<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>38(4)</volume><submitter>Kiepura A</submitter><pubmed_abstract>&lt;h4>Background&lt;/h4>Nonalcoholic fatty liver disease (NAFLD) constitutes an independent risk factor for the development of coronary heart disease. Low-grade inflammation has been shown to play an important role in the development of atherosclerosis and NAFLD. Free fatty acid receptor 4 (FFAR4/GPR120), which is involved in damping inflammatory reactions, may represent a promising target for the treatment of inflammatory diseases. Our objective was to evaluate the effect of TUG-891, the synthetic agonist of FFAR4/GPR120, on fatty liver in vivo.&lt;h4>Methods&lt;/h4>The effect of TUG-891 on fatty liver was investigated in apoE&lt;sup>-/-&lt;/sup> mice fed a high-fat diet (HFD), using microscopic, biochemical, molecular, and proteomic methods.&lt;h4>Results&lt;/h4>Treatment with TUG-891 inhibited the progression</pubmed_abstract><journal>Cardiovascular drugs and therapy</journal><pagination>667-678</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11266261</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>The Influence of the FFAR4 Agonist TUG-891 on Liver Steatosis in ApoE-Knockout Mice.</pubmed_title><pmcid>PMC11266261</pmcid><pubmed_authors>Kus K</pubmed_authors><pubmed_authors>Wisniewska A</pubmed_authors><pubmed_authors>Ulatowska-Bialas M</pubmed_authors><pubmed_authors>Olszanecki R</pubmed_authors><pubmed_authors>Czepiel K</pubmed_authors><pubmed_authors>Stachyra K</pubmed_authors><pubmed_authors>Kiepura A</pubmed_authors><pubmed_authors>Suski M</pubmed_authors></additional><is_claimable>false</is_claimable><name>The Influence of the FFAR4 Agonist TUG-891 on Liver Steatosis in ApoE-Knockout Mice.</name><description>&lt;h4>Background&lt;/h4>Nonalcoholic fatty liver disease (NAFLD) constitutes an independent risk factor for the development of coronary heart disease. Low-grade inflammation has been shown to play an important role in the development of atherosclerosis and NAFLD. Free fatty acid receptor 4 (FFAR4/GPR120), which is involved in damping inflammatory reactions, may represent a promising target for the treatment of inflammatory diseases. Our objective was to evaluate the effect of TUG-891, the synthetic agonist of FFAR4/GPR120, on fatty liver in vivo.&lt;h4>Methods&lt;/h4>The effect of TUG-891 on fatty liver was investigated in apoE&lt;sup>-/-&lt;/sup> mice fed a high-fat diet (HFD), using microscopic, biochemical, molecular, and proteomic methods.&lt;h4>Results&lt;/h4>Treatment with TUG-891 inhibited the progression</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Aug</publication><modification>2026-05-27T12:12:29.638Z</modification><creation>2026-05-27T03:07:28.636Z</creation></dates><accession>S-EPMC11266261</accession><cross_references><pubmed>36705799</pubmed><doi>10.1007/s10557-023-07430-7</doi></cross_references></HashMap>