Evidence map›Paper›PMID 27615138›Full record

ReviewDiabetes, obesity & metabolism2016

β-Cell dysfunction in diabetes: a crisis of identity?

M F Brereton, M Rohm, F M Ashcroft

Abstract readReview
In one paragraph

Review in Diabetes, obesity & metabolism, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
7.2field-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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 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

3 authors at 1 institution in 1 country.

M F BreretonDepartment of Physiology, Anatomy and Genetics and OXION, University of Oxford, Oxford, UK.
M RohmDepartment of Physiology, Anatomy and Genetics and OXION, University of Oxford, Oxford, UK.
F M AshcroftDepartment of Physiology, Anatomy and Genetics and OXION, University of Oxford, Oxford, UK. frances.ashcroft@dpag.ox.ac.uk.
University of Oxford · GB

Funding

European Research Council 322620Wellcome Trust 084655
6 · The paper itself

Abstract

Type 2 diabetes is characterized by insulin resistance and a progressive loss of β-cell function induced by a combination of both β-cell loss and impaired insulin secretion from remaining β-cells. Here, we review the fate of the β-cell under chronic hyperglycaemic conditions with regard to β-cell mass, gene expression, hormone content, secretory capacity and the ability to de- or transdifferentiate into other cell types. We compare data from various in vivo and in vitro models of diabetes with a novel mouse model of inducible, reversible hyperglycaemia (βV59M mice). We suggest that insulin staining using standard histological methods may not always provide an accurate estimation of β-cell mass or number. We consider how β-cell identity is best defined, and whether expression of transcription factors normally found in islet progenitor cells, or in α-cells, implies that mature β-cells have undergone dedifferentiation or transdifferentiation. We propose that even in long-standing diabetes, β-cells predominantly remain β-cells-but not as we know them.

Indexed as

Cell DedifferentiationCell TransdifferentiationAnimalsDiabetes Mellitus, Type 2Glucagon-Secreting CellsHumansHyperglycemiaInsulinInsulin-Secreting CellsInsulin SecretionIn Vitro TechniquesMiceStem CellsInsulindedifferentiationdiabetesinsulin contenttransdifferentiationβ-cell

Identifiers

PMID27615138
PMCPMC5890905
OpenAlexW2519413657

What OpenQuestion holds

Textmetadata
LicenceTDM
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.