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A Hyperandrogenic Mouse Model to Study Polycystic Ovary Syndrome
08:20

A Hyperandrogenic Mouse Model to Study Polycystic Ovary Syndrome

Published on: October 2, 2018

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

Victoria S Sprung1, Helen Jones, Christopher J A Pugh

  • 1*Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, Liverpool, U.K.

Clinical Science (London, England : 1979)
|July 6, 2013
PubMed

Insights

Polycystic ovary syndrome (PCOS) is linked to endothelial dysfunction, a cardiovascular disease risk marker. This dysfunction is not explained by body fat distribution or volume in women with PCOS.

Area of Science:

  • Endocrinology and Metabolism
  • Cardiovascular Health
  • Medical Imaging

Background:

  • Polycystic ovary syndrome (PCOS) is associated with insulin resistance (IR), visceral fat, and non-alcoholic fatty liver disease (NAFLD).
  • These conditions may contribute to endothelial dysfunction, an early indicator of cardiovascular disease (CVD) risk.
  • The relationship between endothelial dysfunction in PCOS and adipose tissue compartments, as well as intracellular triacylglycerol (TAG) pools, requires further investigation.

Purpose of the Study:

  • To examine the relationships between endothelial dysfunction in PCOS, adipose tissue (AT) compartments, and intracellular TAG pools in the liver and skeletal muscle.
  • To assess the role of body fat distribution and volume in endothelial dysfunction in women with PCOS.

Main Methods:

  • Recruitment of 19 women with PCOS and 16 control women.
  • Assessment of endothelial function using brachial artery flow-mediated dilation (FMD).
  • Determination of visceral AT (VAT) and subcutaneous AT (SAT) volume via whole-body MRI, and liver/skeletal muscle TAG via 1H-MRS.

Main Results:

  • Endothelial function (FMD) was significantly impaired in women with PCOS compared to controls (P<0.001).
  • This impairment persisted even after adjusting for visceral and SAT volume and HOMA-IR.
  • The magnitude of FMD impairment was similar in both lean and obese women with PCOS.

Conclusions:

  • Endothelial dysfunction in PCOS is not solely explained by body fat distribution or volume.
  • Flow-mediated dilation (FMD) may serve as an independent prognostic tool for assessing CVD risk in women with PCOS.
  • Further research is warranted to elucidate the precise mechanisms underlying endothelial dysfunction in PCOS.

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