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  • Title: Exercise-Induced ADAR2 Protects against Nonalcoholic Fatty Liver Disease through miR-34a.
    Author: Wang Z, Zhu Y, Xia L, Li J, Song M, Yang C.
    Journal: Nutrients; 2022 Dec 27; 15(1):. PubMed ID: 36615779.
    Abstract:
    Nonalcoholic fatty liver disease (NAFLD) is a growing health problem that is closely associated with insulin resistance and hereditary susceptibility. Exercise is a beneficial approach to NAFLD. However, the relief mechanism of exercise training is still unknown. In this study, mice on a normal diet or a high-fat diet (HFD), combined with Nω-nitro-L-arginine methyl ester, hydrochloride (L-NAME) mice, were either kept sedentary or were subjected to a 12-week exercise running scheme. We found that exercise reduced liver steatosis in mice with diet-induced NAFLD. The hepatic adenosine deaminases acting on RNA 2 (ADAR2) were downregulated in NAFLD and were upregulated in the liver after 12-week exercise. Next, overexpression of ADAR2 inhibited and suppression promoted lipogenesis in HepG2 cells treated with oleic acid (OA), respectively. We found that ADAR2 could down-regulate mature miR-34a in hepatocytes. Functional reverse experiments further proved that miR-34a mimicry eliminated the suppression of ADAR2 overexpression in lipogenesis in vitro. Moreover, miR-34a inhibition and mimicry could also affect lipogenesis in hepatocytes. In conclusion, exercise-induced ADAR2 protects against lipogenesis during NAFLD by editing miR-34a. RNA editing mediated by ADAR2 may be a promising therapeutic candidate for NAFLD.
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