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Higher chylomicron remnants and LDL particle numbers associate with CD36 SNPs and DNA methylation sites that reduce CD36
Washington Univ, Sch Med, Dept Med, Ctr Human Nutr, St Louis, MO 63110 USA..
Washington Univ, Sch Med, Dept Genet, Div Stat Genom, St Louis, MO 63110 USA..
McGill Univ, Dept Human Genet, Montreal, PQ H3A 0G1, Canada.;Genome Quebec Innovat Ctr, Montreal, PQ H3A 0G1, Canada..
Univ Alabama Birmingham, Dept Epidemiol, Birmingham, AL 35294 USA..
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2016 (English)In: Journal of Lipid Research, ISSN 0022-2275, E-ISSN 1539-7262, Vol. 57, no 12, p. 2176-2184Article in journal (Refereed) Published
Abstract [en]

Cluster of differentiation 36 (CD36) variants influence fasting lipids and risk of metabolic syndrome, but their impact on postprandial lipids, an independent risk factor for cardiovascular disease, is unclear. We determined the effects of SNPs within a approximate to 410 kb region encompassing CD36 and its proximal and distal promoters on chylomicron (CM) remnants and LDL particles at fasting and at 3.5 and 6 h following a high-fat meal (Genetics of Lipid Lowering Drugs and Diet Network study, n = 1,117). Five promoter variants associated with CMs, four with delayed TG clearance and five with LDL particle number. To assess mechanisms underlying the associations, we queried expression quantitative trait loci, DNA methylation, and ChIP-seq datasets for adipose and heart tissues that function in postprandial lipid clearance. Several SNPs that associated with higher serum lipids correlated with lower adipose and heart CD36 mRNA and aligned to active motifs for PPAR, a major CD36 regulator. The SNPs also associated with DNA methylation sites that related to reduced CD36 mRNA and higher serum lipids, but mixed-model analyses indicated that the SNPs and methylation independently influence CD36 mRNA. The findings support contributions of CD36 SNPs that reduce adipose and heart CD36 RNA expression to inter-individual variability of postprandial lipid metabolism and document changes in CD36 DNA methylation that influence both CD36 expression and lipids.

Place, publisher, year, edition, pages
2016. Vol. 57, no 12, p. 2176-2184
Keywords [en]
dietary lipids, lipoproteins, dyslipidemia, genetics, cholesterol, metabolism, cluster of differentiation 36, low density lipoprotein, single nucleotide polymorphism, deoxyribonucleic acid
National Category
Biochemistry and Molecular Biology
Identifiers
URN: urn:nbn:se:uu:diva-312651DOI: 10.1194/jlr.P065250ISI: 000389473000008OAI: oai:DiVA.org:uu-312651DiVA, id: diva2:1066955
Available from: 2017-01-19 Created: 2017-01-12 Last updated: 2017-11-29Bibliographically approved

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Molecular epidemiologyScience for Life Laboratory, SciLifeLab
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