistance to insulin action in terms of glucose transport, increased insulin levels may cause hyperandrogenaemia by enhancement of androgen production in the ovaries where insulin acts as co-gonadotrophin. Recent interest in insulin resistance results from the recognition that it predisposes to various metabolic abnormalities, and could be involved in the pathogenesis of atherosclerosis. Women with polycystic ovary syndrome frequently have metabolic disturbances associated with insulin resistance, and recent long-term follow-up studies have indicated that they also have a higher incidence of diabetes and hypertension later in life compared with control populations. This review describes the association of hyperinsulinaemia with hyperandrogenism, metabolic and circulatory changes in women with polycystic ovary syndrome. Special emphasis is placed on recent studies of molecular mechanisms of insulin resistance in polycystic ovary syndrome and clinical implications of hyperinsulinaemia in these women.
Prelevic
G M
GM
Department of Medicine, University College London Medical School, UK.
D000728:Androgens / Q000097:blood; D001786:Blood Glucose / Q000378:metabolism; D005260:Female; D006628:Hirsutism / Q000097:blood / Q000150:complications; D006801:Humans; D006946:Hyperinsulinism / Q000097:blood / Q000150:complications*; D007328:Insulin / Q000097:blood*; D007333:Insulin Resistance; D011085:Polycystic Ovary Syndrome / Q000097:blood / Q000150:complications*
D000728:Androgens; D001786:Blood Glucose; D007328:Insulin