title: Adipokines and incident type 2 diabetes in an Aboriginal Canadian [corrected] population: the Sandy Lake Health and Diabetes Project.
abstract: OBJECTIVE
  The aim of this study was to investigate associations of adiponectin, leptin, C-reactive protein (CRP), interleukin (IL)-6, and serum amyloid A (SAA), individually or in combinations, with risk of incident type 2 diabetes in a Aboriginal Canadian [corrected] population.
  
  
  METHODS
  Of the 606 Sandy Lake Health and Diabetes Project cohort subjects who were free of diabetes at baseline, 540 (89.1%) participated in 10-year follow-up assessments. Concentrations of fasting adiponectin, leptin, CRP, IL-6, SAA, and covariates were measured at baseline. Fasting glucose and a 75-g oral glucose tolerance test were obtained at baseline and follow-up to determine incident type 2 diabetes, defined as clinically diagnosed type 2 diabetes or as fasting plasma glucose > or =7.0 mmol/l or 2-h postload plasma glucose > or =11.1 mmol/l at follow-up.
  
  
  RESULTS
  Low adiponectin, high leptin, and low adiponectin-to-leptin ratio at baseline were associated with increased risk of incident type 2 diabetes after adjustment for age, sex, triglycerides, HDL cholesterol, hypertension, and impaired glucose tolerance (odds ratio 0.63 [95% CI 0.48-0.83], 1.50 [1.02-2.21], and 0.54 [0.37-0.77], respectively). When the models were additionally adjusted for waist circumference or BMI, however, only low adiponectin remained significantly associated with increased incident diabetes (0.68 [0.51-0.90]). Combinations of leptin, CRP, IL-6, and/or SAA with adiponectin, assessed using either the ratio or joint effects, did not improve diabetes prediction.
  
  
  CONCLUSIONS
  Low baseline adiponectin is associated with increased risk of incident type 2 diabetes independent of leptin, CRP, IL-6, SAA, and metabolic syndrome variables including obesity.
authors.affiliation: Department of Nutritional Sciences, University of Toronto, Toronto, Ontario, Canada.
authors.forename: Sylvia H
authors.initials: SH
authors.lastname: Ley
authors.forename: Stewart B
authors.initials: SB
authors.lastname: Harris
authors.forename: Philip W
authors.initials: PW
authors.lastname: Connelly
authors.forename: Mary
authors.initials: M
authors.lastname: Mamakeesick
authors.forename: Joel
authors.initials: J
authors.lastname: Gittelsohn
authors.forename: Robert A
authors.initials: RA
authors.lastname: Hegele
authors.forename: Ravi
authors.initials: R
authors.lastname: Retnakaran
authors.forename: Bernard
authors.initials: B
authors.lastname: Zinman
authors.forename: Anthony J G
authors.initials: AJ
authors.lastname: Hanley
mesh_terms: D054392:Adipokines / Q000097:blood*; D000328:Adult; D002097:C-Reactive Protein / Q000378:metabolism; D002170:Canada / Q000453:epidemiology; D003924:Diabetes Mellitus, Type 2 / Q000453:epidemiology*; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D015994:Incidence; D007333:Insulin Resistance; D004930:Inuit / Q000706:statistics & numerical data*; D020738:Leptin / Q000097:blood; D008297:Male; D009765:Obesity / Q000150:complications
chemical_list: D054392:Adipokines; D020738:Leptin; D002097:C-Reactive Protein