Evidence map›Paper›PMID 25145789›Full record

ArticleNature communications2014

Reversible changes in pancreatic islet structure and function produced by elevated blood glucose.

Melissa F Brereton, Michaela Iberl, Kenju Shimomura, Quan Zhang, Alice E Adriaenssens, Peter Proks, Ioannis I Spiliotis, William Dace, Katia K Mattis, Reshma Ramracheya and 5 more

Open access · hybridAbstract read
In one paragraph

Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 160 papers.

0numbers the graph read from it
0cells of the map it votes in
160citing papers in PubMed
17.0field-weighted citation impact, top 1% 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

160 citing papers in PubMed, 251 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Review
  4. Review
  5. Review
  6. Spatiotemporal Dynamics of Bihormonal Cells in the Developing Human Pancreas.Bulletin of experimental biology and medicine · 2026
    Article
  7. Article
  8. Article
  9. Article
  10. Prolonging Partial Remission in Type 1 Diabetes: The Role of Low-Carbohydrate Diet: A Literature Review.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026
    Review
  11. The role of chromogranin A cleavage products in onset of type 1 and 2 diabetes.Frontiers in clinical diabetes and healthcare · 2026
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. β-Cell Dedifferentiation in HOMA-βlow and HOMA-βhigh Subjects.The Journal of clinical endocrinology and metabolism · 2025
    Article
  18. Article
  19. Review
  20. Article

100 more citing papers are in PubMed but not listed here.

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 1 country.

Melissa F BreretonHenry Wellcome Centre for Gene Function, Department of Physiology, Anatomy and Genetics and OXION, University of Oxford, Parks Road, Oxford OX1 3PT, UK.
Michaela Iberl1] Henry Wellcome Centre for Gene Function, Department of Physiology, Anatomy and Genetics and OXION, University of Oxford, Parks Road, Oxford OX1 3PT, UK [2].
Kenju Shimomura1] Henry Wellcome Centre for Gene Function, Department of Physiology, Anatomy and Genetics and OXION, University of Oxford, Parks Road, Oxford OX1 3PT, UK [2].
Quan Zhang1] Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Churchill Hospital, Oxford OX3 7LE, UK [2].
Alice E Adriaenssens1] Cambridge Institute for Medical Research, Addenbrooke's Hospital, Hills Road, Cambridge CB2 0XY, UK [2].
Peter ProksHenry Wellcome Centre for Gene Function, Department of Physiology, Anatomy and Genetics and OXION, University of Oxford, Parks Road, Oxford OX1 3PT, UK.
Ioannis I SpiliotisHenry Wellcome Centre for Gene Function, Department of Physiology, Anatomy and Genetics and OXION, University of Oxford, Parks Road, Oxford OX1 3PT, UK.
William DaceHenry Wellcome Centre for Gene Function, Department of Physiology, Anatomy and Genetics and OXION, University of Oxford, Parks Road, Oxford OX1 3PT, UK.
Katia K MattisHenry Wellcome Centre for Gene Function, Department of Physiology, Anatomy and Genetics and OXION, University of Oxford, Parks Road, Oxford OX1 3PT, UK.
Reshma RamracheyaOxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Churchill Hospital, Oxford OX3 7LE, UK.
Fiona M GribbleCambridge Institute for Medical Research, Addenbrooke's Hospital, Hills Road, Cambridge CB2 0XY, UK.
Frank ReimannCambridge Institute for Medical Research, Addenbrooke's Hospital, Hills Road, Cambridge CB2 0XY, UK.
Anne ClarkOxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Churchill Hospital, Oxford OX3 7LE, UK.
Patrik RorsmanOxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Churchill Hospital, Oxford OX3 7LE, UK.
Frances M AshcroftHenry Wellcome Centre for Gene Function, Department of Physiology, Anatomy and Genetics and OXION, University of Oxford, Parks Road, Oxford OX1 3PT, UK.
Addenbrooke's Hospital · GBChurchill Hospital · GBUniversity of Oxford · GB

Funding

European Research Council 322620Medical Research Council MC_UU_12012/3Wellcome Trust 084655Wellcome Trust 088357Wellcome Trust 089795Wellcome Trust 095531Wellcome Trust 095531/Z/11/ZWellcome Trust 884655Wellcome Trust WT-084210Z/07/ZWellcome Trust WT088357Z/09/Z
6 · The paper itself

Abstract

Diabetes is characterized by hyperglycaemia due to impaired insulin secretion and aberrant glucagon secretion resulting from changes in pancreatic islet cell function and/or mass. The extent to which hyperglycaemia per se underlies these alterations remains poorly understood. Here we show that β-cell-specific expression of a human activating KATP channel mutation in adult mice leads to rapid diabetes and marked alterations in islet morphology, ultrastructure and gene expression. Chronic hyperglycaemia is associated with a dramatic reduction in insulin-positive cells and an increase in glucagon-positive cells in islets, without alterations in cell turnover. Furthermore, some β-cells begin expressing glucagon, whilst retaining many β-cell characteristics. Hyperglycaemia, rather than KATP channel activation, underlies these changes, as they are prevented by insulin therapy and fully reversed by sulphonylureas. Our data suggest that many changes in islet structure and function associated with diabetes are attributable to hyperglycaemia alone and are reversed when blood glucose is normalized.

Indexed as

AnimalsBlood GlucoseDiabetes Mellitus, ExperimentalDisease Models, AnimalElectrophysiologyGlyburideHumansHyperglycemiaInsulinIslets of LangerhansKATP ChannelsKcnj11 ChannelMice, TransgenicMutationPotassium Channels, Inwardly RectifyingBlood GlucoseGlyburideInsulinKATP ChannelsKcnj11 ChannelPotassium Channels, Inwardly Rectifying

Identifiers

PMID25145789
PMCPMC4143961
OpenAlexW2025410324

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.