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dc.contributor.authorSprung, Victoria
dc.contributor.authorJones, Helen
dc.contributor.authorPugh, Christopher J. A.
dc.contributor.authorAziz, Nabil F.
dc.contributor.authorDaousi, Christina
dc.contributor.authorKemp, Graham
dc.contributor.authorGreen, Daniel
dc.contributor.authorCable, Timothy
dc.contributor.authorCuthbertson, Daniel J.
dc.date.accessioned2018-10-10T18:55:24Z
dc.date.available2018-10-10T18:55:24Z
dc.date.issued2014-01-31
dc.identifier.citationSprung, V.S., Jones, H., Pugh, C.J., Aziz, N.F., Daousi, C., Kemp, G.J., Green, D.J., Cable, N.T. and Cuthbertson, D.J. (2014) 'Endothelial dysfunction in hyperandrogenic polycystic ovary syndrome is not explained by either obesity or ectopic fat deposition', Clinical Science, 126(1), pp.67-74en_US
dc.identifier.urihttp://hdl.handle.net/10369/10136
dc.descriptionCopy not available from this repositoryen_US
dc.description.abstractPCOS (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.en_US
dc.language.isoenen_US
dc.publisherPortland Pressen_US
dc.relation.ispartofseriesClinical Science;
dc.titleEndothelial dysfunction in hyperandrogenic polycystic ovary syndrome is not explained by either obesity or ectopic fat depositionen_US
dc.typeArticleen_US
dc.identifier.doihttps://doi.org/10.1042/CS20130186
rioxxterms.versionNAen_US


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