title: Hyperglycemia-induced oxidative stress is independent of excess abdominal adiposity in normal-weight women with polycystic ovary syndrome.
abstract: OBJECTIVE
  What is the effect of glucose ingestion on leukocytic reactive oxygen species (ROS) generation in normal-weight women with polycystic ovary syndrome (PCOS) with and without excess abdominal adiposity (AA)?
  
  
  CONCLUSIONS
  Normal-weight women with PCOS exhibit an increase in leukocytic ROS generation in response to glucose ingestion, and this increase is independent of excess AA.
  
  
  BACKGROUND
  Excess adipose tissue is a source of oxidative stress. Normal-weight women with PCOS exhibit oxidative stress and can have excess AA.
  
  
  METHODS
  This is a cross-sectional study involving 30 reproductive-age women.
  
  
  METHODS
  Fourteen normal-weight women with PCOS (6 normal AA, 8 excess AA) and 16 body composition-matched controls (8 normal AA, 8 excess AA) underwent body composition assessment by dual-energy absorptiometry and an oral glucose tolerance test (OGTT) at a university medical center. Insulin sensitivity was derived from the OGTT (IS(OGTT)). Blood was drawn while fasting and 2 h after glucose ingestion to measure leukocytic ROS generation and p47(phox) protein content and plasma thiobarbituric acid-reactive substances (TBARS) and C-reactive protein (CRP).
  
  
  RESULTS
  Compared with controls, both PCOS groups exhibited lower IS(OGTT) (43-54%) and greater percentage change (% change) in ROS generation (96-140%), p47(phox) protein (18-28%) and TBARS (17-48%). Compared with women with PCOS with excess AA, those with normal AA exhibited higher testosterone levels (29%) and lower CRP levels (70%). For the combined groups, IS(OGTT) was negatively correlated with the % change in ROS generation and p47(phox) protein. CRP was positively correlated with abdominal fat. The % change in p47(phox) protein was positively correlated with CRP and androgens.
  
  
  CONCLUSIONS
  Although this study is adequately powered to assess differences in ROS generation between the women with PCOS and control participants, the modest sample size merits caution when interpreting the corroborative results of the additional measures of oxidative stress and inflammation.
  
  
  CONCLUSIONS
  This study highlights the unique pro-oxidant contribution of circulating leukocytes in the development of insulin resistance and hyperandrogenism in PCOS.
  
  
  BACKGROUND
  Supported by NIH grant HD-048535 to F.G. The authors have nothing to disclose.
authors.affiliation: Department of Obstetrics and Gynecology, Indiana University School of Medicine, AOC Room 6046, 550 N University Boulevard, Indianapolis, IN 46202, USA. gonzalef@iupui.edu
authors.forename: Frank
authors.initials: F
authors.lastname: González
authors.forename: Chang Ling
authors.initials: CL
authors.lastname: Sia
authors.forename: Marguerite K
authors.initials: MK
authors.lastname: Shepard
authors.forename: Neal S
authors.initials: NS
authors.lastname: Rote
authors.forename: Judi
authors.initials: J
authors.lastname: Minium
mesh_terms: D050153:Abdominal Fat / Q000378:metabolism*; D000328:Adult; D003430:Cross-Sectional Studies; D005260:Female; D005951:Glucose Tolerance Test; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology; D007962:Leukocytes / Q000378:metabolism; D019255:NADPH Oxidases / Q000378:metabolism; D011085:Polycystic Ovary Syndrome / Q000097:blood / Q000378:metabolism*; D017382:Reactive Oxygen Species / Q000378:metabolism*
chemical_list: D017382:Reactive Oxygen Species; D019255:NADPH Oxidases; C060505:neutrophil cytosolic factor 1