Abstract

Polycystic ovary syndrome (PCOS) affects 6–10% of women of childbearing age. It is defined by hyperandrogenism, chronic anovulation or polycystic ovaries (two of three criteria), after exclusion of secondary causes. Insulin resistance probably plays a role in the syndrome's pathogenesis and its association with cardiovascular disease. The microcirculatory system has a role in the delivery of insulin to muscle tissue and therefore insulin action. We hypothesized that microvascular dysfunction may contribute to insulin resistance in PCOS. Capillary function is impaired in healthy obese compared with lean women. As far as we know capillary function has never been measured in women with PCOS. Case control study. 18 lean PCOS women (mean age: 28.0 ± 4.5 years, BMI: 22.0 ± 2.3 kg/m2), 17 obese PCOS women (mean age: 30.5 ± 4.2 years, BMI: 36.4 ± 6.1 kg/m2), and 16 lean controls (mean age: 27.0 ± 4.8 years, BMI: 22.1 ± 1.7 kg/m2) were included. Microcirculatory function was measured as post-occlusive capillary recruitment, i.e. the absolute increase in the number of perfused capillaries after arterial occlusion, as assessed by capillary microscopy in the skin. Insulin-mediated glucose uptake was measured as the glucose infusion rate during the second hour of a hyperinsulinemic euglycemic clamp, expressed per kilogram body weight. Insulin-mediated glucose uptake (IMGU) did not differ between in lean PCOS women and controls. In contrast, obese women with PCOS demonstrated a decreased IMGU as compared to both lean PCOS women and controls (2.7 ± 1.4, 7.0 ± 2.6 and 8.0 ± 2.0 mg . kg−1. min−1, respectively; P<0.001). There were no differences in baseline capillary perfusion between the three groups. Post-occlusive capillary recruitment was reduced in lean and obese women with PCOS compared to controls (31.1 ± 8.6, 34.3 ± 10.7 and 40.5 ± 11.4 n/mm2, respectively, P<0.05 by one-way ANOVA). PCOS per se is associated with reduced post-occlusive capillary recruitment. Disturbed microcirculatory function is present in lean and obese women with PCOS, but insulin resistance only in obese PCOS. These data suggest that microcirculatory dysfunction alone does not fully explain the presence of insulin resistance in PCOS.

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