Evidence map›Paper›PMID 20627640›Full record

ArticleGrowth hormone & IGF research : official journal of the Growth Hormone Research Society and the International IGF Research Society2010

IGF2BP1, IGF2BP2 and IGF2BP3 genotype, haplotype and genetic model studies in metabolic syndrome traits and diabetes.

S Rodriguez, G Eiriksdottir, T R Gaunt, T B Harris, L J Launer, V Gudnason, I N M Day

Abstract read
In one paragraph

Article in Growth hormone & IGF research : official journal of the Growth Hormone Research Society and the International IGF Research Society, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 2 pooled it
2.1field-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

20 citing papers in PubMed, 2 syntheses or guidelines pooled it, 49 citations in OpenAlex.

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  16. [Effect of liraglutide in treatment of non-alcoholic fatty liver disease: mechanism of action and research advances].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2017
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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

7 authors at 4 institutions in 3 countries.

S RodriguezDepartment of Social Medicine, University of Bristol, Bristol, United Kingdom. santi.rodriguez@bristol.ac.uk
G Eiriksdottir
T R Gaunt
T B Harris
L J Launer
V Gudnason
I N M Day
University of Bristol · GBNational Institute on Aging · USIcelandic Heart Association · ISUniversity of Iceland · IS

Funding

CLINICAL PROJECT: Age, Gene/Environment Susceptibility Study on the Multi-omics of Aging: A clinical epidemiologic prospective studyZIAAG007380 · NIA · NATIONAL INSTITUTE ON AGING · PI LAUNER, LENORE J · 2009 to 2025
$6.1M
Genetic analysis of AGES-Reykjavik Study and the Health ABCZIAAG006000 · NIA · NATIONAL INSTITUTE ON AGING · PI HARRIS, TAMARA · 2009 to 2017
$1.3M
AGES STUDY-THE REYKJAVIK STUDY OF HEALTHY AGING FOR THE NEW MILLENNIUM-26012100N01AG012100 · NIA · ICELANDIC HEART ASSOCIATION · 2002 to 2004
–
Intramural NIH HHSMedical Research Council G0600705NIA NIH HHS N01 AG012100
6 · The paper itself

Abstract

objectiveGenetic variation at the insulin-like binding protein 2 (IGF2BP2) gene has been associated with type 2 diabetes (T2D) by genome-wide association studies and by replication analyses. Our aim was to explore the underlying genetic model and mechanism of action, factors accounting for non-replications of the associations, and the effect of variation from pathway-related genes IGF2BP1 and IGF2BP3.

methodWe analysed here the association between T2D (and related traits) and rs4402960 and rs1470579 in IGF2BP2, and rs46522 and rs6949019 (marking IGF2BP1 and IGF2BP3 respectively) from the Age, Gene/Environment Susceptibility (AGES)-Reykjavik Study (N approximately 2500 aged 65-96 years). We undertook a retrospective analysis of the deviations from the multiplicative model in previous studies and the present study.

resultsWe replicated an association between rs4402960 and T2D status, and reported significant associations with anthropometric traits, fasting insulin, HOMA-IR and HOMA-%B. These associations were also observed for rs1470579, but not for the SNPs marking IGF2BP1 and IGF2BP3.

conclusionsThe lower fasting insulin levels and the impaired beta-cell function associated with IGF2BP2 SNPs are independent of obesity phenotypes. The action of these SNPs on T2D may result from an effect on beta-cell function. This could lead to lower insulin levels, the association with anthropometric traits being secondary. We discuss possible mechanisms of action relating IGF2BP2 with T2D traits. The occurrence of null alleles, the inclusion of T2D patients in analyses of metabolic syndrome risk traits and the genetic model, are possible factors accounting for non-replications of IGF2BP2 associations with T2D.

Indexed as

AgedAged, 80 and overCohort StudiesDiabetes Mellitus, Type 2FemaleGenetic Predisposition to DiseaseGenetic VariationGenotypeHaplotypesHumansInsulin-Like Growth Factor Binding Protein 1Insulin-Like Growth Factor Binding Protein 2Insulin-Like Growth Factor Binding Protein 3MaleMetabolic SyndromeModels, GeneticInsulin-Like Growth Factor Binding Protein 1Insulin-Like Growth Factor Binding Protein 2Insulin-Like Growth Factor Binding Protein 3

Identifiers

PMID20627640
PMCPMC3268182
OpenAlexW1996432120

What OpenQuestion holds

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LicenceTDM
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.