miR204 potentially promotes non-alcoholic fatty liver disease by inhibition of cpt1a in mouse hepatocytes View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2022-09-21

AUTHORS

Seonhee Kim, Ikjun Lee, Shuyu Piao, Harsha Nagar, Su-jeong Choi, Young-Rae Kim, Kaikobad Irani, Byeong Hwa Jeon, Cuk-Seong Kim

ABSTRACT

Non-alcoholic fatty liver disease (NAFLD) is associated with hepatic metabolism dysfunction. However, the mechanistic role of miR204 in the development of NAFLD is unknown. We investigate the functional significance of miR204 in the evolution of NAFLD. IDH2 KO mice feed a normal diet (ND) or HFD increased body weight, epididymal fat-pad weight, lipid droplet in liver, blood parameter and inflammation compared to WT mice fed a ND or HFD. Moreover, the expression of miR204 is increased in mice with IDH2 deficiency. Increased miR204 by IDH2 deficiency regulates carnitine palmitoyltransferase 1a (cpt1a) synthesis, which inhibits fatty acid β-oxidation. Inhibition of miR204 prevents the disassembly of two fatty acid-related genes by activating CPT1a expression, which decreases lipid droplet in liver, inflammatory cytokines, epididymal fat pad weight, blood parameters. Increased miR204 by IDH2 deficiency promotes the pathogenesis of HFD-induced NAFLD by regulating hepatic fatty acid metabolism and inflammation. More... »

PAGES

1002

References to SciGraph publications

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  • 2017-10-25. miR-204 is associated with an endocrine phenotype in human pancreatic islets but does not regulate the insulin mRNA through MAFA in SCIENTIFIC REPORTS
  • 2016-09-02. Vascular microRNA-204 is remotely governed by the microbiome and impairs endothelium-dependent vasorelaxation by downregulating Sirtuin1 in NATURE COMMUNICATIONS
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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/s42003-022-03945-1

    DOI

    http://dx.doi.org/10.1038/s42003-022-03945-1

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1151184393

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/36130994


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