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miR204 potentially promotes non-alcoholic fatty liver disease by inhibition of cpt1a in mouse hepatocytes
Journal article   Open access   Peer reviewed

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

Seonhee Kim, Ikjun Lee, Shuyu Piao, Harsha Nagar, Su-jeong Choi, Young-Rae Kim, Kaikobad Irani, Byeong Hwa Jeon and Cuk-Seong Kim
Communications biology, Vol.5(1), pp.1002-1002
09/21/2022
DOI: 10.1038/s42003-022-03945-1
PMCID: PMC9492679
PMID: 36130994
url
https://doi.org/10.1038/s42003-022-03945-1View
Published (Version of record) Open Access

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. miR204 is found to inhibit cpt1a in mouse hepatocytes, which could play a role in promoting non-alcoholic fatty liver disease.
Fat metabolism Metabolic syndrome

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