title: Sex differences in the association between plasma copeptin and incident type 2 diabetes: the Prevention of Renal and Vascular Endstage Disease (PREVEND) study.
abstract: OBJECTIVE
  Vasopressin plays a role in osmoregulation, glucose homeostasis and inflammation. Therefore, plasma copeptin, the stable C-terminal portion of the precursor of vasopressin, has strong potential as a biomarker for the cardiometabolic syndrome and diabetes. Previous results were contradictory, which may be explained by differences between men and women in responsiveness of the vasopressin system. The aim of this study was to evaluate the usefulness of copeptin for prediction of future type 2 diabetes in men and women separately.
  
  
  METHODS
  From the Prevention of Renal and Vascular Endstage Disease (PREVEND) study, 4,063 women and 3,909 men without diabetes at baseline were included. A total of 208 women and 288 men developed diabetes during a median follow-up of 7.7 years.
  
  
  RESULTS
  In multivariable-adjusted models, we observed a stronger association of copeptin with risk of future diabetes in women (OR 1.49 [95% CI 1.24, 1.79]) than in men (OR 1.01 [95% CI 0.85, 1.19]) (p (interaction) < 0.01). The addition of copeptin to the Data from the Epidemiological Study on the Insulin Resistance Syndrome (DESIR) clinical model improved the discriminative value (C-statistic,+0.007, p = 0.02) and reclassification (integrated discrimination improvement [IDI] = 0.004, p < 0.01) in women. However, we observed no improvement in men. The additive value of copeptin in women was maintained when other independent predictors, such as glucose, high sensitivity C-reactive protein (hs-CRP) and 24 h urinary albumin excretion (UAE), were included in the model.
  
  
  CONCLUSIONS
  The association of plasma copeptin with the risk of developing diabetes was stronger in women than in men. Plasma copeptin alone, and along with existing biomarkers (glucose, hs-CRP and UAE), significantly improved the risk prediction for diabetes in women.
authors.affiliation: Department of Epidemiology, University of Groningen, University Medical Center Groningen, Hanzeplein 1, PO Box 30.001, 9700 RB Groningen, the Netherlands. a.abbasi@umcg.nl
authors.forename: A
authors.initials: A
authors.lastname: Abbasi
authors.forename: E
authors.initials: E
authors.lastname: Corpeleijn
authors.forename: E
authors.initials: E
authors.lastname: Meijer
authors.forename: D
authors.initials: D
authors.lastname: Postmus
authors.forename: R T
authors.initials: RT
authors.lastname: Gansevoort
authors.forename: R O B
authors.initials: RO
authors.lastname: Gans
authors.forename: J
authors.initials: J
authors.lastname: Struck
authors.forename: H L
authors.initials: HL
authors.lastname: Hillege
authors.forename: R P
authors.initials: RP
authors.lastname: Stolk
authors.forename: G
authors.initials: G
authors.lastname: Navis
authors.forename: S J L
authors.initials: SJ
authors.lastname: Bakker
mesh_terms: D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood; D015331:Cohort Studies; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000453:epidemiology; D003925:Diabetic Angiopathies / Q000097:blood* / Q000453:epidemiology / Q000517:prevention & control; D003928:Diabetic Nephropathies / Q000097:blood* / Q000453:epidemiology / Q000517:prevention & control; D005260:Female; D005500:Follow-Up Studies; D006020:Glycopeptides / Q000097:blood*; D006801:Humans; D007676:Kidney Failure, Chronic / Q000097:blood* / Q000453:epidemiology / Q000517:prevention & control; D008297:Male; D008875:Middle Aged; D009426:Netherlands / Q000453:epidemiology; D011237:Predictive Value of Tests; D011498:Protein Precursors / Q000097:blood; D012307:Risk Factors; D012737:Sex Factors; D013997:Time Factors
chemical_list: D015415:Biomarkers; D006020:Glycopeptides; D011498:Protein Precursors; C048197:copeptins