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Biochemical and biophysical research communications v.494 no.3/4, 2017년, pp.687 - 692   SCI SCIE
본 등재정보는 저널의 등재정보를 참고하여 보여주는 베타서비스로 정확한 논문의 등재여부는 등재기관에 확인하시기 바랍니다.

MiR-150 deficiency ameliorated hepatosteatosis and insulin resistance in nonalcoholic fatty liver disease via targeting CASP8 and FADD-like apoptosis regulator

Zhuge, Baozhong (Department of Clinical Laboratory, Linyi People's Hospital, Linyi, Shandong, 276000, China ); Li, Guohong (Department of Clinical Laboratory, Dezhou Municiple Hospital, Dezhou, Shandong, 253000, China );
  • 초록  

    Abstract The prevalence of Non-alcoholic fatty liver diseases (NAFLD) increased rapidly in the world. However, the pathogenesis of is still unclear. Hepatic steatosis and insulin resistance are considered to be central to the pathophysiology of NAFLD. MicroRNAs are short non-coding RNAs and has been reported to be involved in pathogenesis of NAFLD and related metabolic diseases. Here, we investigated the mechanisms by which miR-150 regulate hepatic steatosis and insulin resistance in high fat diet (HFD) induced NAFLD model. The expression of miR-150 was up-regulated dramatically in both human NAFLD patients and HFD mice model, as well as in hepatocytes treated with oleic acid. miR-150 deficiency ameliorated the hepatic steatosis and insulin resistance significantly in NAFLD mice. miR-150 deficiency decreased the expression of genes related to fatty acid uptake, synthesis and gluconeogenesis, while increased the expression of genes related to fatty acid β-oxidation. Further, we identified that CFLAR is a direct downstream target of miR-150. Overexpression of miR-150 reduced both the mRNA and protein levels of CFLAR in vitro . And overexpression of miR-150 significantly inhibited the luciferase activity of CFLAR 3′-UTR, while the effect of miR-150 was blocked when the binding site of miR-150 within the CFLAR 3′-UTR was mutated. We also found that miR-150 deficiency decreased the expression of p -Jnk1 and p-Ask1, while the effect of miR-150 on steatosis and insulin signaling was blocked by CFLAR overexpression. In conclusion, our data indicated that miR-150 potentially contributes to the hepatic steatosis and insulin resistance in NAFLD. miR-150/CFLAR pathway may be a new therapeutic strategy against NAFLD.


  • 주제어

    miR-150 .   NAFLD .   Hepatic steatosis .   Insulin resistance .   CFLAR.  

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