<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Daniel N</submitter><funding>Quebec Cardiometabolic Health, Diabetes and Obesity</funding><funding>Canadian Institutes of Health Research</funding><funding>CIHR</funding><pagination>zqac069</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9909367</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>4(2)</volume><pubmed_abstract>We compared endogenous ω-3 PUFA production to supplementation for improving obesity-related metabolic dysfunction. Fat-1 transgenic mice, who endogenously convert exogenous ω-6 to ω-3 PUFA, and wild-type littermates were fed a high-fat diet and a daily dose of either ω-3 or ω-6 PUFA-rich oil for 12 wk. The endogenous ω-3 PUFA production improved glucose intolerance and insulin resistance but not hepatic steatosis. Conversely, ω-3 PUFA supplementation fully prevented hepatic steatosis but failed to improve insulin resistance. Both models increased hepatic levels of ω-3 PUFA-containing 2-monoacylglycerol and N-acylethanolamine congeners, and reduced levels of ω-6 PUFA-derived endocannabinoids with ω-3 PUFA supplementation being more efficacious. Reduced hepatic lipid accumulation associated </pubmed_abstract><journal>Function (Oxford, England)</journal><pubmed_title>Comparing Transgenic Production to Supplementation of ω-3 PUFA Reveals Distinct But Overlapping Mechanisms Underlying Protection Against Metabolic and Hepatic Disorders.</pubmed_title><pmcid>PMC9909367</pmcid><funding_grant_id>FDN-746 143247</funding_grant_id><pubmed_authors>Le Barz M</pubmed_authors><pubmed_authors>Garofalo C</pubmed_authors><pubmed_authors>Jobin C</pubmed_authors><pubmed_authors>Julien IB</pubmed_authors><pubmed_authors>Gauthier J</pubmed_authors><pubmed_authors>Kang JX</pubmed_authors><pubmed_authors>Chassaing B</pubmed_authors><pubmed_authors>Farabos D</pubmed_authors><pubmed_authors>Flamand N</pubmed_authors><pubmed_authors>Mitchell PL</pubmed_authors><pubmed_authors>Di Marzo V</pubmed_authors><pubmed_authors>Varin TV</pubmed_authors><pubmed_authors>Daniel N</pubmed_authors><pubmed_authors>Levy E</pubmed_authors><pubmed_authors>Lamaziere A</pubmed_authors><pubmed_authors>Roy D</pubmed_authors><pubmed_authors>Raymond F</pubmed_authors><pubmed_authors>Barbier O</pubmed_authors><pubmed_authors>Silvestri C</pubmed_authors><pubmed_authors>Pilon G</pubmed_authors><pubmed_authors>Trottier J</pubmed_authors><pubmed_authors>Marette A</pubmed_authors></additional><is_claimable>false</is_claimable><name>Comparing Transgenic Production to Supplementation of ω-3 PUFA Reveals Distinct But Overlapping Mechanisms Underlying Protection Against Metabolic and Hepatic Disorders.</name><description>We compared endogenous ω-3 PUFA production to supplementation for improving obesity-related metabolic dysfunction. Fat-1 transgenic mice, who endogenously convert exogenous ω-6 to ω-3 PUFA, and wild-type littermates were fed a high-fat diet and a daily dose of either ω-3 or ω-6 PUFA-rich oil for 12 wk. The endogenous ω-3 PUFA production improved glucose intolerance and insulin resistance but not hepatic steatosis. Conversely, ω-3 PUFA supplementation fully prevented hepatic steatosis but failed to improve insulin resistance. Both models increased hepatic levels of ω-3 PUFA-containing 2-monoacylglycerol and N-acylethanolamine congeners, and reduced levels of ω-6 PUFA-derived endocannabinoids with ω-3 PUFA supplementation being more efficacious. Reduced hepatic lipid accumulation associated </description><dates><release>2023-01-01T00:00:00Z</release><publication>2023</publication><modification>2025-04-04T20:17:47.946Z</modification><creation>2025-02-19T03:30:42.692Z</creation></dates><accession>S-EPMC9909367</accession><cross_references><pubmed>36778746</pubmed><doi>10.1093/function/zqac069</doi></cross_references></HashMap>