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

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Abstract

BACKGROUND: 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. METHODS: 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. RESULTS: The cumulative 10-year incidence of type 2 diabetes was 17.5%. High concentrations of apo B, triglycerides, 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. CONCLUSIONS: 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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Ley, S. H., Harris, S. B., Connelly, P. W., Mamakeesick, M., Gittelsohn, J., Wolever, T. M., … Hanley, A. J. (2010). Association of apolipoprotein B with incident type 2 diabetes in an aboriginal Canadian population. Clinical Chemistry, 56(4), 666–670. https://doi.org/10.1373/clinchem.2009.136994

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