<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Horakova O</submitter><funding>European Commission FP7</funding><pagination>e43764</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3432031</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>7(8)</volume><pubmed_abstract>Insulin resistance, the key defect in type 2 diabetes (T2D), is associated with a low capacity to adapt fuel oxidation to fuel availability, i.e., metabolic inflexibility. This, in turn, contributes to a further damage of insulin signaling. Effectiveness of T2D treatment depends in large part on the improvement of insulin sensitivity and metabolic adaptability of the muscle, the main site of whole-body glucose utilization. We have shown previously in mice fed an obesogenic high-fat diet that a combined use of n-3 long-chain polyunsaturated fatty acids (n-3 LC-PUFA) and thiazolidinediones (TZDs), anti-diabetic drugs, preserved metabolic health and synergistically improved muscle insulin sensitivity. We investigated here whether n-3 LC-PUFA could elicit additive beneficial effects on metabol</pubmed_abstract><journal>PloS one</journal><pubmed_title>Preservation of metabolic flexibility in skeletal muscle by a combined use of n-3 PUFA and rosiglitazone in dietary obese mice.</pubmed_title><pmcid>PMC3432031</pmcid><funding_grant_id>FP7_244995</funding_grant_id><pubmed_authors>Bardova K</pubmed_authors><pubmed_authors>Kopecky J</pubmed_authors><pubmed_authors>Hensler M</pubmed_authors><pubmed_authors>Rossmeisl M</pubmed_authors><pubmed_authors>Kus V</pubmed_authors><pubmed_authors>Medrikova D</pubmed_authors><pubmed_authors>Kuda O</pubmed_authors><pubmed_authors>Keijer J</pubmed_authors><pubmed_authors>Illig T</pubmed_authors><pubmed_authors>Horakova O</pubmed_authors><pubmed_authors>Adamski J</pubmed_authors><pubmed_authors>Prehn C</pubmed_authors><pubmed_authors>Bunschoten A</pubmed_authors><pubmed_authors>Janovska P</pubmed_authors><pubmed_authors>Wang-Sattler R</pubmed_authors><pubmed_authors>Flachs P</pubmed_authors><pubmed_authors>van Schothorst EM</pubmed_authors></additional><is_claimable>false</is_claimable><name>Preservation of metabolic flexibility in skeletal muscle by a combined use of n-3 PUFA and rosiglitazone in dietary obese mice.</name><description>Insulin resistance, the key defect in type 2 diabetes (T2D), is associated with a low capacity to adapt fuel oxidation to fuel availability, i.e., metabolic inflexibility. This, in turn, contributes to a further damage of insulin signaling. Effectiveness of T2D treatment depends in large part on the improvement of insulin sensitivity and metabolic adaptability of the muscle, the main site of whole-body glucose utilization. We have shown previously in mice fed an obesogenic high-fat diet that a combined use of n-3 long-chain polyunsaturated fatty acids (n-3 LC-PUFA) and thiazolidinediones (TZDs), anti-diabetic drugs, preserved metabolic health and synergistically improved muscle insulin sensitivity. We investigated here whether n-3 LC-PUFA could elicit additive beneficial effects on metabol</description><dates><release>2012-01-01T00:00:00Z</release><publication>2012</publication><modification>2026-05-04T07:29:13.52Z</modification><creation>2019-03-26T23:11:15Z</creation></dates><accession>S-EPMC3432031</accession><cross_references><pubmed>22952760</pubmed><doi>10.1371/journal.pone.0043764</doi></cross_references></HashMap>