Evidence map›Paper›PMID 27615136›Full record

ReviewDiabetes, obesity & metabolism2016

Stress-induced adaptive islet cell identity changes.

V Cigliola, F Thorel, S Chera, P L Herrera

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 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing 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

24 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. GABA signalling in human pancreatic islets.Frontiers in endocrinology · 2023
    Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. GABAInternational journal of molecular sciences · 2020
    Article
  18. Review
  19. Pancreatic Progenitors: There and Back Again.Trends in endocrinology and metabolism: TEM · 2019
    Review
  20. Article
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

4 authors at 2 institutions in 2 countries.

V CigliolaDepartment of Genetic Medicine and Development, Faculty of Medicine, Institute of Genetics and Genomics in Geneva (iGE3), and Centre facultaire du diabète, University of Geneva, Geneva, Switzerland.
F ThorelDepartment of Genetic Medicine and Development, Faculty of Medicine, Institute of Genetics and Genomics in Geneva (iGE3), and Centre facultaire du diabète, University of Geneva, Geneva, Switzerland.
S CheraDepartment of Clinical Science, Faculty of Medicine and Dentistry, University of Bergen, Bergen, Norway.
P L HerreraDepartment of Genetic Medicine and Development, Faculty of Medicine, Institute of Genetics and Genomics in Geneva (iGE3), and Centre facultaire du diabète, University of Geneva, Geneva, Switzerland. Pedro.Herrera@unige.ch.
University of Geneva · CHUniversity of Bergen · NO

Funding

Beta-cell Regeneration by Islet Cell Type Interconversion: Exploiting Islet Cell Plasticity for Diabetes RecoveryUC4DK104209 · NIDDK · UNIVERSITY OF GENEVA · PI HERRERA, PEDRO L · 2014 to 2014
$2.4M
Beta Cell Regeneration by Reprogramming of Adult Pancreatic CellsU01DK089566 · NIDDK · UNIVERSITY OF GENEVA · PI HERRERA, PEDRO L · 2010 to 2014
$1.0M
NIDDK NIH HHS U01 DK089566NIDDK NIH HHS UC4 DK104209
6 · The paper itself

Abstract

The different forms of diabetes mellitus differ in their pathogenesis but, ultimately, they are all characterized by progressive islet β-cell loss. Restoring the β-cell mass is therefore a major goal for future therapeutic approaches. The number of β-cells found at birth is determined by proliferation and differentiation of pancreatic progenitor cells, and it has been considered to remain mostly unchanged throughout adult life. Recent studies in mice have revealed an unexpected plasticity in islet endocrine cells in response to stress; under certain conditions, islet non-β-cells have the potential to reprogram into insulin producers, thus contributing to restore the β-cell mass. Here, we discuss the latest findings on pancreas and islet cell plasticity upon physiological, pathological and experimental conditions of stress. Understanding the mechanisms involved in cell reprogramming in these models will allow the development of new strategies for the treatment of diabetes, by exploiting the intrinsic regeneration capacity of the pancreas.

Indexed as

Cell PlasticityCellular ReprogrammingStress, PhysiologicalAnimalsDiabetes MellitusHumansInsulinInsulin-Secreting CellsInsulin SecretionIslets of LangerhansMiceRegenerationStem CellsInsulinadaptive cell plasticitycell conversioncell dedifferentiationcell fate changecell identitycell reprogrammingcell transdifferentiationdiabetesdiabetes treatmentisletpancreastransgenic

Identifiers

PMID27615136
PMCPMC5021189
OpenAlexW2519210235

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.