title: PCOS is associated with increased CD11c expression and crown-like structures in adipose tissue and increased central abdominal fat depots independent of obesity.
abstract: BACKGROUND
  Adipose tissue macrophage (ATM) infiltration is a major pathway for obesity-induced insulin resistance but has not been studied as a mechanism for insulin resistance in PCOS.
  
  
  OBJECTIVE
  We tested whether polycystic ovary syndrome (PCOS) is associated with increased ATM infiltration, especially of inflammatory subtype identified by the CD11c marker.
  
  
  METHODS
  We conducted a case-control study at an academic medical center in the United States.
  
  
  METHODS
  Fourteen PCOS and 14 control women of similar age and body mass index (BMI) underwent a gluteal fat biopsy. Markers of ATM, integrins, TNF-α, and adiponectin, were analyzed by quantitative RT-PCR using a standard curve method. Crown-like structures (CLS) were identified by immunohistochemistry. Abdominal magnetic resonance imaging and frequently sampled i.v. glucose tolerance test were performed to assess abdominal fat and insulin sensitivity (SI).
  
  
  RESULTS
  Women with PCOS were compared with control women of similar age and BMI for ATM markers, CLS density, adipose tissue expression of inflammatory cytokines and adiponectin, SI, and abdominal fat depots.
  
  
  RESULTS
  Women with PCOS had an increase in CD11c expression (P = 0.03), CLS density (P = 0.001), α5 expression (P = 0.009), borderline increase in TNF-α expression (P = 0.08), and a decrease in adiponectin expression (P = 0.02) in gluteal adipose tissue. Visceral (P = 0.009) and sc abdominal fat (P = 0.005) were increased in PCOS. SI was lower in PCOS (P = 0.008).
  
  
  CONCLUSIONS
  PCOS is associated with an increase in CD11c expression and CLS density and a decrease in adiponectin expression in sc adipose tissue. Additionally, PCOS is associated with higher central abdominal fat depots independent of BMI. These alterations are present among mostly nonobese women and could represent mechanisms for insulin resistance.
authors.affiliation: Department of Medicine, Section of Endocrinology, Diabetes, and Metabolism (MC 797), University of Illinois at Chicago, 1819 West Polk Street, Chicago, Illinois 60612, USA.
authors.forename: Zhi Hua
authors.initials: ZH
authors.lastname: Huang
authors.forename: Buvana
authors.initials: B
authors.lastname: Manickam
authors.forename: Victoria
authors.initials: V
authors.lastname: Ryvkin
authors.forename: Xiaohong Joe
authors.initials: XJ
authors.lastname: Zhou
authors.forename: Giamila
authors.initials: G
authors.lastname: Fantuzzi
authors.forename: Theodore
authors.initials: T
authors.lastname: Mazzone
authors.forename: Susan
authors.initials: S
authors.lastname: Sam
mesh_terms: D050153:Abdominal Fat / Q000378:metabolism / Q000473:pathology*; D000273:Adipose Tissue / Q000378:metabolism / Q000473:pathology / Q000648:ultrastructure*; D000328:Adult; D015992:Body Mass Index; D039521:CD11c Antigen / Q000235:genetics* / Q000378:metabolism; D016022:Case-Control Studies; D005260:Female; D006801:Humans; D007333:Insulin Resistance / Q000235:genetics / Q000502:physiology; D009765:Obesity / Q000150:complications / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D011085:Polycystic Ovary Syndrome / Q000150:complications / Q000235:genetics* / Q000378:metabolism / Q000473:pathology*; D050151:Subcutaneous Fat / Q000378:metabolism / Q000473:pathology; D015854:Up-Regulation / Q000235:genetics / Q000502:physiology; D055815:Young Adult
chemical_list: D039521:CD11c Antigen