Evidence map›Paper›PMID 21708048›Full record

ArticleBMC medical genomics2011

Genome wide association study identifies KCNMA1 contributing to human obesity.

Hong Jiao, Peter Arner, Johan Hoffstedt, David Brodin, Beatrice Dubern, Sébastien Czernichow, Ferdinand van't Hooft, Tomas Axelsson, Oluf Pedersen, Torben Hansen and 7 more

Open access · goldAbstract read
In one paragraph

Article in BMC medical genomics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 5 pooled it
19.1field-weighted citation impact, top 1% 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

51 citing papers in PubMed, 5 syntheses or guidelines pooled it, 181 citations in OpenAlex.

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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

17 authors at 9 institutions in 4 countries.

Hong JiaoDepartment of Biosciences and Nutrition, Karolinska Institutet, SE-141 83 Huddinge, Sweden. hong.jiao@ki.se
Peter Arner
Johan Hoffstedt
David Brodin
Beatrice Dubern
Sébastien Czernichow
Ferdinand van't Hooft
Tomas Axelsson
Oluf Pedersen
Torben Hansen
Thorkild I A Sørensen
Johannes Hebebrand
Juha Kere
Karin Dahlman-Wright
Anders Hamsten
Karine Clement
Ingrid Dahlman
Karolinska Institutet · SEKarolinska University Hospital · SEUniversity of Copenhagen · DKAssistance Publique – Hôpitaux de Paris · FRConservatoire National des Arts et Métiers · FRCopenhagen University Hospital · DKPitié-Salpêtrière Hospital · FRUniversity of Duisburg-Essen · DEUppsala University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRecent genome-wide association (GWA) analyses have identified common single nucleotide polymorphisms (SNPs) that are associated with obesity. However, the reported genetic variation in obesity explains only a minor fraction of the total genetic variation expected to be present in the population. Thus many genetic variants controlling obesity remain to be identified. The aim of this study was to use GWA followed by multiple stepwise validations to identify additional genes associated with obesity.

methodsWe performed a GWA analysis in 164 morbidly obese subjects (BMI:body mass index>40 kg/m2) and 163 Swedish subjects (>45 years) who had always been lean. The 700 SNPs displaying the strongest association with obesity in the GWA were analyzed in a second cohort comprising 460 morbidly obese subjects and 247 consistently lean Swedish adults. 23 SNPs remained significantly associated with obesity (nominal P<0.05) and were in a step-wise manner followed up in five additional cohorts from Sweden, France, and Germany together comprising 4214 obese and 5417 lean or population-based control individuals. Three samples, n=4133, were used to investigate the population-based associations with BMI. Gene expression in abdominal subcutaneous adipose tissue in relation to obesity was investigated for14 adults.

resultsPotassium channel, calcium activated, large conductance, subfamily M, alpha member (KCNMA1) rs2116830*G and BDNF rs988712*G were associated with obesity in five of six investigated case-control cohorts. In meta-analysis of 4838 obese and 5827 control subjects we obtained genome-wide significant allelic association with obesity for KCNMA1 rs2116830*G with P=2.82×10(-10) and an odds ratio (OR) based on cases vs controls of 1.26 [95% C.I. 1.12-1.41] and for BDNF rs988712*G with P=5.2×10(-17) and an OR of 1.36 [95% C.I. 1.20-1.55]. KCNMA1 rs2116830*G was not associated with BMI in the population-based samples. Adipose tissue (P=0.0001) and fat cell (P=0.04) expression of KCNMA1 was increased in obesity.

conclusionsWe have identified KCNMA1 as a new susceptibility locus for obesity, and confirmed the association of the BDNF locus at the genome-wide significant level.

Indexed as

Genome, HumanAllelesBody Mass IndexCase-Control StudiesCohort StudiesFemaleFranceGenetic Predisposition to DiseaseGenome-Wide Association StudyGermanyHumansLarge-Conductance Calcium-Activated Potassium Channel alpha SubunitsMaleMiddle AgedObesity, MorbidPolymorphism, Single NucleotideKCNMA1 protein, humanLarge-Conductance Calcium-Activated Potassium Channel alpha Subunits

Identifiers

PMID21708048
PMCPMC3148553
OpenAlexW2126992918

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.