Evidence map›Paper›PMID 19847392›Full record

ArticleDiabetologia2010

Genetic association analysis of LARS2 with type 2 diabetes.

E Reiling, B Jafar-Mohammadi, E van 't Riet, M N Weedon, J V van Vliet-Ostaptchouk, T Hansen, R Saxena, T W van Haeften, P A Arp, S Das and 21 more

Open access · hybridAbstract read
In one paragraph

Article in Diabetologia, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.0field-weighted citation impact, top 20% 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

4 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. 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

31 authors at 15 institutions in 6 countries.

E ReilingDepartment of Molecular Cell Biology, Leiden University Medical Center (LUMC), 2300RC Leiden, the Netherlands.
B Jafar-Mohammadi
E van 't Riet
M N Weedon
J V van Vliet-Ostaptchouk
T Hansen
R Saxena
T W van Haeften
P A Arp
S Das
G Nijpels
M J Groenewoud
E C van Hove
A G Uitterlinden
J W A Smit
A D Morris
A S F Doney
C N A Palmer
C Guiducci
A T Hattersley
T M Frayling
O Pedersen
P E Slagboom
D M Altshuler
L Groop
J A Romijn
J A Maassen
M H Hofker
J M Dekker
M I McCarthy
L M 't Hart
Leiden University Medical Center · NLNinewells Hospital · GBPeninsula College of Medicine and Dentistry · GBEMGO Institute for Health and Care Research · NLErasmus MC · NLHarvard University · USNational Institute for Health Research · GBUniversity Medical Center Groningen · NLAmsterdam UMC Location VUmc · NLBroad Institute · USSteno Diabetes Center · DKUniversity Medical Center Utrecht · NLUniversity of Copenhagen · DKUniversity of Helsinki · FIUniversity of Oxford · GB

Funding

Medical Research Council G0000934Medical Research Council G0601261Wellcome TrustWellcome Trust 068545/Z/02Wellcome Trust 076113Wellcome Trust GR072960
6 · The paper itself

Abstract

aims/hypothesisLARS2 has been previously identified as a potential type 2 diabetes susceptibility gene through the low-frequency H324Q (rs71645922) variant (minor allele frequency [MAF] 3.0%). However, this association did not achieve genome-wide levels of significance. The aim of this study was to establish the true contribution of this variant and common variants in LARS2 (MAF > 5%) to type 2 diabetes risk.

methodsWe combined genome-wide association data (n = 10,128) from the DIAGRAM consortium with independent data derived from a tagging single nucleotide polymorphism (SNP) approach in Dutch individuals (n = 999) and took forward two SNPs of interest to replication in up to 11,163 Dutch participants (rs17637703 and rs952621). In addition, because inspection of genome-wide association study data identified a cluster of low-frequency variants with evidence of type 2 diabetes association, we attempted replication of rs9825041 (a proxy for this group) and the previously identified H324Q variant in up to 35,715 participants of European descent.

resultsNo association between the common SNPs in LARS2 and type 2 diabetes was found. Our replication studies for the two low-frequency variants, rs9825041 and H324Q, failed to confirm an association with type 2 diabetes in Dutch, Scandinavian and UK samples (OR 1.03 [95% CI 0.95-1.12], p = 0.45, n = 31,962 and OR 0.99 [0.90-1.08], p = 0.78, n = 35,715 respectively). CONCLUSIONS/

interpretationIn this study, the largest study examining the role of sequence variants in LARS2 in type 2 diabetes susceptibility, we found no evidence to support previous data indicating a role in type 2 diabetes susceptibility.

Indexed as

Genome-Wide Association StudyAgedAmino Acid SubstitutionAmino Acyl-tRNA SynthetasesBody Mass IndexCohort StudiesDiabetes Mellitus, Type 2Genetic Predisposition to DiseaseHumansLinkage DisequilibriumMitochondrial ProteinsPolymorphism, Single NucleotideAmino Acyl-tRNA SynthetasesLARS2 protein, humanMitochondrial Proteins

Identifiers

PMID19847392
PMCPMC2789927
OpenAlexW2151742484

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.