Evidence map›Paper›PMID 27516442›Full record

ArticleThe EMBO journal2016

IGFBP1 increases β-cell regeneration by promoting α- to β-cell transdifferentiation.

Jing Lu, Ka-Cheuk Liu, Nadja Schulz, Christos Karampelias, Jérémie Charbord, Agneta Hilding, Linn Rautio, Philippe Bertolino, Claes-Göran Östenson, Kerstin Brismar and 1 more

Open access · greenAbstract read
In one paragraph

Article in The EMBO journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 1 pooled it
6.3field-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

55 citing papers in PubMed, 1 synthesis or guideline pooled it, 87 citations in OpenAlex.

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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

11 authors at 3 institutions in 2 countries.

Jing LuDepartment of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden.
Ka-Cheuk LiuDepartment of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden.
Nadja SchulzDepartment of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden.
Christos KarampeliasDepartment of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden.
Jérémie CharbordDepartment of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden.
Agneta HildingDepartment of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden Department of Endocrinology, Metabolism and Diabetes, Karolinska University Hospital, Stockholm, Sweden.
Linn RautioDepartment of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden.
Philippe BertolinoCentre de Recherche en Cancérologie de Lyon, Inserm U1052, CNRS UMR5286, Université Lyon 1, Lyon, France.
Claes-Göran ÖstensonDepartment of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden Department of Endocrinology, Metabolism and Diabetes, Karolinska University Hospital, Stockholm, Sweden.
Kerstin BrismarDepartment of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden Department of Endocrinology, Metabolism and Diabetes, Karolinska University Hospital, Stockholm, Sweden.
Olov AnderssonDepartment of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden olov.andersson@ki.se.ORCID 0000-0001-6715-781X
Karolinska Institutet · SEKarolinska University Hospital · SEUniversité Claude Bernard Lyon 1 · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

There is great interest in therapeutically harnessing endogenous regenerative mechanisms to increase the number of β cells in people with diabetes. By performing whole-genome expression profiling of zebrafish islets, we identified 11 secreted proteins that are upregulated during β-cell regeneration. We then tested the proteins' ability to potentiate β-cell regeneration in zebrafish at supraphysiological levels. One protein, insulin-like growth factor (Igf) binding-protein 1 (Igfbp1), potently promoted β-cell regeneration by potentiating α- to β-cell transdifferentiation. Using various inhibitors and activators of the Igf pathway, we show that Igfbp1 exerts its regenerative effect, at least partly, by inhibiting Igf signaling. Igfbp1's effect on transdifferentiation appears conserved across species: Treating mouse and human islets with recombinant IGFBP1 in vitro increased the number of cells co-expressing insulin and glucagon threefold. Moreover, a prospective human study showed that having high IGFBP1 levels reduces the risk of developing type-2 diabetes by more than 85%. Thus, we identify IGFBP1 as an endogenous promoter of β-cell regeneration and highlight its clinical importance in diabetes.

Indexed as

Cell TransdifferentiationRegenerationAnimalsGlucagon-Secreting CellsHumansInsulin-Like Growth Factor Binding Protein 1Insulin-Secreting CellsMiceZebrafishIGFBP1 protein, humanInsulin-Like Growth Factor Binding Protein 1diabetesinsulinregenerationzebrafishβ cell

Identifiers

PMID27516442
PMCPMC5116948
OpenAlexW2511018787

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.