Evidence map›Paper›PMID 24504152›Full record

ArticleEpigenetics2014

Epipolymorphisms within lipoprotein genes contribute independently to plasma lipid levels in familial hypercholesterolemia.

Simon-Pierre Guay, Diane Brisson, Benoit Lamarche, Daniel Gaudet, Luigi Bouchard

Open access · bronzeAbstract read
In one paragraph

Article in Epigenetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 3 pooled it
8.8field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

34 citing papers in PubMed, 3 syntheses or guidelines pooled it, 73 citations in OpenAlex.

  1. Pooled it
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  7. Methylation status ofEpigenomics · 2024
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  20. A preliminary study of the association between theMolecular biology research communications · 2018
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 2 countries.

Simon-Pierre GuayDepartment of Biochemistry; Université de Sherbrooke; Sherbrooke, QC Canada; ECOGENE-21 and Lipid Clinic; Chicoutimi Hospital; Saguenay, QC Canada.
Diane BrissonECOGENE-21 and Lipid Clinic; Chicoutimi Hospital; Saguenay, QC Canada; Department of Medicine; Université de Montréal; Montréal, QC Canada.
Benoit LamarcheInstitute of Nutrition and Functional Foods; Université Laval; Québec, QC Canada.
Daniel GaudetECOGENE-21 and Lipid Clinic; Chicoutimi Hospital; Saguenay, QC Canada; Department of Medicine; Université de Montréal; Montréal, QC Canada.
Luigi BouchardDepartment of Biochemistry; Université de Sherbrooke; Sherbrooke, QC Canada; ECOGENE-21 and Lipid Clinic; Chicoutimi Hospital; Saguenay, QC Canada.
Cégep de Chicoutimi · CAUniversité de Sherbrooke · CAUniversité Laval · CA

Funding

Canadian Institutes of Health Research CTP-82941
6 · The paper itself

Abstract

Gene polymorphisms associated so far with plasma lipid concentrations explain only a fraction of their heritability, which can reach up to 60%. Recent studies suggest that epigenetic modifications (DNA methylation) could contribute to explain part of this missing heritability. We therefore assessed whether the DNA methylation of key lipoprotein metabolism genes is associated with high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C) and triglyceride levels in patients with familial hypercholesterolemia (FH). Untreated FH patients (61 men and 37 women) were recruited for the measurement of blood DNA methylation levels at the ABCG1, LIPC, PLTP and SCARB1 gene loci using bisulfite pyrosequencing. ABCG1, LIPC and PLTP DNA methylation was significantly associated with HDL-C, LDL-C and triglyceride levels in a sex-specific manner (all P<0.05). FH subjects with previous history of coronary artery disease (CAD) had higher LIPC DNA methylation levels compared with FH subjects without CAD (P = 0.02). Sex-specific multivariable linear regression models showed that new and previously reported epipolymorphisms (ABCG1-CpGC3, LIPC-CpGA2, mean PLTP-CpGC, LPL-CpGA3, CETP-CpGA2, and CETP-CpGB2) significantly contribute to variations in plasma lipid levels (all P<0.001 in men and P<0.02 in women), independently of traditional predictors such as age, waist circumference, blood pressure, fasting plasma lipids and glucose levels. These results suggest that epigenetic perturbations of key lipoprotein metabolism genes are associated with plasma lipid levels, contribute to the interindividual variability and might partially explain the missing heritability of plasma lipid levels, at least in FH.

Indexed as

Polymorphism, GeneticAdultATP-Binding Cassette TransportersATP Binding Cassette Transporter, Subfamily G, Member 1Cholesterol, HDLCholesterol, LDLCoronary Artery DiseaseCpG IslandsDNA MethylationEpigenesis, GeneticFemaleGenetic LociHumansHyperlipoproteinemia Type IILipaseLipoproteinsABCG1 protein, humanATP-Binding Cassette TransportersATP Binding Cassette Transporter, Subfamily G, Member 1Cholesterol, HDLCholesterol, LDLLipaseLIPC protein, humanLipoproteinsPhospholipid Transfer ProteinsPLTP protein, humanSCARB1 protein, humanScavenger Receptors, Class BTriglyceridescandidate genescoronary artery diseaseDNA methylationmissing heritabilityplasma lipid levels

Identifiers

PMID24504152
PMCPMC4063831
OpenAlexW1964011698

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.