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Clin Chem. 2010 Apr;56(4):666-70. doi: 10.1373/clinchem.2009.136994. Epub 2010 Jan 28.

Association of apolipoprotein B with incident type 2 diabetes in an aboriginal Canadian population.

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Department of Nutritional Sciences, University of Toronto, Toronto, Ontario, Canada.



Expanding evidence indicates that apolipoprotein B (apo B) is superior to LDL cholesterol as a marker of vascular disease. Although traditional lipid measures are known to predict type 2 diabetes, limited data are available regarding apo B. We assessed the association of apo B with incident type 2 diabetes and compared it with traditional lipid variables as a risk predictor in aboriginal Canadians.


Of an initial cohort of 606 individuals without diabetes in 1993-1995, 540 were contacted for the 10-year follow-up evaluation in 2003-2005. Fasting and 2-h postload glucose concentrations were obtained at baseline and follow-up to determine incident type 2 diabetes. Baseline fasting serum lipids were measured with standard laboratory procedures.


The cumulative 10-year incidence of type 2 diabetes was 17.5%. High concentrations of apo B, triglycerides, and LDL cholesterol, and low concentrations of HDL cholesterol were individually associated with incident type 2 diabetes in univariate analyses. Comparing C statistics of univariate models showed apo B to be a superior determinant of incident diabetes compared with LDL (P = 0.026) or HDL (P = 0.004) cholesterol. With multivariate adjustment including waist circumference, apo B (odds ratio, 1.50; 95% CI, 1.11-2.02) and triglycerides (odds ratio, 1.49; 95% CI, 1.12-1.98) remained associated with incident diabetes, whereas LDL and HDL cholesterol became nonsignificant.


The association of plasma apo B with incident type 2 diabetes and its better prediction of risk compared with LDL or HDL cholesterol suggest the potential for the use of apo B in type 2 diabetes risk communication and prevention.

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Conflict of interest statement

Authors’ Disclosures of Potential Conflicts of Interest: Upon manuscript submission, all authors completed the Disclosures of Potential Conflict of Interest form. Potential conflicts of interest: Employment or Leadership: None declared. Consultant or Advisory Role: None declared. Stock Ownership: None declared. Honoraria: None declared. Research Funding: This work was supported by grants from the Canadian Institutes of Health Research (CIHR). S.H. Ley, CIHR Frederick Banting and Charles Best Canada Graduate Scholarship; S.B. Harris, the Canadian Diabetes Association (CDA) Chair in Diabetes Management and the Ian McWhinney Chair in Family Medicine at the University of Western Ontario; R.A. Hegele, the Edith Schulich Vinet Canada Research Chair (Tier I) in Human Genetics, the Martha Blackburn Chair in Cardiovascular Genetics, and the Jacob J. Wolfe Distinguished Medical Research Chair at the University of Western Ontario; B. Zinman, the Sam and Judy Pencer Family Chair in Diabetes Research at Mount Sinai Hospital and University of Toronto; A.J. Hanley, CIHR Canada Research Chair in the Epidemiology of Type 2 Diabetes and Ontario Ministry of Research and Innovation Early Researcher Award. Expert Testimony: None declared.

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