Evidence map›Paper›PMID 39159974›Full record

ArticleLife science alliance2024

Examining the liver-pancreas crosstalk reveals a role for the molybdenum cofactor in β-cell regeneration.

Christos Karampelias, Bianca Băloiu, Birgit Rathkolb, Patricia da Silva-Buttkus, Etty Bachar-Wikström, Susan Marschall, Helmut Fuchs, Valerie Gailus-Durner, Lianhe Chu, Martin Hrabě de Angelis and 1 more

Abstract read
In one paragraph

Article in Life science alliance, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. 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

11 authors.

Christos KarampeliasDepartment of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden christos.karampelias@helmholtz-munich.de.ORCID 0000-0002-9990-5760
Bianca BăloiuDepartment of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden.ORCID 0009-0001-8047-3515
Birgit RathkolbInstitute of Experimental Genetics, German Mouse Clinic, Helmholtz Zentrum München, Neuherberg, Germany.
Patricia da Silva-ButtkusInstitute of Experimental Genetics, German Mouse Clinic, Helmholtz Zentrum München, Neuherberg, Germany.ORCID 0000-0003-4705-3399
Etty Bachar-WikströmDepartment of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden.ORCID 0000-0002-3283-6721
Susan MarschallInstitute of Experimental Genetics, German Mouse Clinic, Helmholtz Zentrum München, Neuherberg, Germany.
Helmut FuchsInstitute of Experimental Genetics, German Mouse Clinic, Helmholtz Zentrum München, Neuherberg, Germany.
Valerie Gailus-DurnerInstitute of Experimental Genetics, German Mouse Clinic, Helmholtz Zentrum München, Neuherberg, Germany.
Lianhe ChuDepartment of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden.
Martin Hrabě de AngelisInstitute of Experimental Genetics, German Mouse Clinic, Helmholtz Zentrum München, Neuherberg, Germany.
Olov AnderssonDepartment of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden olov.andersson@ki.se olov.andersson@mcb.uu.se.ORCID 0000-0001-6715-781X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Regeneration of insulin-producing β-cells is an alternative avenue to manage diabetes, and it is crucial to unravel this process in vivo during physiological responses to the lack of β-cells. Here, we aimed to characterize how hepatocytes can contribute to β-cell regeneration, either directly or indirectly via secreted proteins or metabolites, in a zebrafish model of β-cell loss. Using lineage tracing, we show that hepatocytes do not directly convert into β-cells even under extreme β-cell ablation conditions. A transcriptomic analysis of isolated hepatocytes after β-cell ablation displayed altered lipid- and glucose-related processes. Based on the transcriptomics, we performed a genetic screen that uncovers a potential role of the molybdenum cofactor (Moco) biosynthetic pathway in β-cell regeneration and glucose metabolism in zebrafish. Consistently, molybdenum cofactor synthesis 2 (

Indexed as

CoenzymesGlucoseHepatocytesInsulin-Secreting CellsLiverMetalloproteinsMolybdenum CofactorsPteridinesZebrafishAnimalsMicePancreasRegenerationZebrafish ProteinsCoenzymesGlucoseMetalloproteinsMolybdenum CofactorsmolybdopterinPteridinesZebrafish Proteins

Identifiers

PMID39159974
PMCPMC11333758

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.