Evidence map›Paper›PMID 20855566›Full record

ArticleJournal of lipid research2010

ACC2 gene polymorphisms, metabolic syndrome, and gene-nutrient interactions with dietary fat.

Catherine M Phillips, Louisa Goumidi, Sandrine Bertrais, Martyn R Field, L Adrienne Cupples, Jose M Ordovas, Jolene McMonagle, Catherine Defoort, Julie A Lovegrove, Christian A Drevon 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 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

16 citing papers in PubMed, 35 citations in OpenAlex.

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  13. Structure and function of biotin-dependent carboxylases.Cellular and molecular life sciences : CMLS · 2013
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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 13 institutions in 9 countries.

Catherine M PhillipsNutrigenomics Research Group, UCD School of Public Health and Population Science, UCD Conway Institute, University College Dublin, Dublin, Ireland.
Louisa Goumidi
Sandrine Bertrais
Martyn R Field
L Adrienne Cupples
Jose M Ordovas
Jolene McMonagle
Catherine Defoort
Julie A Lovegrove
Christian A Drevon
Ellen E Blaak
Beata Kiec-Wilk
Ulf Riserus
Jose Lopez-Miranda
Ross McManus
Serge Hercberg
Denis Lairon
Richard Planells
Helen M Roche
Inserm · FRUniversity College Dublin · IEBoston University · USEquipe de Recherche en Epidémiologie Nutritionnelle · FRInstitut de Neurobiologie de la Méditerranée · FRInstituto Maimónides de Investigación Biomédica de Córdoba · ESJagiellonian University · PLJean Mayer Human Nutrition Research Center on Aging · USMaastricht University · NLTrinity College Dublin · IEUniversity of Oslo · NOUniversity of Reading · GBUppsala University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acetyl-CoA carboxylase β (ACC2) plays a key role in fatty acid synthesis and oxidation pathways. Disturbance of these pathways is associated with impaired insulin responsiveness and metabolic syndrome (MetS). Gene-nutrient interactions may affect MetS risk. This study determined the relationship between ACC2 polymorphisms (rs2075263, rs2268387, rs2284685, rs2284689, rs2300453, rs3742023, rs3742026, rs4766587, and rs6606697) and MetS risk, and whether dietary fatty acids modulate this in the LIPGENE-SU.VI.MAX study of MetS cases and matched controls (n = 1754). Minor A allele carriers of rs4766587 had increased MetS risk (OR 1.29 [CI 1.08, 1.58], P = 0.0064) compared with the GG homozygotes, which may in part be explained by their increased body mass index (BMI), abdominal obesity, and impaired insulin sensitivity (P < 0.05). MetS risk was modulated by dietary fat intake (P = 0.04 for gene-nutrient interaction), where risk conferred by the A allele was exacerbated among individuals with a high-fat intake (>35% energy) (OR 1.62 [CI 1.05, 2.50], P = 0.027), particularly a high intake (>5.5% energy) of n-6 polyunsaturated fat (PUFA) (OR 1.82 [CI 1.14, 2.94], P = 0.01; P = 0.05 for gene-nutrient interaction). Saturated and monounsaturated fat intake did not modulate MetS risk. Importantly, we replicated some of these findings in an independent cohort. In conclusion, the ACC2 rs4766587 polymorphism influences MetS risk, which was modulated by dietary fat, suggesting novel gene-nutrient interactions.

Indexed as

Polymorphism, GeneticAcetyl-CoA CarboxylaseAllelesBody Mass IndexDietary FatsFatty AcidsFatty Acids, UnsaturatedGenotypeHumansInsulin ResistanceMetabolic SyndromeObesity, AbdominalRisk FactorsAcetyl-CoA CarboxylaseDietary FatsFatty AcidsFatty Acids, Unsaturated

Identifiers

PMID20855566
PMCPMC2975722
OpenAlexW2159009886

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.