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image/svg+xml Jakob Voss, based on art designer at PLoS, modified by Wikipedia users Nina and Beao Closed Access logo, derived from PLoS Open Access logo. This version with transparent background. http://commons.wikimedia.org/wiki/File:Closed_Access_logo_transparent.svg Jakob Voss, based on art designer at PLoS, modified by Wikipedia users Nina and Beao
Clinical Genetics
Article . 2006 . Peer-reviewed
License: Wiley Online Library User Agreement
Data sources: Crossref
Clinical Genetics
Article . 2006
Data sources: Pure Amsterdam UMC
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Common variants of multiple genes that control reverse cholesterol transport together explain only a minor part of the variation of HDL cholesterol levels

Authors: Boekholdt, S. M.; Souverein, O. W.; Tanck, M. W. T.; Hovingh, G. K.; Kuivenhoven, J. A.; Peters, R. I. G.; Jansen, H.; +7 Authors

Common variants of multiple genes that control reverse cholesterol transport together explain only a minor part of the variation of HDL cholesterol levels

Abstract

It is assumed that the combined effects of multiple common genetic variants explain a large part of variation of high‐density lipoprotein cholesterol (HDL‐C) plasma levels, but little evidence exists to corroborate this assumption. It was our objective to study the contribution of multiple common genetic variants of HDL‐C‐related genes to variation of HDL‐C plasma levels. A well‐characterized cohort of 546 Caucasian men with documented coronary artery disease was genotyped for common functional variants in genes that control reverse cholesterol transport: ATP‐binding cassette transporter A1, apolipoprotein A‐I and apolipoprotein‐E, cholesteryl ester transfer protein, hepatic lipase, lecithin : cholesterol‐acyl transferase, lipoprotein lipase, and scavenger receptor class B type 1. Multivariate linear regression showed that these variants, in conjunction, explain 12.4% (95% confidence interval: 6.9–17.9%) of variation in HDL‐C plasma levels. When the covariates smoking and body mass index were taken into account, the explained variation increased to 15.3% (9.4–21.2%), and when 10 two‐way interactions were incorporated, this percentage rose to 25.2% (18.9–31.5%). This study supports the hypothesis that multiple, mildly penetrant, but highly prevalent genetic variants explain part of the variation of HDL‐C plasma levels, albeit to a very modest extent. Multiple environmental and genetic influences on HDL‐C plasma levels still have to be elucidated.

Country
Netherlands
Keywords

Male, HDL, Scavenger Receptors, Genotype, Active, EMC COEUR-01-43-01, Biological Transport, Active, Coronary Artery Disease, Phosphatidylcholine-Sterol O-Acyltransferase, Cohort Studies, Apolipoproteins E, Models, Humans, Alleles, Glycoproteins, Apolipoprotein A-I, Cholesterol, HDL, Genetic Variation, Biological Transport, Lipase, Middle Aged, Biological, Cholesterol Ester Transfer Proteins, Lipoprotein Lipase, Cholesterol, ATP-Binding Cassette Transporters, Class B, Carrier Proteins, ATP Binding Cassette Transporter 1

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citations
This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Citations provided by BIP!
popularity
This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.
BIP!Popularity provided by BIP!
influence
This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).
BIP!Influence provided by BIP!
impulse
This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.
BIP!Impulse provided by BIP!
42
Average
Top 10%
Top 10%