Evidence map›Paper›PMID 37864157›Full record

ArticleMolecular medicine (Cambridge, Mass.)2023

Knockout of STE20-type kinase TAOK3 does not attenuate diet-induced NAFLD development in mice.

Ying Xia, Emma Andersson, Mara Caputo, Emmelie Cansby, Francesca Sedda, Ferran Font-Gironès, Johan Ruud, Yeshwant Kurhe, Bengt Hallberg, Hanns-Ulrich Marschall and 4 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact, top 73% of its field
1 · What the graph read from it

What it found

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2 · The registry

The trial behind it

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3 · Its place in the literature

Who cites it

0 citing papers in PubMed, 0 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

14 authors at 3 institutions in 2 countries.

Ying XiaDepartment of Chemistry and Molecular Biology, University of Gothenburg and Sahlgrenska University Hospital, Gothenburg, Sweden.
Emma AnderssonDepartment of Chemistry and Molecular Biology, University of Gothenburg and Sahlgrenska University Hospital, Gothenburg, Sweden.
Mara CaputoDepartment of Chemistry and Molecular Biology, University of Gothenburg and Sahlgrenska University Hospital, Gothenburg, Sweden.
Emmelie CansbyDepartment of Chemistry and Molecular Biology, University of Gothenburg and Sahlgrenska University Hospital, Gothenburg, Sweden.
Francesca SeddaDepartment of Molecular and Clinical Medicine/Wallenberg Laboratory, Institute of Medicine, University of Gothenburg and Sahlgrenska University Hospital, Gothenburg, Sweden.
Ferran Font-GironèsDepartment of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Johan RuudDepartment of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Yeshwant KurheDepartment of Medical Biochemistry and Cell Biology, Institute of Biomedicine, University of Gothenburg and Sahlgrenska University Hospital, Gothenburg, Sweden.
Bengt HallbergDepartment of Medical Biochemistry and Cell Biology, Institute of Biomedicine, University of Gothenburg and Sahlgrenska University Hospital, Gothenburg, Sweden.
Hanns-Ulrich MarschallDepartment of Molecular and Clinical Medicine/Wallenberg Laboratory, Institute of Medicine, University of Gothenburg and Sahlgrenska University Hospital, Gothenburg, Sweden.
Ingrid Wernstedt AsterholmDepartment of Physiology, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Stefano RomeoDepartment of Molecular and Clinical Medicine/Wallenberg Laboratory, Institute of Medicine, University of Gothenburg and Sahlgrenska University Hospital, Gothenburg, Sweden.
Matthias BlüherHelmholtz Institute for Metabolic, Obesity, and Vascular Research (HI-MAG) of the Helmholtz Zentrum München, University of Leipzig and University Hospital Leipzig, Leipzig, Germany.
Margit MahlapuuDepartment of Chemistry and Molecular Biology, University of Gothenburg and Sahlgrenska University Hospital, Gothenburg, Sweden. margit.mahlapuu@gu.se.ORCID 0000-0001-8740-8874
Sahlgrenska University Hospital · SEUniversity of Gothenburg · SEHelmholtz Zentrum München · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveNon-alcoholic fatty liver disease (NAFLD), the primary hepatic consequence of obesity, is affecting about 25% of the global adult population. The aim of this study was to examine the in vivo role of STE20-type protein kinase TAOK3, which has been previously reported to regulate hepatocellular lipotoxicity in vitro, in the development of NAFLD and systemic insulin resistance in the context of obesity.

methodsTaok3 knockout mice and wild-type littermates were challenged with a high-fat diet. Various in vivo tests were performed to characterize the whole-body metabolism. NAFLD progression in the liver, and lipotoxic damage in adipose tissue, kidney, and skeletal muscle were compared between the genotypes by histological assessment, immunofluorescence microscopy, protein and gene expression profiling, and biochemical assays. Intracellular lipid accumulation and oxidative/ER stress were analyzed in cultured human and mouse hepatocytes where TAOK3 was knocked down by small interfering RNA. The expression of TAOK3-related STE20-type kinases was quantified in different organs from high-fat diet-fed Taok3

resultsTAOK3 deficiency had no impact on body weight or composition, food consumption, locomotor activity, or systemic glucose or insulin homeostasis in obese mice. Consistently, Taok3

conclusionsIn contrast to the in vitro observations, genetic deficiency of TAOK3 in mice failed to mitigate the detrimental metabolic consequences of chronic exposure to dietary lipids, which may be partly attributable to the activation of liver-specific compensation response for the genetic loss of TAOK3 by related STE20-type kinases.

Indexed as

Non-alcoholic Fatty Liver DiseaseAdultAnimalsDiet, High-FatHumansLipidsLiverMiceMice, Inbred C57BLMice, KnockoutObesityProtein Serine-Threonine KinasesLipidsProtein Serine-Threonine KinasesTack3 kinase, mouseGenetic compensationNon-alcoholic fatty liver diseaseNon-alcoholic steatohepatitisSystemic glucose and insulin homeostasisTAOK3

Identifiers

PMID37864157
PMCPMC10589923
OpenAlexW4387808878

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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.