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Published online March 13, 2008
Diabetes Care 31:1410-1415, 2008
DOI: 10.2337/dc08-0036
© 2008 by the American Diabetes Association
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Cardiovascular and Metabolic Risk
Original Research

Adipokines and Incident Type 2 Diabetes in an Aboriginal Canadian Population

The Sandy Lake Health and Diabetes Project

Sylvia H. Ley, RD1, Stewart B. Harris, MD2, Philip W. Connelly, PHD3,4, Mary Mamakeesick, RPN5, Joel Gittelsohn, PHD6, Robert A. Hegele, MD7, Ravi Retnakaran, MD8,9, Bernard Zinman, MD8,9,10 and Anthony J.G. Hanley, PHD1,8,9

1 Department of Nutritional Sciences, University of Toronto, Toronto, Ontario, Canada
2 Center for Studies in Family Medicine, Schulich School of Medicine and Dentistry, University of Western Ontario, London, Ontario, Canada
3 Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada
4 Keenan Research Centre of the Li Ka Shing Knowledge Institute, St. Michael's Hospital, Toronto, Ontario, Canada
5 Sandy Lake Health and Diabetes Project, Sandy Lake, Ontario, Canada
6 Center for Human Nutrition, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland
7 Robarts Research Institute and University of Western Ontario, London, Ontario, Canada
8 Division of Endocrinology, University of Toronto, Toronto, Ontario, Canada
9 Leadership Sinai Centre for Diabetes, Mount Sinai Hospital, Toronto, Ontario, Canada
10 Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada

Corresponding author: Anthony J.G. Hanley, anthony.hanley{at}utoronto.ca

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 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 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.


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