title: Endothelial dysfunction in hyperandrogenic polycystic ovary syndrome is not explained by either obesity or ectopic fat deposition.
abstract: PCOS (polycystic ovary syndrome) is associated with IR (insulin resistance), increased visceral fat and NAFLD (non-alcoholic fatty liver disease) all of which may contribute to endothelial dysfunction, an early marker of CVD (cardiovascular disease) risk. Our objective was to examine the relationships between endothelial dysfunction in PCOS, the volume of AT (adipose tissue) compartments and the size of intracellular TAG (triacylglycerol) pools in liver and skeletal muscle. A total of 19 women with PCOS (means±S.D.; 26±6 years, 36±5 kg/m2) and 16 control women (31±8 years, 30±6 kg/m2) were recruited. Endothelial function was assessed in the brachial artery using FMD (flow-mediated dilation). VAT (visceral AT) and abdominal SAT (subcutaneous AT) volume were determined by whole body MRI, and liver and skeletal muscle TAG by 1H-MRS (proton magnetic resonance spectroscopy). Cardiorespiratory fitness and HOMA-IR (homoeostasis model assessment of IR) were also determined. Differences between groups were analysed using independent Student's t tests and ANCOVA (analysis of co-variance). FMD was impaired in PCOS by 4.6% [95% CI (confidence interval), 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 SAT 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 distribution or volume. FMD might be a useful independent prognostic tool to assess CVD risk in this population.
authors.affiliation: *Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, Liverpool, U.K.
authors.forename: Victoria S
authors.initials: VS
authors.lastname: Sprung
authors.forename: Helen
authors.initials: H
authors.lastname: Jones
authors.forename: Christopher J A
authors.initials: CJ
authors.lastname: Pugh
authors.forename: Nabil F
authors.initials: NF
authors.lastname: Aziz
authors.forename: Christina
authors.initials: C
authors.lastname: Daousi
authors.forename: Graham J
authors.initials: GJ
authors.lastname: Kemp
authors.forename: Daniel J
authors.initials: DJ
authors.lastname: Green
authors.forename: N Timothy
authors.initials: NT
authors.lastname: Cable
authors.forename: Daniel J
authors.initials: DJ
authors.lastname: Cuthbertson
mesh_terms: D000273:Adipose Tissue / Q000473:pathology*; D050154:Adiposity / Q000502:physiology; D000328:Adult; D000886:Anthropometry / Q000379:methods; D001916:Brachial Artery / Q000503:physiopathology; D016022:Case-Control Studies; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D006801:Humans; D017588:Hyperandrogenism / Q000150:complications / Q000503:physiopathology*; D007333:Insulin Resistance / Q000502:physiology; D008099:Liver / Q000378:metabolism; D008279:Magnetic Resonance Imaging; D009682:Magnetic Resonance Spectroscopy; D018482:Muscle, Skeletal / Q000378:metabolism; D009765:Obesity / Q000150:complications / Q000473:pathology / Q000503:physiopathology*; D011085:Polycystic Ovary Syndrome / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D011379:Prognosis; D014280:Triglycerides / Q000378:metabolism; D014664:Vasodilation / Q000502:physiology; D055815:Young Adult
chemical_list: D014280:Triglycerides