Adipocyte insulin action following ovulation in polycystic ovarian syndrome.

The role of anovulation and insulin resistance in the pathogenesis of polycystic ovarian syndrome (PCOS) remains to be determined. The aim of this study was to investigate whether the metabolic abnormality of insulin resistance in PCOS reflects, rather than causes, the ovarian dysfunction. Eight subjects with classical PCOS were studied on two occasions. Adipocyte insulin sensitivity together with hormonal and metabolic changes were investigated in patients with PCOS following prolonged amenorrhoea and then again in the early follicular phase after ovulation. Insulin receptor binding in amenorrhoeic 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 stimulated 3-O-methylglucose uptake was 0.70 +/- 0. 14 during amenorrhoea and increased to 1.08 +/- 0.25 pmol/10 cm(2) cell membrane (P < 0.05). Plasma testosterone fell (4.0 +/- 0.4 to 2. 3 +/- 0.2 nmol/l; P < 0.001), luteinizing hormone fell (17.6 +/- 2.3 to 6.7 +/- 0.8 IU/l; P < 0.001) but plasma insulin concentrations remained unchanged following ovulation (14.6 +/- 1.9 and 15.7 +/- 3. 8 pmol/l during amenorrhoea and after ovulation respectively). The results of this study suggest that chronic anovulation per se appears to modify the factors contributing to cellular insulin resistance seen in PCOS.