Evidence map›Paper›PMID 21953277›Full record

Trial reportDiabetologia2012

Association studies of novel obesity-related gene variants with quantitative metabolic phenotypes in a population-based sample of 6,039 Danish individuals.

K S Burgdorf, A P Gjesing, N Grarup, J M Justesen, C H Sandholt, D R Witte, T Jørgensen, S Madsbad, T Hansen, O Pedersen

Abstract readRandomized Controlled Trial
PubMed Publisher
In one paragraph

Trial report in Diabetologia, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 2 pooled it
2.6field-weighted citation impact, top 10% 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

21 citing papers in PubMed, 2 syntheses or guidelines pooled it, 39 citations in OpenAlex.

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  6. Distinct Driver Pathway Enrichments and a High Prevalence ofInternational journal of molecular sciences · 2024
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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

10 authors at 6 institutions in 1 country.

K S BurgdorfThe Novo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health Sciences, University of Copenhagen, Universitetsparken 1, DIKU Building, Room 1.1.N121, DK-2100 Copenhagen, Denmark. Kristoffer.Burgdorf@sund.ku.dk
A P Gjesing
N Grarup
J M Justesen
C H Sandholt
D R Witte
T Jørgensen
S Madsbad
T Hansen
O Pedersen
University of Copenhagen · DKGlostrup Hospital · DKHvidovre Hospital · DKNovo Nordisk Foundation · DKSteno Diabetes Center · DKUniversity of Southern Denmark · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aims/hypothesisGenome-wide association studies have identified novel WHR and BMI susceptibility loci. The aim of this study was to elucidate if any of these loci had an effect on quantitative measures of glucose homeostasis, including estimates of insulin release and insulin sensitivity in an epidemiological setting.

methodsBy applying an additive genetic model, 14 WHR-associated gene variants and 18 BMI-associated variants were investigated for their relationships with glucose-related metabolic traits in treatment-naive individuals from the population-based Inter99 study sample (n = 6,039).

resultsOf the variants associated with BMI, the QPCTL rs2287019 C allele was associated with an increased insulinogenic index of 7.4% per risk allele (p = 4.0 × 10⁻⁷) and increased disposition index of 5.6% (p = 6.4 × 10⁻⁵). The LRP1B rs2890652 C allele was associated with insulin resistance, showing a 3.3% increase (p = 0.0011) using the HOMA-insulin resistance (HOMA-IR) index and a 2.2% reduction (p = 0.0014) with the Matsuda index. Of the variants associated with WHR, LYPLAL1/SLC30A10 rs4846567 G allele carriers showed a 5.2% lower HOMA-IR (p = 0.00086) in women, indicating improved insulin sensitivity. Female carriers of the VEGFA rs6905288 A allele were insulin resistant, with a 3.7% increase in HOMA-IR (p = 0.00036) and 4.0% decrease in Matsuda index (p = 2 × 10⁻⁴).

conclusionsOur correlative findings from analysing single-locus data suggest that some variation in validated BMI and WHR loci are associated with either increased or decreased insulin sensitivity and thereby potentially with metabolically healthy or metabolically unhealthy subsets of obesity. The results call for testing in larger study samples and for further physiological exploration of the possible metabolic implications of these loci.

Indexed as

Polymorphism, Single NucleotideAminoacyltransferasesBody Mass IndexCarrier StateCross-Sectional StudiesDenmarkFemaleGenetic Association StudiesHumansHyperinsulinismInsulin ResistanceLysophospholipaseMaleMiddle AgedModels, GeneticObesityAminoacyltransferasesglutaminyl-peptide cyclotransferaseLRP1B protein, humanLYPLAL1 protein, humanLysophospholipaseReceptors, LDLVascular Endothelial Growth Factor AVEGFA protein, human

Identifiers

PMID21953277
OpenAlexW2000035786

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.