title: Polycystic ovary syndrome with hyperandrogenism is characterized by an increased risk of hepatic steatosis compared to nonhyperandrogenic PCOS phenotypes and healthy controls, independent of obesity and insulin resistance.
abstract: BACKGROUND
  Nonalcoholic fatty liver disease may be evident in women with polycystic ovary syndrome (PCOS), both conditions being associated with obesity and insulin resistance. However, few studies have accounted for the high prevalence of obesity in PCOS.
  
  
  OBJECTIVE
  The aim of this study was to determine whether PCOS is independently associated with hepatic steatosis, compared with healthy controls of similar age and body mass index (BMI), and whether steatosis is associated with hyperandrogenemia.
  
  
  METHODS
  We conducted a cross-sectional, case-control study at two tertiary referral centers.
  
  
  METHODS
  Twenty-nine women with PCOS diagnosed by the Rotterdam criteria [aged 28 yr; 95% confidence interval (CI), 26-31; BMI, 33 kg/m2; 95% CI, 31-36] and 22 healthy controls (aged 29 yr; 95% CI, 28-31; BMI, 30 kg/m2; 95% CI, 28-33) were studied.
  
  
  METHODS
  Proton-magnetic resonance spectroscopy quantified hepatic and skeletal muscle fat; whole body magnetic resonance imaging quantified internal, visceral, and sc adipose tissue volumes. Differences were assessed between PCOS and controls using t tests, and between hyperandrogenic (HA) PCOS, PCOS with normal androgens (NA), and controls using analysis of covariance.
  
  
  RESULTS
  After statistical adjustment for BMI, HA-PCOS had significantly higher liver fat vs. NA-PCOS (3.7%; 95% CI, 0.6-13.1) and vs. controls (2.1%; 95% CI, 0.3-6.6). Similarly, after adjustment for homeostasis model assessment for insulin resistance, internal and visceral adipose tissue volumes, liver fat remained significantly greater in HA-PCOS compared to NA-PCOS and controls.
  
  
  CONCLUSIONS
  These data suggest that HA-PCOS is associated with hepatic steatosis, independent of obesity and insulin resistance.
authors: Research Institute for Sport and Exercise Sciences, John Moores University, and Department of Obesity and Endocrinology, University Hospital Aintree, Liverpool L9 7AL, United Kingdom.
authors: Helen
authors: H
authors: Jones
authors: Victoria S
authors: VS
authors: Sprung
authors: Christopher J A
authors: CJ
authors: Pugh
authors: Christina
authors: C
authors: Daousi
authors: Andrew
authors: A
authors: Irwin
authors: Nabil
authors: N
authors: Aziz
authors: Valerie L
authors: VL
authors: Adams
authors: E Louise
authors: EL
authors: Thomas
authors: Jimmy D
authors: JD
authors: Bell
authors: Graham J
authors: GJ
authors: Kemp
authors: Daniel J
authors: DJ
authors: Cuthbertson
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism / Q000473:pathology; D000328:Adult; D001823:Body Composition / Q000502:physiology; D016022:Case-Control Studies; D003430:Cross-Sectional Studies; D005234:Fatty Liver / Q000453:epidemiology* / Q000378:metabolism / Q000473:pathology; D005260:Female; D006801:Humans; D017588:Hyperandrogenism / Q000453:epidemiology* / Q000378:metabolism / Q000473:pathology; D007333:Insulin Resistance / Q000502:physiology; D008099:Liver / Q000378:metabolism / Q000473:pathology; D018482:Muscle, Skeletal / Q000378:metabolism / Q000473:pathology; D065626:Non-alcoholic Fatty Liver Disease; D009765:Obesity / Q000453:epidemiology* / Q000378:metabolism / Q000473:pathology; D010641:Phenotype; D011085:Polycystic Ovary Syndrome / Q000453:epidemiology* / Q000378:metabolism / Q000473:pathology; D015995:Prevalence; D012307:Risk Factors