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Oxidized LDL autoantibodies are related to apolipoprotein E phenotype, independently of postprandial change in plasma triglycerides and LDL size, among patients with angiographically verified coronary artery disease and healthy controls

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Journal of Biomedical Science

Abstract

Objective: Oxidized low-density liporotein (LDL) autoantibodies (oxLDLab), apolipoprotein E (apoE) phenotype, postprandial triglyceride changes and LDL size are suggested to be risk factors for coronary artery disease (CAD). Our aim was to study the interaction between these new risk factors among patients with CAD and healthy controls.Methods: oxLDLab from 31 men with angiographically verified CAD and 31 healthy men were analyzed by enzyme-linked immunosorbent assay. Iso-electric focusing and immunoblotting were used for apoE phenotyping. Triglyceride level was measured after 12 h of fasting and 3, 5 and 7 h after a high-fat meal. Nondenaturing gradient gel electrophoresis was used to separate LDL particles according to size.Results: oxLDLab levels increased according to apoE phenotype in the following order: E2<E3<E4 (p=0.004, ANOVA). The postprandial response of triglycerides, the size of LDL particles and the concentration of LDL and high-density lipoprotein (HDL) cholesterol did not differ between apoE phenotypes, and the use of these variables as covariates did not change the statistically significant difference in oxLDLab levels between apoE phenotypes (p=0.01, ANCOVA). oxLDLab levels did not differ between the patient and control groups.Conclusion: We found an association between apoE allele ɛ2 and decreased levels of oxLDLab, which was independent of the postprandial response of triglycerides, the size of LDL particles and plasma LDL and HDL cholesterol levels. The mechanism by which apoE affects oxidation of LDL remains unknown.

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Metso, S., Nikkilä, M., Laippala, P. et al. Oxidized LDL autoantibodies are related to apolipoprotein E phenotype, independently of postprandial change in plasma triglycerides and LDL size, among patients with angiographically verified coronary artery disease and healthy controls. J Biomed Sci 10, 345–351 (2003). https://doi.org/10.1007/BF02256454

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