Evidence map›Paper›PMID 25225679›Full record

ArticleJournal of lipid research2014

Adiposity significantly modifies genetic risk for dyslipidemia.

Christopher B Cole, Majid Nikpay, Paulina Lau, Alexandre F R Stewart, Robert W Davies, George A Wells, Robert Dent, Ruth McPherson

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

23 citing papers in PubMed, 36 citations in OpenAlex.

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  14. Genetic Markers for Coronary Artery Disease.Medicina (Kaunas, Lithuania) · 2018
    Review
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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

8 authors at 2 institutions in 1 country.

Christopher B ColeAtherogenomics Laboratory, University of Ottawa Heart Institute, Ottawa, Canada Ruddy Cardiovascular Genetics Centre, University of Ottawa Heart Institute, Ottawa, Canada.
Majid NikpayAtherogenomics Laboratory, University of Ottawa Heart Institute, Ottawa, Canada Ruddy Cardiovascular Genetics Centre, University of Ottawa Heart Institute, Ottawa, Canada.
Paulina LauAtherogenomics Laboratory, University of Ottawa Heart Institute, Ottawa, Canada Ruddy Cardiovascular Genetics Centre, University of Ottawa Heart Institute, Ottawa, Canada.
Alexandre F R StewartRuddy Cardiovascular Genetics Centre, University of Ottawa Heart Institute, Ottawa, Canada.
Robert W DaviesCardiovascular Research Methods Centre, University of Ottawa Heart Institute, Ottawa, Canada.
George A WellsCardiovascular Research Methods Centre, University of Ottawa Heart Institute, Ottawa, Canada.
Robert DentBariatric Centre of Excellence, Ottawa Hospital, Ottawa, Canada.
Ruth McPhersonAtherogenomics Laboratory, University of Ottawa Heart Institute, Ottawa, Canada Ruddy Cardiovascular Genetics Centre, University of Ottawa Heart Institute, Ottawa, Canada.
University of Ottawa · CAOttawa Hospital · CA

Funding

Canadian Institutes of Health Research MOP2390941Canadian Institutes of Health Research OPB134211
6 · The paper itself

Abstract

Recent genome-wide association studies have identified multiple loci robustly associated with plasma lipids, which also contribute to extreme lipid phenotypes. However, these common genetic variants explain <12% of variation in lipid traits. Adiposity is also an important determinant of plasma lipoproteins, particularly plasma TGs and HDL cholesterol (HDLc) concentrations. Thus, interactions between genes and clinical phenotypes may contribute to this unexplained heritability. We have applied a weighted genetic risk score (GRS) for both plasma TGs and HDLc in two large cohorts at the extremes of BMI. Both BMI and GRS were strongly associated with these lipid traits. A significant interaction between obese/lean status and GRS was noted for each of TG (P(Interaction) = 2.87 × 10(-4)) and HDLc (P(Interaction) = 1.05 × 10(-3)). These interactions were largely driven by SNPs tagging APOA5, glucokinase receptor (GCKR), and LPL for TG, and cholesteryl ester transfer protein (CETP), GalNAc-transferase (GALNT2), endothelial lipase (LIPG), and phospholipid transfer protein (PLTP) for HDLc. In contrast, the GRSLDL cholesterol × adiposity interaction was not significant. Sexual dimorphism was evident for the GRSHDL on HDLc in obese (P(Interaction) = 0.016) but not lean subjects. SNP by BMI interactions may provide biological insight into specific genetic associations and missing heritability.

Indexed as

AdiposityGenetic Predisposition to DiseaseAgedBody Mass IndexCholesterol, HDLDyslipidemiasFemaleGenome-Wide Association StudyHumansMaleMiddle AgedPolymorphism, Single NucleotideTriglyceridesCholesterol, HDLTriglyceridesgenetic risk scorelipoproteinsobesitysingle nucleotide polymorphismstatistical interaction

Identifiers

PMID25225679
PMCPMC4617143
OpenAlexW2158984209

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.