<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Yang W</submitter><funding>NIDDK NIH HHS</funding><funding>NIAID NIH HHS</funding><funding>National Institutes of Health</funding><pagination>150-165</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8678294</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>162(1)</volume><pubmed_abstract>&lt;h4>Background &amp; aims&lt;/h4>G protein-coupled receptor (GPR) 120 has been implicated in regulating metabolic syndromes with anti-inflammatory function. However, the role of GPR120 in intestinal inflammation is unknown. Here, we investigated whether and how GPR120 regulates CD4&lt;sup>+&lt;/sup> T cell function to inhibit colitis development.&lt;h4>Methods&lt;/h4>Dextran sodium sulfate (DSS)-induced colitis model, Citrobacter rodentium infection model, and CD4&lt;sup>+&lt;/sup> T cell adoptive transfer model were used to analyze the role of GPR120 in regulating colitis development. The effect of GPR120 on CD4&lt;sup>+&lt;/sup> T cell functions was analyzed by RNA sequencing, flow cytometry, and Seahorse metabolic assays. Mice were administered GPR120 agonist for investigating the potential of GPR120 agonist in preve</pubmed_abstract><journal>Gastroenterology</journal><pubmed_title>GPR120 Inhibits Colitis Through Regulation of CD4&lt;sup>+&lt;/sup> T Cell Interleukin 10 Production.</pubmed_title><pmcid>PMC8678294</pmcid><funding_grant_id>R21 AI150210</funding_grant_id><funding_grant_id>R01 DK125011</funding_grant_id><funding_grant_id>R01 DK124132</funding_grant_id><pubmed_authors>Liu H</pubmed_authors><pubmed_authors>Xu L</pubmed_authors><pubmed_authors>Zhang H</pubmed_authors><pubmed_authors>Zuo X</pubmed_authors><pubmed_authors>Yao S</pubmed_authors><pubmed_authors>Barnes S</pubmed_authors><pubmed_authors>Zhao X</pubmed_authors><pubmed_authors>Yang W</pubmed_authors><pubmed_authors>Li Y</pubmed_authors><pubmed_authors>Dann SM</pubmed_authors><pubmed_authors>Zhao Q</pubmed_authors><pubmed_authors>Yu T</pubmed_authors><pubmed_authors>Cong Y</pubmed_authors><pubmed_authors>Cohn SM</pubmed_authors></additional><is_claimable>false</is_claimable><name>GPR120 Inhibits Colitis Through Regulation of CD4&lt;sup>+&lt;/sup> T Cell Interleukin 10 Production.</name><description>&lt;h4>Background &amp; aims&lt;/h4>G protein-coupled receptor (GPR) 120 has been implicated in regulating metabolic syndromes with anti-inflammatory function. However, the role of GPR120 in intestinal inflammation is unknown. Here, we investigated whether and how GPR120 regulates CD4&lt;sup>+&lt;/sup> T cell function to inhibit colitis development.&lt;h4>Methods&lt;/h4>Dextran sodium sulfate (DSS)-induced colitis model, Citrobacter rodentium infection model, and CD4&lt;sup>+&lt;/sup> T cell adoptive transfer model were used to analyze the role of GPR120 in regulating colitis development. The effect of GPR120 on CD4&lt;sup>+&lt;/sup> T cell functions was analyzed by RNA sequencing, flow cytometry, and Seahorse metabolic assays. Mice were administered GPR120 agonist for investigating the potential of GPR120 agonist in preve</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Jan</publication><modification>2025-04-21T14:26:58.01Z</modification><creation>2025-02-18T22:34:23.376Z</creation></dates><accession>S-EPMC8678294</accession><cross_references><pubmed>34536451</pubmed><doi>10.1053/j.gastro.2021.09.018</doi></cross_references></HashMap>