Adipokines and Incident Type 2 Diabetes in an Aboriginal Canadian Population: The Sandy Lake Health and Diabetes Project

  1. Sylvia H. Ley, RD1,
  2. Stewart B. Harris, MD2,
  3. Philip W. Connelly, PHD3,,4,
  4. Mary Mamakeesick, RPN5,
  5. Joel Gittelsohn, PHD6,
  6. Robert A. Hegele, MD7,
  7. Ravi Retnakaran, MD8,,9,
  8. Bernard Zinman, MD8,,9,,10 and
  9. Anthony J.G. Hanley, PHD (anthony.hanley{at}utoronto.ca)1,,8,,9
  1. 1Department of Nutritional Sciences, University of Toronto, Toronto, Ontario, Canada
  2. 2Center for Studies in Family Medicine, Schulich School of Medicine and Dentistry, University of Western Ontario, London, Ontario, Canada
  3. 3Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada
  4. 4Keenan Research Centre of the Li Ka Shing Knowledge Institute, St. Michael's Hospital, Toronto, Ontario, Canada
  5. 5Sandy Lake Health and Diabetes Project, Sandy Lake, Ontario, Canada
  6. 6Center for Human Nutrition, Johns Hopkins Bloomberg School of Public Health, Baltimore,
  7. 7Robarts Research Institute and University of Western Ontario, London, Ontario, Canada
  8. 8Division of Endocrinology, University of Toronto, Toronto, Ontario, Canada
  9. 9Leadership Sinai Centre for Diabetes, Mount Sinai Hospital, Toronto, Canada
  10. 10Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Canada

    Abstract

    Objective: The aim of this study was to investigate associations of adiponectin, leptin, C-reactive protein (CRP), interleukin 6 (IL-6), and serum amyloid A (SAA), individually or in combinations, with risk of incident type 2 diabetes in an Aboriginal Canadian population.

    Research Design and 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 ≥7.0 mmol/l or 2-h postload plasma glucose ≥11.1 mmol/l at follow-up.

    Results: Low adiponectin, high leptin and the low adiponectin-to-leptin ratio at baseline were associated with increased risk of incident type 2 diabetes after adjustment for age, sex, triglyceride, HDL cholesterol, hypertension, and impaired glucose tolerance (odds ratio [OR] 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 (OR 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.

    Footnotes

      • Received January 7, 2008.
      • Accepted February 23, 2008.