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dc.contributor.authorTurner, Nigel
dc.contributor.authorBruce, Clinton R.
dc.contributor.authorBeale, Susan M.
dc.contributor.authorHoehn, Kyle L.
dc.contributor.authorSo, Trina
dc.contributor.authorRolph, Michael S.
dc.contributor.authorCooney, Gregory J.
dc.date.accessioned2017-05-03T16:02:16Z
dc.date.available2017-05-03T16:02:16Z
dc.date.issued2007
dc.date.modified2011-05-30T06:56:35Z
dc.identifier.issn00121797
dc.identifier.doi10.2337/db07-0093
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.
dc.description.peerreviewedYes
dc.description.publicationstatusYes
dc.languageEnglish
dc.language.isoeng
dc.publisherAmerican Diabetes Association
dc.publisher.placeUnited States
dc.relation.ispartofstudentpublicationN
dc.relation.ispartofpagefrom2085
dc.relation.ispartofpageto2092
dc.relation.ispartofissue8
dc.relation.ispartofjournalDiabetes
dc.relation.ispartofvolume56
dc.rights.retentionY
dc.subject.fieldofresearchMetabolic Medicine
dc.subject.fieldofresearchMedical and Health Sciences
dc.subject.fieldofresearchcode110107
dc.subject.fieldofresearchcode11
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 rodents
dc.typeJournal article
dc.type.descriptionC1 - Articles
dc.type.codeC - Journal Articles
gro.date.issued2007
gro.hasfulltextNo Full Text
gro.griffith.authorRolph, Michael S.


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