Lipoprotein lipase gene polymorphism and lipid profile in coronary artery disease.

Abstract

Lipoprotein lipase (LPL) plays a central role in lipid metabolism, hydrolyzing triglyceride in chylomicrons and very-low-density lipoproteins. The PvuII polymorphic variant of LPL gene is common and might affect risk of coronary artery disease (CAD). Our aim was to determine whether LPL- PvuII polymorphism can be considered to be an independent risk factor or a predictor for CAD in Turkish subjects. We used polymerase chain reaction and restriction enzyme digestion to determine the distribution of the previously described C-->T transition that causes a PvuII polymorphism in intron 6 among healthy blood donors of Turkish origin and among angiographically confirmed CAD patients with comparable ethnic backgrounds. For the PvuII genotypes, within the CAD group (n = 80), the +/- genotype was found in 39 individuals (48.8%), whereas 25 (31.3%) carried the +/+ genotype, and 14 (17.5%) carried the -/- genotype. Within the control group (n = 49), the -/- genotype was found in 19 individuals (38.8%), 16 (32.7%) carried the +/- genotype, and 14 (28.6%) carried the +/+ genotype. The genotype frequency distribution was significantly different (P =.049) in the CAD and control study groups. The most frequent genotype among CAD patients was +/-; this genotype was more frequent in patients than in control subjects. However, the -/- genotype was more prevalent in the control group. Lipoprotein lipase-PvuII polymorphism was found to be associated with fasting total cholesterol and low-density lipoprotein cholesterol levels. The +/+ genotype was found to have higher levels of total cholesterol and low-density lipoprotein cholesterol in both the CAD and control groups. There was a difference in the distribution of LPL-PvuII genotypes between the healthy subjects and the patients with CAD. Lipoprotein lipase-PvuII polymorphisms were not detected as independent risk factors for CAD in this study group, but had associations with lipid levels.