Evidence map›Paper›PMID 20176858›Full record

ArticleJournal of lipid research2010

Gene-nutrient interactions with dietary fat modulate the association between genetic variation of the ACSL1 gene and metabolic syndrome.

Catherine M Phillips, Louisa Goumidi, Sandrine Bertrais, Martyn R Field, L Adrienne Cupples, Jose M Ordovas, Catherine Defoort, Julie A Lovegrove, Christian A Drevon, Michael J Gibney and 9 more

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 12% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 citations in OpenAlex.

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  16. Emerging roles of long non-coding RNAs in tumor metabolism.Journal of hematology & oncology · 2018
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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

19 authors at 12 institutions in 9 countries.

Catherine M PhillipsNutrigenomics Research Group, UCD School of Public Health and Population Science, UCD Conway Institute, and Institute of Food and Health, University College Dublin, Ireland.
Louisa Goumidi
Sandrine Bertrais
Martyn R Field
L Adrienne Cupples
Jose M Ordovas
Catherine Defoort
Julie A Lovegrove
Christian A Drevon
Michael J Gibney
Ellen E Blaak
Beata Kiec-Wilk
Britta Karlstrom
Jose Lopez-Miranda
Ross McManus
Serge Hercberg
Denis Lairon
Richard Planells
Helen M Roche
Inserm · FRUniversity College Dublin · IEConservatoire National des Arts et Métiers · FRBoston University · USJagiellonian University · PLMaastricht University · NLTrinity College Dublin · IETufts University · USUniversity of Córdoba · ESUniversity of Oslo · NOUniversity of Reading · GBUppsala University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long-chain acyl CoA synthetase 1 (ACSL1) plays an important role in fatty acid metabolism and triacylglycerol (TAG) synthesis. Disturbance of these pathways may result in dyslipidemia and insulin resistance, hallmarks of the metabolic syndrome (MetS). Dietary fat is a key environmental factor that may interact with genetic determinants of lipid metabolism to affect MetS risk. We investigated the relationship between ACSL1 polymorphisms (rs4862417, rs6552828, rs13120078, rs9997745, and rs12503643) and MetS risk and determined potential interactions with dietary fat in the LIPGENE-SU.VI.MAX study of MetS cases and matched controls (n = 1,754). GG homozygotes for rs9997745 had increased MetS risk {odds ratio (OR) 1.90 [confidence interval (CI) 1.15, 3.13]; P = 0.01}, displayed elevated fasting glucose (P = 0.001) and insulin concentrations (P = 0.002) and increased insulin resistance (P = 0.03) relative to the A allele carriers. MetS risk was modulated by dietary fat, whereby the risk conferred by GG homozygosity was abolished among individuals consuming either a low-fat (<35% energy) or a high-PUFA diet (>5.5% energy). In conclusion, ACSL1 rs9997745 influences MetS risk, most likely via disturbances in fatty acid metabolism, which was modulated by dietary fat consumption, particularly PUFA intake, suggesting novel gene-nutrient interactions.

Indexed as

FoodGenetic VariationAdultBiomarkersCoenzyme A LigasesDietary FatsFatty AcidsFemaleGenetic Predisposition to DiseaseGenotypeHaplotypesHumansInsulin ResistanceIsoenzymesLong-Chain-Fatty-Acid-CoA LigaseMaleBiomarkersCoenzyme A LigasesDietary FatsFatty AcidsIsoenzymesLong-Chain-Fatty-Acid-CoA Ligase

Identifiers

PMID20176858
PMCPMC2882737
OpenAlexW2151802038

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.