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  • Title: Up-regulation of microRNA-367 promotes liver steatosis through repressing TBL1 in obese mice.
    Author: Li DD, Liu Y, Xue L, Su DY, Pang WY.
    Journal: Eur Rev Med Pharmacol Sci; 2017 Apr; 21(7):1598-1603. PubMed ID: 28429344.
    Abstract:
    OBJECTIVE: Increasing evidence has demonstrated that microRNAs (miRNAs) play a critical role in the progression of metabolic disorders, including obesity-induced non-alcoholic fatty liver disease (NAFLD). In the present study, the expression and function of miR-367 were investigated. MATERIALS AND METHODS: C57BL/6 male mice aged 8 weeks were fed with a normal diet (ND) or high-fat-diet (HFD). The expression levels of miR-367 were analyzed in livers from two groups of mice by quantitative real-time PCR. Adenovirus containing miR-367 or negative control (NC) were constructed and administrated into C57BL/6 mice by tail vain injection. Potential targets of miR-367 were screened by miRWalk software and luciferase reporter assays. Mutagenesis analysis and Western blots were used to further determine the target of miR-367 in obese mice. RESULTS: We found that the expression of hepatic miR-367 was up-regulated in obese mice. In vitro and in vivo studies further demonstrated that overexpression of miR-367 mimics promoted triglyceride accumulation in cells and lean mice. At the molecular level, transducin beta-like 1 (TBL1), a coactivator of nuclear receptor peroxisome proliferator-activated receptor (PPAR) α, was identified as a direct target of miR-367. As a result, miR-367 overexpression resulted in an inhibition of fatty acid oxidation, leading to hepatosteatosis. CONCLUSIONS: Our data suggest miR-367/TBL1 regulatory pathway might have an important role for in the development of NAFLD.
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