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dc.contributor.authorTurner, Nigelen_US
dc.contributor.authorR. Bruce, Clintonen_US
dc.contributor.authorM. Beale, Susanen_US
dc.contributor.authorL. Hoehn, Kyleen_US
dc.contributor.authorSo, Trinaen_US
dc.contributor.authorS. Rolph, Michaelen_US
dc.contributor.authorJ. Cooney, Gregoryen_US
dc.date.accessioned2017-05-03T16:02:16Z
dc.date.available2017-05-03T16:02:16Z
dc.date.issued2007en_US
dc.date.modified2011-05-30T06:56:35Z
dc.identifier.issn00121797en_US
dc.identifier.doi10.2337/db07-0093en_AU
dc.identifier.urihttp://hdl.handle.net/10072/38874
dc.description.abstractA reduced capacity for mitochondrial fatty acid oxidation in skeletal muscle has been proposed as a major factor leading to the accumulation of intramuscular lipids and their subsequent deleterious effects on insulin action. Here, we examine markers of mitochondrial fatty acid oxidative capacity in rodent models of insulin resistance associated with an oversupply of lipids. C57BL/6J mice were fed a high-fat diet for either 5 or 20 weeks. Several markers of muscle mitochondrial fatty acid oxidative capacity were measured, including 14C-palmitate oxidation, palmitoyl-CoA oxidation in isolated mitochondria, oxidative enzyme activity (citrate synthase, ߭hydroxyacyl CoA dehydrogenase, medium-chain acyl-CoA dehydrogenase, and carnitine palmitoyl-transferase 1), and expression of proteins involved in mitochondrial metabolism. Enzyme activity and mitochondrial protein expression were also examined in muscle from other rodent models of insulin resistance. Compared with standard diet-fed controls, muscle from fat-fed mice displayed elevated palmitate oxidation rate (5 weeks +23%, P < 0.05, and 20 weeks +29%, P < 0.05) and increased palmitoyl-CoA oxidation in isolated mitochondria (20 weeks +49%, P < 0.01). Furthermore, oxidative enzyme activity and protein expression of peroxisome proliferator-activated receptor ? coactivator (PGC)-1a, uncoupling protein (UCP) 3, and mitochondrial respiratory chain subunits were significantly elevated in fat-fed animals. A similar pattern was present in muscle of fat-fed rats, obese Zucker rats, and db/db mice, with increases observed for oxidative enzyme activity and expression of PGC-1a, UCP3, and subunits of the mitochondrial respiratory chain. These findings suggest that high lipid availability does not lead to intramuscular lipid accumulation and insulin resistance in rodents by decreasing muscle mitochondrial fatty acid oxidative capacity.en_US
dc.description.peerreviewedYesen_US
dc.description.publicationstatusYesen_AU
dc.languageEnglishen_US
dc.language.isoen_AU
dc.publisherAmerican Diabetes Associationen_US
dc.publisher.placeUnited Statesen_US
dc.relation.ispartofstudentpublicationNen_AU
dc.relation.ispartofpagefrom2085en_US
dc.relation.ispartofpageto2092en_US
dc.relation.ispartofissue8en_US
dc.relation.ispartofjournalDiabetesen_US
dc.relation.ispartofvolume56en_US
dc.rights.retentionYen_AU
dc.subject.fieldofresearchMetabolic Medicineen_US
dc.subject.fieldofresearchcode110107en_US
dc.titleExcess lipid availability increases mitochondrial fatty acid oxidative capacity in muscle: evidence against a role for reduced fatty acid oxidation in lipid-induced insulin resistance in rodentsen_US
dc.typeJournal articleen_US
dc.type.descriptionC1 - Peer Reviewed (HERDC)en_US
dc.type.codeC - Journal Articlesen_US
gro.date.issued2007
gro.hasfulltextNo Full Text


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