Evidence map›Paper›PMID 28442507›Full record

ArticleThe Journal of endocrinology2017

Protein kinase STK25 aggravates the severity of non-alcoholic fatty pancreas disease in mice.

Esther Nuñez-Durán, Belén Chanclón, Silva Sütt, Joana Real, Hanns-Ulrich Marschall, Ingrid Wernstedt Asterholm, Emmelie Cansby, Margit Mahlapuu

Open access · hybridAbstract read
In one paragraph

Article in The Journal of endocrinology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

13 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Review
  3. Pathophysiological Mechanisms and Clinical Associations of Non-Alcoholic Fatty Pancreas Disease.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024
    Review
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  6. Article
  7. Review
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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 at 2 institutions in 1 country.

Esther Nuñez-DuránDepartment of Molecular and Clinical MedicineLundberg Laboratory for Diabetes Research, Institute of Medicine, University of Gothenburg, Sahlgrenska University Hospital, Gothenburg, Sweden.
Belén ChanclónDepartment of Molecular and Clinical MedicineLundberg Laboratory for Diabetes Research, Institute of Medicine, University of Gothenburg, Sahlgrenska University Hospital, Gothenburg, Sweden.
Silva SüttDepartment of Molecular and Clinical MedicineLundberg Laboratory for Diabetes Research, Institute of Medicine, University of Gothenburg, Sahlgrenska University Hospital, Gothenburg, Sweden.
Joana RealDepartment of Metabolic PhysiologyInstitute of Neuroscience and Physiology, University of Gothenburg, Gothenburg, Sweden.
Hanns-Ulrich MarschallDepartment of Molecular and Clinical MedicineWallenberg Laboratory, Institute of Medicine, University of Gothenburg, Sahlgrenska University Hospital, Gothenburg, Sweden.
Ingrid Wernstedt AsterholmDepartment of Metabolic PhysiologyInstitute of Neuroscience and Physiology, University of Gothenburg, Gothenburg, Sweden.
Emmelie CansbyDepartment of Molecular and Clinical MedicineLundberg Laboratory for Diabetes Research, Institute of Medicine, University of Gothenburg, Sahlgrenska University Hospital, Gothenburg, Sweden.
Margit MahlapuuDepartment of Molecular and Clinical MedicineLundberg Laboratory for Diabetes Research, Institute of Medicine, University of Gothenburg, Sahlgrenska University Hospital, Gothenburg, Sweden Margit.Mahlapuu@gu.se.
Sahlgrenska University Hospital · SEUniversity of Gothenburg · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Characterising the molecular networks that negatively regulate pancreatic β-cell function is essential for understanding the underlying pathogenesis and developing new treatment strategies for type 2 diabetes. We recently identified serine/threonine protein kinase 25 (STK25) as a critical regulator of ectopic fat storage, meta-inflammation, and fibrosis in liver and skeletal muscle. Here, we assessed the role of STK25 in control of progression of non-alcoholic fatty pancreas disease in the context of chronic exposure to dietary lipids in mice. We found that overexpression of STK25 in high-fat-fed transgenic mice aggravated diet-induced lipid storage in the pancreas compared with that of wild-type controls, which was accompanied by exacerbated pancreatic inflammatory cell infiltration, stellate cell activation, fibrosis and apoptosis. Pancreas of

Indexed as

Diet, High-FatAdipose TissueAnimalsBlood GlucoseC-PeptideGene ExpressionGlucose Tolerance TestHippo KinasesInflammationInsulinInsulin-Secreting CellsInsulin SecretionIntracellular Signaling Peptides and ProteinsIslets of LangerhansLeptinLipid MetabolismBlood GlucoseC-PeptideHippo KinasesInsulinIntracellular Signaling Peptides and ProteinsLeptinProtein Serine-Threonine KinasesStk25 protein, mouseectopic lipid storagenon-alcoholic fatty pancreas diseaseβ-cell dysfunction

Identifiers

PMID28442507
PMCPMC5510597
OpenAlexW2609376378

What OpenQuestion holds

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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.