Evidence map›Paper›PMID 25971976›Full record

ArticleThe Journal of biological chemistry2015

Insulin-like Growth Factor 2 Overexpression Induces β-Cell Dysfunction and Increases Beta-cell Susceptibility to Damage.

Alba Casellas, Cristina Mallol, Ariana Salavert, Veronica Jimenez, Miquel Garcia, Judith Agudo, Mercè Obach, Virginia Haurigot, Laia Vilà, Maria Molas and 5 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

38 citing papers in PubMed, 69 citations in OpenAlex.

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  10. Humero-femoral index and diabetes risk in the US population- a case study.Journal of diabetes and metabolic disorders · 2023
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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

15 authors at 3 institutions in 2 countries.

Alba CasellasFrom the Center of Animal Biotechnology and Gene Therapy, Departments of Biochemistry and Molecular Biology and Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas, 08036-Barcelona, Spain.
Cristina MallolFrom the Center of Animal Biotechnology and Gene Therapy, Departments of Biochemistry and Molecular Biology and Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas, 08036-Barcelona, Spain.
Ariana SalavertFrom the Center of Animal Biotechnology and Gene Therapy.
Veronica JimenezFrom the Center of Animal Biotechnology and Gene Therapy, Departments of Biochemistry and Molecular Biology and Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas, 08036-Barcelona, Spain.
Miquel GarciaFrom the Center of Animal Biotechnology and Gene Therapy, Departments of Biochemistry and Molecular Biology and Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas, 08036-Barcelona, Spain.
Judith AgudoFrom the Center of Animal Biotechnology and Gene Therapy, Departments of Biochemistry and Molecular Biology and Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas, 08036-Barcelona, Spain.
Mercè ObachFrom the Center of Animal Biotechnology and Gene Therapy, Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas, 08036-Barcelona, Spain.
Virginia HaurigotFrom the Center of Animal Biotechnology and Gene Therapy, Departments of Biochemistry and Molecular Biology and Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas, 08036-Barcelona, Spain.
Laia VilàFrom the Center of Animal Biotechnology and Gene Therapy, Departments of Biochemistry and Molecular Biology and Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas, 08036-Barcelona, Spain.
Maria MolasFrom the Center of Animal Biotechnology and Gene Therapy, Departments of Biochemistry and Molecular Biology and Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas, 08036-Barcelona, Spain.
Ricardo LageFrom the Center of Animal Biotechnology and Gene Therapy, Departments of Biochemistry and Molecular Biology and Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas, 08036-Barcelona, Spain.
Meritxell MorróFrom the Center of Animal Biotechnology and Gene Therapy, Departments of Biochemistry and Molecular Biology and Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas, 08036-Barcelona, Spain.
Estefania CasanaFrom the Center of Animal Biotechnology and Gene Therapy, Departments of Biochemistry and Molecular Biology and Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas, 08036-Barcelona, Spain.
Jesús RuberteFrom the Center of Animal Biotechnology and Gene Therapy, Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas, 08036-Barcelona, Spain Animal Health and Anatomy, School of Veterinary Medicine, Universitat Autònoma Barcelona, 08193-Bellaterra and.
Fatima BoschFrom the Center of Animal Biotechnology and Gene Therapy, Departments of Biochemistry and Molecular Biology and Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas, 08036-Barcelona, Spain fatima.bosch@uab.es.
Gene Therapy Laboratory · FRCentro de Investigación Biomédica en Red Diabetes y Enfermedades Metabólicas Asociadas · ESDépartement Santé Animale · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The human insulin-like growth factor 2 (IGF2) and insulin genes are located within the same genomic region. Although human genomic studies have demonstrated associations between diabetes and the insulin/IGF2 locus or the IGF2 mRNA-binding protein 2 (IGF2BP2), the role of IGF2 in diabetes pathogenesis is not fully understood. We previously described that transgenic mice overexpressing IGF2 specifically in β-cells (Tg-IGF2) develop a pre-diabetic state. Here, we characterized the effects of IGF2 on β-cell functionality. Overexpression of IGF2 led to β-cell dedifferentiation and endoplasmic reticulum stress causing islet dysfunction in vivo. Both adenovirus-mediated overexpression of IGF2 and treatment of adult wild-type islets with recombinant IGF2 in vitro further confirmed the direct implication of IGF2 on β-cell dysfunction. Treatment of Tg-IGF2 mice with subdiabetogenic doses of streptozotocin or crossing these mice with a transgenic model of islet lymphocytic infiltration promoted the development of overt diabetes, suggesting that IGF2 makes islets more susceptible to β-cell damage and immune attack. These results indicate that increased local levels of IGF2 in pancreatic islets may predispose to the onset of diabetes. This study unravels an unprecedented role of IGF2 on β-cells function.

Indexed as

AnimalsCell DedifferentiationCell Line, TumorDiabetes MellitusHumansInsulinInsulin-Like Growth Factor IIInsulin-Secreting CellsIslets of LangerhansMiceMice, Inbred C57BLMice, TransgenicRatsIGF2 protein, humanInsulinInsulin-Like Growth Factor IIbeta cell (B-cell)diabetesendoplasmic reticulum stress (ER stress)insulin-like growth factor (IGF)islet

Identifiers

PMID25971976
PMCPMC4505425
OpenAlexW1646497768

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.