<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Xiao J</submitter><funding>Shanghai Municipal Education Commission</funding><funding>National Natural Science Foundation of China</funding><funding>China Postdoctoral Science Foundation</funding><funding>Shanghai University of Sport</funding><funding>Chinese Foundation for Hepatitis Prevention and Control of the WBN Research Foundation</funding><pagination>204-16</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4727558</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>20(2)</volume><pubmed_abstract>Non-alcoholic fatty liver disease (NAFLD) is associated with obesity and lifestyle, while exercise is beneficial for NAFLD. Dysregulated microRNAs (miRs) control the pathogenesis of NAFLD. However, whether exercise could prevent NAFLD via targeting microRNA is unknown. In this study, normal or high-fat diet (HF) mice were either subjected to a 16-week running program or kept sedentary. Exercise attenuated liver steatosis in HF mice. MicroRNA array and qRT-PCR demonstrated that miR-212 was overexpressed in HF liver, while reduced by exercise. Next, we investigated the role of miR-212 in lipogenesis using HepG2 cells with/without long-chain fatty acid treatment (± FFA). FFA increased miR-212 in HepG2 cells. Moreover, miR-212 promoted lipogenesis in HepG2 cells (± FFA). Fibroblast growth fact</pubmed_abstract><journal>Journal of cellular and molecular medicine</journal><pubmed_title>miR-212 downregulation contributes to the protective effect of exercise against non-alcoholic fatty liver via targeting FGF-21.</pubmed_title><pmcid>PMC4727558</pmcid><funding_grant_id>81370559</funding_grant_id><funding_grant_id>81400647</funding_grant_id><funding_grant_id>2014M561456</funding_grant_id><funding_grant_id>81400635</funding_grant_id><funding_grant_id>81170406</funding_grant_id><funding_grant_id>TQGB20140141</funding_grant_id><funding_grant_id>13YZ014</funding_grant_id><funding_grant_id>sdcx2012038</funding_grant_id><funding_grant_id>81200169</funding_grant_id><funding_grant_id>81570362</funding_grant_id><funding_grant_id>81070343</funding_grant_id><pubmed_authors>Kuang D</pubmed_authors><pubmed_authors>Yang W</pubmed_authors><pubmed_authors>Liu J</pubmed_authors><pubmed_authors>Li J</pubmed_authors><pubmed_authors>Yang Y</pubmed_authors><pubmed_authors>Zhou Q</pubmed_authors><pubmed_authors>Xiao J</pubmed_authors><pubmed_authors>Dimitrova-Shumkovska J</pubmed_authors><pubmed_authors>Xiang Y</pubmed_authors><pubmed_authors>Wang F</pubmed_authors><pubmed_authors>Yang C</pubmed_authors><pubmed_authors>Bei Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>miR-212 downregulation contributes to the protective effect of exercise against non-alcoholic fatty liver via targeting FGF-21.</name><description>Non-alcoholic fatty liver disease (NAFLD) is associated with obesity and lifestyle, while exercise is beneficial for NAFLD. Dysregulated microRNAs (miRs) control the pathogenesis of NAFLD. However, whether exercise could prevent NAFLD via targeting microRNA is unknown. In this study, normal or high-fat diet (HF) mice were either subjected to a 16-week running program or kept sedentary. Exercise attenuated liver steatosis in HF mice. MicroRNA array and qRT-PCR demonstrated that miR-212 was overexpressed in HF liver, while reduced by exercise. Next, we investigated the role of miR-212 in lipogenesis using HepG2 cells with/without long-chain fatty acid treatment (± FFA). FFA increased miR-212 in HepG2 cells. Moreover, miR-212 promoted lipogenesis in HepG2 cells (± FFA). Fibroblast growth fact</description><dates><release>2016-01-01T00:00:00Z</release><publication>2016 Feb</publication><modification>2025-04-04T20:30:34.011Z</modification><creation>2019-08-04T07:56:29Z</creation></dates><accession>S-EPMC4727558</accession><cross_references><pubmed>26648452</pubmed><doi>10.1111/jcmm.12733</doi></cross_references></HashMap>