Evidence map›Paper›PMID 33404684›Full record

ArticleDiabetologia2021

SUR1-mutant iPS cell-derived islets recapitulate the pathophysiology of congenital hyperinsulinism.

Väinö Lithovius, Jonna Saarimäki-Vire, Diego Balboa, Hazem Ibrahim, Hossam Montaser, Tom Barsby, Timo Otonkoski

Open access · hybridAbstract read
PubMed Publisher
In one paragraph

Article in Diabetologia, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
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

27 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
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  8. Article
  9. Thymidylate synthase disruption to limit cell proliferation in cell therapies.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
    Article
  10. Article
  11. Review
  12. Article
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  14. CaBiomedicines · 2023
    Review
  15. Review
  16. β cell replacement therapy for the cure of diabetes.Journal of diabetes investigation · 2022
    Review
  17. Article
  18. Article
  19. Stem Cell-Derived Islets for Type 2 Diabetes.International journal of molecular sciences · 2022
    Review
  20. Review
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

7 authors at 1 institution in 2 countries.

Väinö LithoviusStem Cells and Metabolism Research Program in the Faculty of Medicine of the University of Helsinki, Helsinki, Finland. vaino.lithovius@helsinki.fi.ORCID 0000-0002-1537-5548
Jonna Saarimäki-VireStem Cells and Metabolism Research Program in the Faculty of Medicine of the University of Helsinki, Helsinki, Finland.ORCID 0000-0002-8865-7060
Diego BalboaStem Cells and Metabolism Research Program in the Faculty of Medicine of the University of Helsinki, Helsinki, Finland.ORCID 0000-0002-4784-5452
Hazem IbrahimStem Cells and Metabolism Research Program in the Faculty of Medicine of the University of Helsinki, Helsinki, Finland.ORCID 0000-0003-0165-2660
Hossam MontaserStem Cells and Metabolism Research Program in the Faculty of Medicine of the University of Helsinki, Helsinki, Finland.
Tom BarsbyStem Cells and Metabolism Research Program in the Faculty of Medicine of the University of Helsinki, Helsinki, Finland.
Timo OtonkoskiStem Cells and Metabolism Research Program in the Faculty of Medicine of the University of Helsinki, Helsinki, Finland. timo.otonkoski@helsinki.fi.ORCID 0000-0001-9190-2496
University of Helsinki · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aims/hypothesisCongenital hyperinsulinism caused by mutations in the K

methodsWe derived iPSCs from a patient carrying a homozygous ABCC8

resultsSUR1-mutant and -corrected iPSC lines both differentiated towards the endocrine lineage, but SUR1-mutant stem cells generated 32% more beta-like cells (SC-beta cells) (64.6% vs 49.0%, p = 0.02) and 26% fewer alpha-like cells (16.1% vs 21.8% p = 0.01). SUR1-mutant SC-beta cells were 61% more proliferative (1.23% vs 0.76%, p = 0.006), and this phenotype could be induced in SUR1-corrected cells with pharmacological K CONCLUSIONS/

interpretationWe have created a model recapitulating the known pathophysiology of K

Indexed as

AnimalsCell DifferentiationCell LineCell ProliferationCongenital HyperinsulinismFemaleGenetic Predisposition to DiseaseHumansInduced Pluripotent Stem CellsInsulin SecretionIslets of LangerhansIslets of Langerhans TransplantationMaleMiceMice, Inbred NODMice, SCIDABCC8 protein, humanSulfonylurea ReceptorsBeta cellsCongenital hyperinsulinismDisease modellingInduced pluripotent stem cellsKATP-channelPancreatic islet developmentStem cell-derived islets

Identifiers

PMID33404684
OpenAlexW3120241853

What OpenQuestion holds

Textmetadata
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.