Evidence map›Paper›PMID 18008060›Full record

ArticleDiabetologia2008

The GCKR rs780094 polymorphism is associated with elevated fasting serum triacylglycerol, reduced fasting and OGTT-related insulinaemia, and reduced risk of type 2 diabetes.

T Sparsø, G Andersen, T Nielsen, K S Burgdorf, A P Gjesing, A L Nielsen, A Albrechtsen, S S Rasmussen, T Jørgensen, K Borch-Johnsen and 5 more

Erratum issuedOpen access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Diabetologia, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 107 papers, 14 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
107citing papers in PubMed, 14 pooled it
8.8field-weighted citation impact, top 2% 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

107 citing papers in PubMed, 14 syntheses or guidelines pooled it, 172 citations in OpenAlex.

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47 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

15 authors at 5 institutions in 1 country.

T SparsøSteno Diabetes Center, Niels Steensens Vej 1, NLC2.13, DK-2820, Gentofte, Denmark. tspr@steno.dk
G Andersen
T Nielsen
K S Burgdorf
A P Gjesing
A L Nielsen
A Albrechtsen
S S Rasmussen
T Jørgensen
K Borch-Johnsen
A Sandbaek
T Lauritzen
S Madsbad
T Hansen
O Pedersen
Steno Diabetes Center · DKAarhus University · DKGlostrup Hospital · DKHvidovre Hospital · DKUniversity of Copenhagen · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aims/hypothesisRecent genome-wide association studies have suggested that a polymorphism in GCKR, the gene encoding the glucokinase regulatory protein, is involved in triacylglycerol regulation. Our aim was to examine in large-scale studies the common GCKR rs780094 polymorphism in relation to metabolic traits (mainly fasting hypertriacylglycerolaemia) and traits related to pancreatic beta cell function.

methodsThe polymorphism was genotyped in 16,853 Danes using Taqman allelic discrimination. Association was analysed in case-control studies and quantitative trait analyses. We also analysed the possible interactive effect between the GCK -30G>A polymorphism and the GCKR rs780094 variant on metabolic traits.

resultsThe minor GCKR A-allele of rs780094 is associated with an increased level of fasting serum triacylglycerol (p = 6 x 10(-14)), impaired fasting (p = 0.001) and OGTT-related insulin release (p = 3 x 10(-6)), reduced homeostasis model assessment of insulin resistance (p = 0.0004), WHO-defined dyslipidaemia (p = 6 x 10(-9)) and a modestly decreased risk of type 2 diabetes (p = 0.01). Significantly increased fasting serum insulin concentrations were demonstrated when analysing the GCK -30A and GCKR rs780094 G-alleles in an additive model. CONCLUSIONS/

interpretationThe GCKR rs780094 polymorphism, or another variant with which it is in tight linkage disequilibrium, is likely to increase glucokinase regulatory protein activity to induce improved glycaemic regulation at the expense of hypertriacylglycerolaemia as reflected in the present study of 16,853 Danes. We also suggest an additive effect of GCK and GCKR risk alleles on [corrected] serum insulin release.

Indexed as

Polymorphism, GeneticAdultDiabetes Mellitus, Type 2FemaleGlucokinaseGlucoseGlucose Tolerance TestHumansInsulinMaleMiddle AgedPhenotypeReceptors, Cytoplasmic and NuclearRiskTriglyceridesGlucokinaseglucokinase receptorGlucoseInsulinReceptors, Cytoplasmic and NuclearTriglycerides

Identifiers

PMID18008060
OpenAlexW2113052184

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.