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, PHD34,
- Mary Mamakeesick, RPN5,
- Joel Gittelsohn, PHD6,
- Robert A. Hegele, MD7,
- Ravi Retnakaran, MD89,
- Bernard Zinman, MD8910 and
- Anthony J.G. Hanley, PHD189
- 1Department of Nutritional Sciences, University of Toronto, Toronto, Ontario, Canada
- 2Center for Studies in Family Medicine, Schulich School of Medicine and Dentistry, University of Western Ontario, London, Ontario, Canada
- 3Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada
- 4Keenan Research Centre of the Li Ka Shing Knowledge Institute, St. Michael's Hospital, Toronto, Ontario, Canada
- 5Sandy Lake Health and Diabetes Project, Sandy Lake, Ontario, Canada
- 6Center for Human Nutrition, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland
- 7Robarts Research Institute and University of Western Ontario, London, Ontario, Canada
- 8Division of Endocrinology, University of Toronto, Toronto, Ontario, Canada
- 9Leadership Sinai Centre for Diabetes, Mount Sinai Hospital, Toronto, Ontario, Canada
- 10Samuel Lunenfeld Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada
- Corresponding author: Anthony J.G. Hanley, anthony.hanley{at}utoronto.ca
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 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.
Footnotes
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Published ahead of print at http://care.diabetesjournals.org on 20 March 2008.
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- Accepted February 23, 2008.
- Received January 7, 2008.
- DIABETES CARE
