Evidence map›Paper›PMID 40295334›Full record

ArticleDiabetologia2025

Pancreatic exocrine damage induces beta cell stress in zebrafish larvae.

Noura Faraj, Willem M H Hoogaars, B H Peter Duinkerken, Anouk H G Wolters, Kim Kats, Mette C Dekkers, Arnaud Zaldumbide, Ben N G Giepmans

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Diabetologia, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–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

1 citing paper in PubMed.

  1. 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

8 authors.

Noura FarajDepartment of Biomedical Sciences, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands.ORCID http://orcid.org/0000-0003-1458-9402
Willem M H HoogaarsDepartment of Biomedical Sciences, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands.ORCID http://orcid.org/0000-0001-6061-2576
B H Peter DuinkerkenDepartment of Biomedical Sciences, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands.ORCID http://orcid.org/0000-0003-0699-0001
Anouk H G WoltersDepartment of Biomedical Sciences, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands.ORCID http://orcid.org/0000-0002-9060-9850
Kim KatsDepartment of Biomedical Sciences, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands.ORCID http://orcid.org/0000-0001-5300-2139
Mette C DekkersDepartment of Cell and Chemical Biology, Leiden University Medical Center, Leiden, the Netherlands.ORCID http://orcid.org/0000-0001-6894-759X
Arnaud ZaldumbideDepartment of Cell and Chemical Biology, Leiden University Medical Center, Leiden, the Netherlands.ORCID http://orcid.org/0000-0001-6680-4456
Ben N G GiepmansDepartment of Biomedical Sciences, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands. b.n.g.giepmans@umcg.nl.ORCID http://orcid.org/0000-0001-5105-5915

Funding

Juvenile Diabetes Research Foundation International 5-SRA-2018-557-Q-RNederlandse Organisatie voor Wetenschappelijk Onderzoek 019.030Nederlandse Organisatie voor Wetenschappelijk Onderzoek 184.034.014ZonMw 09120012010107ZonMw 91111.006
6 · The paper itself

Abstract

aims/hypothesisExcessive endoplasmic reticulum (ER) stress in beta cells can impair proliferation and contribute to autoimmune responses such as the destruction of beta cells in type 1 diabetes. Exocrine-beta cell interactions affect beta cell growth and function. Notably, exocrine abnormalities are frequently observed alongside overloaded beta cells in different types of diabetes, suggesting that exocrine stress may induce beta cell ER stress and loss. While a cause-consequence relationship between exocrine stress and beta cell function cannot be addressed in humans, it can be studied in a zebrafish model. Larvae develop a pancreas with a human-like morphology by 120 h post-fertilisation, providing a valuable dynamic model for studying pancreatic interactions. Our aim was to target exocrine cells specifically and address beta cell status using transgenic zebrafish models and reporters.

methodsTo explore the impact of exocrine damage on beta cell fitness, we generated a novel zebrafish model allowing exocrine pancreas ablation, using a nifurpirinol-nitroreductase system. We subsequently assessed the in vivo effects on beta cells by live-monitoring dynamic cellular events, such as ER stress, apoptosis and changes in beta cell number and volume.

resultsExocrine damage in zebrafish decreased pancreas volume by approximately 50% and changed its morphology. The resulting exocrine damage induced ER stress in 60-90% of beta cells and resulted in a ~50% reduction in their number. CONCLUSIONS/

interpretationThe zebrafish model provides a robust platform for investigating the interplay between exocrine cells and beta cells, thereby enhancing further insights into the mechanisms driving pancreatic diseases such as type 1 diabetes.

Indexed as

Endoplasmic Reticulum StressInsulin-Secreting CellsPancreas, ExocrineAnimalsAnimals, Genetically ModifiedApoptosisLarvaZebrafishBeta cell functionBeta cell stressDiabetesExocrine damageZebrafish larvae

Identifiers

PMID40295334
PMCPMC12245981

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.