Apolipoprotein L-I is positively associated with hyperglycemia and plasma triglycerides in CAD patients with low HDL

Timothy S.E. Albert, Philippe N. Duchateau, Samir S. Deeb, Clive R. Pullinger, Min H. Cho, David C. Heilbron, Mary J. Malloy, John P. Kane, and B. Greg Brown

Medicine, Duke University Medical Center, Durham, NC 27710

Corresponding Author: alber016{at}mc.duke.edu

Apolipoprotein L-I (apol-I) is present on a subset of HDL particles and is positively correlated with plasma triglycerides (TG). We measured plasma apoL-I levels in CAD subjects with low HDL who were enrolled in an angiographic, CAD prevention trial. At baseline, apoL-I levels (n=136, range: 2.2-64.1 $mu$ g/ml) were right skewed with a large degree of variability. Mutlivariate analysis for biological determinants of apoL-I revealed that the log of VLDL-TG (+0.17, P < 0.05) and hyperglycemia (+0.26, P < 0.005) independently predicted apoL-I level. Hyperglycemic patients (n = 24) had mean apoL-I levels >50% higher than normoglycemics (n = 112) (13.2 vs. 8.3 $mu$ g/ml, respectively, P < 0.001). No relationship between apoL-I level and change in CAD was found (r = 0.06, P = 0.49). Simvastatin-niacin therapy did not alter apoL-I levels (n = 34, P = 0.27), whereas antioxidant vitamins alone increased apoL-I by >50% (n = 36, P < 0.01). Genotyping of a known apoL-I polymorphism (Lys166Glu) did not independently account for any of the variability in apoL-I levels. In conclusion, we found TG and hyperglycemia to be the strongest predictors of apoL-I within a dyslipidemic CAD population. These data provide further characterization of the novel HDL associated apolipoprotein L-I.

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