title: The altered mononuclear cell-derived cytokine response to glucose ingestion is not regulated by excess adiposity in polycystic ovary syndrome.
abstract: BACKGROUND
  Excess adipose tissue is a source of inflammation. Polycystic ovary syndrome (PCOS) is a proinflammatory state and is often associated with excess abdominal adiposity (AA) alone and/or frank obesity.
  
  
  OBJECTIVE
  To determine the effect of glucose ingestion on cytokine release from mononuclear cells (MNC) in women with PCOS with and without excess AA and/or obesity.
  
  
  METHODS
  A cross-sectional study.
  
  
  METHODS
  Academic medical center.
  
  
  METHODS
  Twenty-three women with PCOS (seven normal weight with normal AA, eight normal weight with excess AA, eight obese) and 24 ovulatory controls (eight normal weight with normal AA, eight normal weight with excess AA, eight obese).
  
  
  METHODS
  Three-hour 75-g oral glucose tolerance test (OGTT).
  
  
  METHODS
  Body composition was measured by dual energy x-ray absorptiometry. Insulin sensitivity was derived from the OGTT (ISOGTT). TNFα, IL-6, and IL-1β release was measured in supernatants of cultured MNC isolated from blood samples drawn while fasting and 2 hours after glucose ingestion.
  
  
  RESULTS
  Insulin sensitivity was lower in obese subjects regardless of PCOS status and in normal-weight women with PCOS compared with normal-weight controls regardless of body composition status. In response to glucose ingestion, MNC-derived TNFα, IL-6, and IL-1β release decreased in both normal-weight control groups but failed to suppress in either normal-weight PCOS group and in obese women regardless of PCOS status. For the combined groups, the cytokine responses were negatively correlated with insulin sensitivity and positively correlated with abdominal fat and androgens.
  
  
  CONCLUSIONS
  Women with PCOS fail to suppress MNC-derived cytokine release in response to glucose ingestion, and this response is independent of excess adiposity. Nevertheless, a similar response is also a feature of obesity per se. Circulating MNC and excess adipose tissue are separate and distinct sources of inflammation in this population.
authors: Department of Obstetrics and Gynecology (F.G., C.L.S., M.K.S.), Indiana University School of Medicine, Indianapolis, Indiana 46202; and Department of Reproductive Biology (N.S.R., J.M.), Case Western Reserve University School of Medicine, Cleveland, Ohio 44109.
authors: Frank
authors: F
authors: González
authors: Chang Ling
authors: CL
authors: Sia
authors: Marguerite K
authors: MK
authors: Shepard
authors: Neal S
authors: NS
authors: Rote
authors: Judi
authors: J
authors: Minium
mesh_terms: D050154:Adiposity / Q000276:immunology*; D000328:Adult; D001823:Body Composition / Q000502:physiology; D003430:Cross-Sectional Studies; D005260:Female; D005947:Glucose / Q000008:administration & dosage*; D005951:Glucose Tolerance Test; D006801:Humans; D053583:Interleukin-1beta / Q000378:metabolism*; D015850:Interleukin-6 / Q000378:metabolism*; D007963:Leukocytes, Mononuclear / Q000187:drug effects* / Q000378:metabolism; D011085:Polycystic Ovary Syndrome / Q000276:immunology* / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*; D055815:Young Adult
chemical_list: D053583:Interleukin-1beta; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D005947:Glucose