Polymorphisms in APOA1 and LPL genes are statistically independently associated with fasting TG in men with CAD
Open Access
- 19 January 2005
- journal article
- research article
- Published by Springer Nature in European Journal of Human Genetics
- Vol. 13 (4) , 445-451
- https://doi.org/10.1038/sj.ejhg.5201362
Abstract
The objective of this paper was to identify the single nucleotide polymorphisms (SNPs) that show unshared effects on plasma triglyceride (TG) levels and to investigate whether these SNPs show statistically independent effects on plasma TG levels. In total, 59 polymorphisms in 20 genes involved in lipid metabolism were investigated. Polymorphisms were selected for a multivariate ANOVA model if they showed an univariate association with TG (after adjustment for HDL-C and LDL-C) in more than 50% of bootstrap samples that were made from the original data. The multivariate model included 512 men with coronary artery disease from the REGRESS study who were completely genotyped for eight polymorphisms selected in the univariate procedure (ie, APOA1 G(−75)A, ABCA1 C(−477)T, ABCA1 G1051A, APOC3 T3206G, APOE Arg158Cys, LIPC C(−514)T, LPL Asn291Ser and LPL Ser447Stop). The gene variants APOA1 G(−75)A (P=0.04) and LPL Asn291Ser (P=0.03) were significantly associated with plasma TG levels in this multivariate analysis. The eight polymorphisms explained 8.9% of the variation in plasma TG levels. In conclusion, this study showed statistically independent effects of gene variants in the APOA1 and LPL genes on fasting plasma levels of TG. Nevertheless, only a small part of variation in TG levels could be explained by the polymorphisms.Keywords
This publication has 46 references indexed in Scilit:
- Effects of covariates: A summary of Group 5 contributionsGenetic Epidemiology, 2003
- Cholesteryl Ester Transfer ProteinArteriosclerosis, Thrombosis, and Vascular Biology, 2003
- Lipoprotein lipase: structure, function, regulation, and role in diseaseJournal of Molecular Medicine, 2002
- Relative contribution of variation within the APOC3/A4/A5 gene cluster in determining plasma triglyceridesHuman Molecular Genetics, 2002
- Power to Localize the Major Gene for Disease Liability Is Increased After Accounting for the Effects of Related Quantitative PhenotypesGenetic Epidemiology, 2001
- Evidence that triglycerides are an independent coronary heart disease risk factorThe American Journal of Cardiology, 2000
- Dissecting the Genetic Architecture of Lipids, Lipoproteins, and ApolipoproteinsArteriosclerosis, Thrombosis, and Vascular Biology, 1999
- Two common mutations (D9N, N291S) in lipoprotein lipase: a cumulative analysis of their influence on plasma lipids and lipoproteins in men and womenClinical Genetics, 1999
- Lipoprotein Lipase Mutations, Plasma Lipids and Lipoproteins, and Risk of Ischemic Heart DiseaseCirculation, 1999
- Effects of Lipid Lowering by Pravastatin on Progression and Regression of Coronary Artery Disease in Symptomatic Men With Normal to Moderately Elevated Serum Cholesterol LevelsCirculation, 1995