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Journal of Lipid Research, Vol. 47, 2064-2070, September 2006
Copyright © 2006 by American Society for Biochemistry and Molecular Biology
* Department of Vascular Medicine, Academic Medical Center, Amsterdam, The Netherlands
Department of Clinical Epidemiology and Biostatistics, Academic Medical Center, Amsterdam, The Netherlands
** Department of Cardiology, Academic Medical Center, Amsterdam, The Netherlands
The Liver Center, Academic Medical Center, Amsterdam, The Netherlands
Department of Advanced Medical Technology and Development, BML, Inc., Saitama, Japan
Institute of Public Health and Primary Care, Institute of Public Health, University of Cambridge, Cambridge, UK
*** Medical Research Council Dunn Nutrition Unit, Cambridge, UK
Department of Medicine, Rayne Institute, University College Medical School, London, UK
Medical Research Council Epidemiology Unit, Cambridge, UK
Published, JLR Papers in Press, June 12, 2006.
1 S. F. C. Vaessen and F. G. Schaap contributed equally to this study.
2 To whom correspondence should be addressed. e-mail: j.a.kuivenhoven{at}amc.uva.nl
In mouse models, apolipoprotein A-V (apoA-V) exhibits triglyceride (TG)-lowering effects. We investigated the apoA-V/TG relationship and the association of apoA-V with coronary artery disease (CAD) risk by determining serum apoA-V levels and genotypes in a nested case-control (n = 1,034/2,031) study. Both univariate and multivariate apoA-V levels showed no association with future CAD (P = 0.4 and 0.5, respectively). Unexpectedly, there was a significant positive correlation between serum apoA-V and TG in men and women (r = 0.36 and 0.28, respectively, P < 0.001 each) but a negative correlation between apoA-V and LPL mass (r = –0.14 and –0.12 for men and women respectively, P < 0.001 each). The frequency of the c.56C>G polymorphism did not differ between cases and controls despite significant positive association of c.56G with both apoA-V and TG levels. For –1131T>C, the minor allele was significantly associated with lower apoA-V yet higher TG levels and was overrepresented in cases (P = 0.047). The association of –1131T>C with CAD risk, however, was independent of apoA-V levels and likely acts through linkage disequilibrium with APOC3 variants. The positive correlation of apoA-V levels with TG levels, negative correlation with LPL levels, and lack of association with CAD risk highlight the need for further human studies to clarify the role of apoA-V.
Supplementary key words single nucleotide polymorphism • European Prospective Investigation into Cancer and Nutrition • epidemiology
Abbreviations: apoA-V, apolipoprotein A-V; BMI, body mass index; CAD, coronary artery disease; CI, confidence interval; EPIC, European Prospective Investigation into Cancer and Nutrition; OR, odds ratio; SNP, single nucleotide polymorphism; TG, triglyceride
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