Evidence map›Paper›PMID 21810601›Full record

ArticleDiabetes2011

Pleiotropic effects of GIP on islet function involve osteopontin.

Valeriya Lyssenko, Lena Eliasson, Olga Kotova, Kasper Pilgaard, Nils Wierup, Albert Salehi, Anna Wendt, Anna Jonsson, Yang Z De Marinis, Lisa M Berglund and 29 more

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2011. 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 46 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 3 pooled it
7.1field-weighted citation impact, top 3% 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

46 citing papers in PubMed, 3 syntheses or guidelines pooled it, 99 citations in OpenAlex.

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4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

39 authors at 11 institutions in 6 countries.

Valeriya LyssenkoDiabetes and Endocrinology, Department of Clinical Sciences, University Hospital Malmö, Lund University, Malmö, Sweden. valeriya.lyssenko@med.lu.se
Lena Eliasson
Olga Kotova
Kasper Pilgaard
Nils Wierup
Albert Salehi
Anna Wendt
Anna Jonsson
Yang Z De Marinis
Lisa M Berglund
Jalal Taneera
Alexander Balhuizen
Ola Hansson
Peter Osmark
Pontus Dunér
Charlotte Brøns
Alena Stancáková
Johanna Kuusisto
Marco Bugliani
Richa Saxena
Emma Ahlqvist
Timothy J Kieffer
Tiinamaija Tuomi
Bo Isomaa
Olle Melander
Emily Sonestedt
Marju Orho-Melander
Peter Nilsson
Sara Bonetti
Riccardo Bonadonna
Roberto Miccoli
Stefano Delprato
Piero Marchetti
Sten Madsbad
Pernille Poulsen
Allan Vaag
Markku Laakso
Maria F Gomez
Leif Groop
Lund University · SESteno Diabetes Centers · DKUniversity of Pisa · ITUniversity of Eastern Finland · FIUniversity of Verona · ITBroad Institute · USFolkhälsans Forskningscentrum · FIMalmö University · SEUniversity of British Columbia · CAUniversity of Copenhagen · DKUniversity of Helsinki · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThe incretin hormone GIP (glucose-dependent insulinotropic polypeptide) promotes pancreatic β-cell function by potentiating insulin secretion and β-cell proliferation. Recently, a combined analysis of several genome-wide association studies (Meta-analysis of Glucose and Insulin-Related Traits Consortium [MAGIC]) showed association to postprandial insulin at the GIP receptor (GIPR) locus. Here we explored mechanisms that could explain the protective effects of GIP on islet function. RESEARCH DESIGN AND

methodsAssociations of GIPR rs10423928 with metabolic and anthropometric phenotypes in both nondiabetic (N = 53,730) and type 2 diabetic individuals (N = 2,731) were explored by combining data from 11 studies. Insulin secretion was measured both in vivo in nondiabetic subjects and in vitro in islets from cadaver donors. Insulin secretion was also measured in response to exogenous GIP. The in vitro measurements included protein and gene expression as well as measurements of β-cell viability and proliferation.

resultsThe A allele of GIPR rs10423928 was associated with impaired glucose- and GIP-stimulated insulin secretion and a decrease in BMI, lean body mass, and waist circumference. The decrease in BMI almost completely neutralized the effect of impaired insulin secretion on risk of type 2 diabetes. Expression of GIPR mRNA was decreased in human islets from carriers of the A allele or patients with type 2 diabetes. GIP stimulated osteopontin (OPN) mRNA and protein expression. OPN expression was lower in carriers of the A allele. Both GIP and OPN prevented cytokine-induced reduction in cell viability (apoptosis). In addition, OPN stimulated cell proliferation in insulin-secreting cells.

conclusionsThese findings support β-cell proliferative and antiapoptotic roles for GIP in addition to its action as an incretin hormone. Identification of a link between GIP and OPN may shed new light on the role of GIP in preservation of functional β-cell mass in humans.

Indexed as

AllelesDiabetes Mellitus, Type 2Gastric Inhibitory PolypeptideGenome-Wide Association StudyGlucagon-Like Peptide 1HumansInsulinInsulin-Secreting CellsInsulin SecretionIslets of LangerhansMaleOsteopontinGastric Inhibitory PolypeptideGlucagon-Like Peptide 1InsulinOsteopontin

Identifiers

PMID21810601
PMCPMC3161325
OpenAlexW2133754637

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.