title: The determinants of insulin sensitivity, β-cell function, and glucose tolerance are different in patients with polycystic ovary syndrome than in women who do not have hyperandrogenism.
abstract: OBJECTIVE
  To evaluate the pathogenetic mechanisms underlying abnormal glucose tolerance in polycystic ovary syndrome (PCOS).
  
  
  METHODS
  Case-control study.
  
  
  METHODS
  Academic hospital.
  
  
  METHODS
  One hundred twelve patients with PCOS and 86 nonhyperandrogenic control women of similar age and body mass index (BMI).
  
  
  METHODS
  An oral glucose tolerance test (OGTT) served to explore glucose tolerance and to calculate insulin sensitivity, insulin secretion, and insulin disposition indexes.
  
  
  METHODS
  Frequency of abnormal glucose tolerance, indexes of insulin sensitivity, secretion and disposition, and markers of inflammation, androgen excess, and iron stores.
  
  
  RESULTS
  Obesity and age, but not PCOS, were associated with an increased frequency of abnormal glucose tolerance and diabetes. An imbalance between insulin resistance and secretion--translated into decreased insulin disposition index--predicted abnormal glucose tolerance in patients with PCOS and controls, yet these women differed in the factors associated with decreased insulin disposition. In patients with PCOS, hyperandrogenism, chronic inflammation, and family history of diabetes contributed to insulin resistance as the main pathogenetic mechanism. In nonhyperandrogenic women, familial aggregation of defective insulin secretion, adiposity, and increased body iron stores explained most of the decrease in insulin disposition.
  
  
  CONCLUSIONS
  In addition to a major influence of obesity and age, the mechanisms underlying abnormal glucose tolerance are different in patients with PCOS compared with women who do not have hyperandrogenism.
authors.affiliation: Department of Endocrinology, Hospital Universitario Ramón y Cajal and Universidad de Alcalá, Madrid, Madrid, Spain.
authors.forename: Manuel
authors.initials: M
authors.lastname: Luque-Ramírez
authors.forename: Macarena
authors.initials: M
authors.lastname: Alpañés
authors.forename: Héctor F
authors.initials: HF
authors.lastname: Escobar-Morreale
mesh_terms: D052242:Adiponectin / Q000097:blood / Q000378:metabolism; D015415:Biomarkers / Q000032:analysis* / Q000097:blood / Q000378:metabolism; D001786:Blood Glucose / Q000378:metabolism*; D016022:Case-Control Studies; D005260:Female; D005293:Ferritins / Q000097:blood / Q000378:metabolism; D018149:Glucose Intolerance / Q000097:blood / Q000150:complications / Q000175:diagnosis / Q000378:metabolism; D006801:Humans; D017588:Hyperandrogenism / Q000097:blood / Q000378:metabolism / Q000503:physiopathology; D018836:Inflammation Mediators / Q000097:blood / Q000378:metabolism; D007328:Insulin / Q000378:metabolism; D007333:Insulin Resistance / Q000502:physiology*; D000078790:Insulin Secretion; D050417:Insulin-Secreting Cells / Q000502:physiology*; D016017:Odds Ratio; D011085:Polycystic Ovary Syndrome / Q000097:blood / Q000175:diagnosis / Q000378:metabolism* / Q000503:physiopathology*
chemical_list: C499918:ADIPOQ protein, human; D052242:Adiponectin; D015415:Biomarkers; D001786:Blood Glucose; D018836:Inflammation Mediators; D007328:Insulin; D005293:Ferritins