Adipocyte insulin action following ovulation in polycystic ovarian syndrome

The role of anovulation and insulin resistance in the pathogenesis of polyc ystic ovarian syndrome (PCOS) remains to be determined. The aim of this stu dy was to investigate whether the metabolic abnormality of insulin resistan ce in PCOS reflects, rather than causes, the ovarian dysfunction. Eight sub jects with classical PCOS were studied on two occasions. Adipocyte insulin sensitivity together with hormonal and metabolic changes mere investigated in patients with PCOS following prolonged amenorrhoea and then again in the early follicular phase after ovulation. Insulin receptor binding in amenor rhoeic subjects with PCOS was low at 0.78 +/- 0.08% and this increased to 1 .18 +/- 0.19% after an ovulatory cycle (P < 0.05). Maximal insulin stimulat ed 3-O-methylglucose uptake was 0.70 +/- 0.14 during amenorrhoea and increa sed to 1.08 +/- 0.25 pmol/10 cm(2) cell membrane (P < 0.05). Plasma testost erone fell (4.0 +/- 0.4 to 2.3 +/- 0.2 nmol/l; P < 0.001), luteinizing horm one feb (17.6 +/- 2.3 to 6.7 +/- 0.8 IU/l; P < 0.001) but plasma insulin co ncentrations remained unchanged following ovulation (14.6 +/- 1.9 and 15.7 +/- 3.8 pmol/l during amenorrhoea and after ovulation respectively). The re sults of this study suggest that chronic anovulation per se appears to modi fy the factors contributing to cellular insulin resistance seen in PCOS.