Endothelial dysfunction in hyperandrogenic polycystic ovary syndrome is not explained by either obesity or ectopic fat deposition

Polycystic ovary syndrome (PCOS) is associated with insulin resistance, increased visceral fat and non-alcoholic fatty liver disease (NAFLD) all of which may contribute to endothelial dysfunction, an early marker of cardiovascular disease risk. Our objective was to examine the relationships between endothelial dysfunction in PCOS, the volume of adipose tissue compartments and the size of intracellular triglyceride pools in liver and skeletal muscle. Thirty-five women with PCOS (mean±SD; 26±6y, 36±5kg/m2) and 16 control women (31±8y, 30±6kg/m2) were recruited. Endothelial function was assessed in the brachial artery using flow-mediated dilation (FMD). Visceral (VAT) and abdominal subcutaneous adipose tissue (SAT) volume were determined by whole body magnetic resonance imaging, and liver and skeletal muscle triglyceride by 1H magnetic resonance spectroscopy. Cardiorespiratory fitness and insulin resistance (HOMA-IR) were also determined. Differences between groups were analysed using independent t-tests and analysis of covariance. FMD was impaired in PCOS by 4.6% (95% CI=3.0-7.7, P<0.001), and this difference decreased only slightly to 4.2% (95% CI=2.4-6.1, P<0.001) when FMD was adjusted for individual differences in visceral and subcutaneous adipose tissue and HOMA-IR. This magnitude of impairment was also similar in lean and obese PCOS women. The results suggest that endothelial dysfunction in PCOS is not explained by body fat distribu...
Source: Clinical Science - Category: Biomedical Science Authors: Source Type: research