Evidence map›Paper›PMID 20802253›Full record

ArticleDiabetes2010

Glycemia determines the effect of type 2 diabetes risk genes on insulin secretion.

Martin Heni, Caroline Ketterer, Claus Thamer, Silke A Herzberg-Schäfer, Martina Guthoff, Norbert Stefan, Fausto Machicao, Harald Staiger, Andreas Fritsche, Hans-Ulrich Häring

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

24 citing papers in PubMed, 47 citations in OpenAlex.

  1. Trial
  2. Comprehensive overview of disease models for Wolfram syndrome: toward effective treatments.Mammalian genome : official journal of the International Mammalian Genome Society · 2024
    Review
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  5. Glucagon-like peptide 1 (GLP-1).Molecular metabolism · 2019 · on this map
    Review
  6. Transcription factor-7-like 2 (The Journal of biological chemistry · 2018
    Article
  7. Diabetes care · 2018
    Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Lack of Association betweenJournal of diabetes research · 2016
    Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
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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 1 institution in 1 country.

Martin HeniDepartment of Internal Medicine, Division of Endocrinology, Diabetology, Angiology, Nephrology and Clinical Chemistry, Eberhard Karls University Tübingen, Tübingen, Germany.
Caroline Ketterer
Claus Thamer
Silke A Herzberg-Schäfer
Martina Guthoff
Norbert Stefan
Fausto Machicao
Harald Staiger
Andreas Fritsche
Hans-Ulrich Häring
Deutsches Diabetes-Zentrum e.V. · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveSeveral single nucleotide polymorphisms (SNPs) in diabetes risk genes reduce glucose- and/or incretin-induced insulin secretion. Here, we investigated interactions between glycemia and such diabetes risk polymorphisms. RESEARCH DESIGN AND

methodsInsulin secretion was assessed by insulinogenic index and areas under the curve of C-peptide/glucose in 1,576 subjects using an oral glucose tolerance test (OGTT). Participants were genotyped for 10 diabetes risk SNPs associated with β-cell dysfunction: rs5215 (KCNJ11), rs13266634 (SLC30A8), rs7754840 (CDKAL1), rs10811661 (CDKN2A/2B), rs10830963 (MTNR1B), rs7903146 (TCF7L2), rs10010131 (WFS1), rs7923837 (HHEX), rs151290 (KCNQ1), and rs4402960 (IGF2BP2). Furthermore, the impact of the interaction between genetic variation in TCF7L2 and glycemia on changes in insulin secretion was tested in 315 individuals taking part in a lifestyle intervention study.

resultsFor the SNPs in TCF7L2 and WFS1, we found a significant interaction between glucose control and insulin secretion (all P ≤ 0.0018 for glucose × genotype). When plotting insulin secretion against glucose at 120 min OGTT, the compromising SNP effects on insulin secretion are most apparent under high glucose. In the longitudinal study, rs7903146 in TCF7L2 showed a significant interaction with baseline glucose tolerance upon change in insulin secretion (P = 0.0027). Increased glucose levels at baseline predicted an increase in insulin secretion upon improvement of glycemia by lifestyle intervention only in carriers of the risk alleles.

conclusionsFor the diabetes risk genes TCF7L2 and WFS1, which are associated with impaired incretin signaling, the level of glycemia determines SNP effects on insulin secretion. This indicates the increasing relevance of these SNPs during the progression of prediabetes stages toward clinically overt type 2 diabetes.

Indexed as

Polymorphism, Single NucleotideBlood GlucoseC-PeptideDiabetes Mellitus, Type 2Gene Expression RegulationGenetic VariationGenotypeGlucose Tolerance TestIncretinsInsulinInsulin-Secreting CellsInsulin SecretionMembrane ProteinsRisk AssessmentTranscription Factor 7-Like 2 ProteinBlood GlucoseC-PeptideIncretinsInsulinMembrane ProteinsTCF7L2 protein, humanTranscription Factor 7-Like 2 Proteinwolframin protein

Identifiers

PMID20802253
PMCPMC2992789
OpenAlexW2112726367

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

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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.