Evidence map›Paper›PMID 40768044›Full record

ReviewDiabetologia2025

The role of the beta cell in type 2 diabetes: new findings from the last 5 years.

Belinda Yau, Julien Ghislain, Melkam A Kebede, Jing Hughes, Vincent Poitout

Abstract readReview
In one paragraph

Review in Diabetologia, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

22 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  6. Mettl14-mediated mJournal of endocrinological investigation · 2026
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  13. Reuniting diabetes through the islet coordinate framework.The lancet. Diabetes & endocrinology · 2026
    Article
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  15. Mitochondria-associated programmed cell death in pancreatic β cell of T2DM.Apoptosis : an international journal on programmed cell death · 2026
    Review
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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

5 authors.

Belinda YauCharles Perkins Centre, University of Sydney, Camperdown, NSW, Australia.
Julien GhislainUniversity of Montreal Hospital Research Center, Montreal, QC, Canada.
Melkam A KebedeCharles Perkins Centre, University of Sydney, Camperdown, NSW, Australia. melkam.kebede@sydney.edu.au.ORCID http://orcid.org/0000-0001-9686-7378
Jing HughesDepartment of Medicine, Yale University School of Medicine, New Haven, CT, USA. jing.hughes@yale.edu.ORCID http://orcid.org/0000-0003-4397-8175
Vincent PoitoutUniversity of Montreal Hospital Research Center, Montreal, QC, Canada. vincent.poitout@umontreal.ca.ORCID http://orcid.org/0000-0002-6555-5053

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent advances in genome-wide approaches, the availability of isolated human islets for research and the evaluation of novel incretin mimetics in large clinical trials have brought about remarkable progress in our understanding of the role of the pancreatic beta cell in type 2 diabetes. Here, we review key developments in type 2 diabetes initiation, progression and remission, focusing mostly on human studies published in the last 5 years. Progress in multi-omics technologies has enabled researchers to identify links between type 2 diabetes risk variants and gene regulatory networks in islet endocrine cells that control beta cell development, function and stress resilience. These studies support the notion that early abnormalities in insulin secretion, rather than a reduction in beta cell mass, play a fundamental and primary role in early type 2 diabetes pathogenesis. Contributing to these intrinsic beta cell defects are various pathogenic signals from other (endocrine and non-endocrine) islet cells, the exocrine pancreas, the gut and insulin-sensitive tissues. It has also become apparent that beta cells comprise a heterogeneous population that responds differently to stress situations and that sex-related differences in beta cell responses should not be underestimated. Finally, human clinical trials have clearly demonstrated that diabetes remission can be achieved using glucose-lowering therapies and particularly strategies focused on weight loss, including bariatric surgery and, more recently, the use of highly efficient new drugs targeting the incretin system. While progress in the last 5 years has been significant, much remains to be uncovered to bring these advances to the clinic and thereby alleviate the dramatic consequences of type 2 diabetes complications for the hundreds of millions of people who live with this disease.

Indexed as

Diabetes Mellitus, Type 2Insulin-Secreting CellsAnimalsHumansIncretinsIncretinsHuman isletsPancreatic beta cellRemissionReviewType 2 diabetes

Identifiers

PMID40768044
PMCPMC12423227

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.