Evidence map›Paper›PMID 26384018›Full record

ArticleScientific reports2015

Diabetic pdx1-mutant zebrafish show conserved responses to nutrient overload and anti-glycemic treatment.

Robin A Kimmel, Stefan Dobler, Nicole Schmitner, Tanja Walsen, Julia Freudenblum, Dirk Meyer

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
7.1field-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

37 citing papers in PubMed, 63 citations in OpenAlex.

  1. Review
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  7. An inducible model of chronic hyperglycemia.Disease models & mechanisms · 2023
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Characteristics of the New Insulin-Resistant Zebrafish Model.Pharmaceuticals (Basel, Switzerland) · 2021
    Article
  15. Review
  16. Review
  17. Article
  18. Which Hyperglycemic Model of Zebrafish (Frontiers in cell and developmental biology · 2021
    Review
  19. Article
  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

6 authors at 1 institution in 1 country.

Robin A KimmelInstitute of Molecular Biology/CMBI; Leopold-Francis University of Innsbruck, Technikerstrasse 25, A-6020 Innsbruck, Austria.
Stefan DoblerInstitute of Molecular Biology/CMBI; Leopold-Francis University of Innsbruck, Technikerstrasse 25, A-6020 Innsbruck, Austria.
Nicole SchmitnerInstitute of Molecular Biology/CMBI; Leopold-Francis University of Innsbruck, Technikerstrasse 25, A-6020 Innsbruck, Austria.
Tanja WalsenInstitute of Molecular Biology/CMBI; Leopold-Francis University of Innsbruck, Technikerstrasse 25, A-6020 Innsbruck, Austria.
Julia FreudenblumInstitute of Molecular Biology/CMBI; Leopold-Francis University of Innsbruck, Technikerstrasse 25, A-6020 Innsbruck, Austria.
Dirk MeyerInstitute of Molecular Biology/CMBI; Leopold-Francis University of Innsbruck, Technikerstrasse 25, A-6020 Innsbruck, Austria.
Universität Innsbruck · AT

Funding

Austrian Science Fund FWF P 25659
6 · The paper itself

Abstract

Diabetes mellitus is characterized by disrupted glucose homeostasis due to loss or dysfunction of insulin-producing beta cells. In this work, we characterize pancreatic islet development and function in zebrafish mutant for pdx1, a gene which in humans is linked to genetic forms of diabetes and is associated with increased susceptibility to Type 2 diabetes. Pdx1 mutant zebrafish have the key diabetic features of reduced beta cells, decreased insulin and elevated glucose. The hyperglycemia responds to pharmacologic anti-diabetic treatment and, as often seen in mammalian diabetes models, beta cells of pdx1 mutants show sensitivity to nutrient overload. This unique genetic model of diabetes provides a new tool for elucidating the mechanisms behind hyperglycemic pathologies and will allow the testing of novel therapeutic interventions in a model organism that is amenable to high-throughput approaches.

Indexed as

Animal FeedAnimal Nutritional Physiological PhenomenaMutationAmino Acid SequenceAnimalsAnimals, Genetically ModifiedBody SizeCell SurvivalCodon, NonsenseDiabetes Mellitus, Type 2Disease Models, AnimalGene Knockout TechniquesGenotypeGlucoseHomeodomain ProteinsHypoglycemic AgentsCodon, NonsenseGlucoseHomeodomain ProteinsHypoglycemic Agentspancreatic and duodenal homeobox 1 proteinTrans-Activators

Identifiers

PMID26384018
PMCPMC4585597
OpenAlexW2403145859

What OpenQuestion 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 OpenQuestion graph.