Please use this identifier to cite or link to this item: http://hdl.handle.net/1893/26141
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dc.contributor.authorDent, Jessica Ren_UK
dc.contributor.authorMartins, Vitor Fen_UK
dc.contributor.authorSvensson, Kristofferen_UK
dc.contributor.authorLaBarge, Samuel Aen_UK
dc.contributor.authorSchlenk, Noah Cen_UK
dc.contributor.authorEsparza, Mary Cen_UK
dc.contributor.authorBuckner, Elisa Hen_UK
dc.contributor.authorMeyer, Gretchen Aen_UK
dc.contributor.authorHamilton, David Leeen_UK
dc.contributor.authorSchenk, Simonen_UK
dc.contributor.authorPhilp, Andrewen_UK
dc.date.accessioned2018-01-19T00:40:55Z-
dc.date.available2018-01-19T00:40:55Z-
dc.date.issued2017-12en_UK
dc.identifier.urihttp://hdl.handle.net/1893/26141-
dc.description.abstractObjective  Lysine acetylation is an important post-translational modification that regulates metabolic function in skeletal muscle. The acetyltransferase, general control of amino acid synthesis 5 (GCN5), has been proposed as a regulator of mitochondrial biogenesis via its inhibitory action on peroxisome proliferator activated receptor-γ coactivator-1α (PGC-1α). However, the specific contribution of GCN5 to skeletal muscle metabolism and mitochondrial adaptations to endurance exercise in vivo remain to be defined. We aimed to determine whether loss of GCN5 in skeletal muscle enhances mitochondrial density and function, and the adaptive response to endurance exercise training.  Methods  We used Cre-LoxP methodology to generate mice with muscle-specific knockout of GCN5 (mKO) and floxed, wildtype (WT) littermates. We measured whole-body energy expenditure, as well as markers of mitochondrial density, biogenesis, and function in skeletal muscle from sedentary mice, and mice that performed 20 days of voluntary endurance exercise training.  Results  Despite successful knockdown of GCN5 activity in skeletal muscle of mKO mice, whole-body energy expenditure as well as skeletal muscle mitochondrial abundance and maximal respiratory capacity were comparable between mKO and WT mice. Further, there were no genotype differences in endurance exercise-mediated mitochondrial biogenesis or increases in PGC-1α protein content.  Conclusion  These results demonstrate that loss of GCN5 in vivo does not promote metabolic remodeling in mouse skeletal muscle.en_UK
dc.language.isoenen_UK
dc.publisherElsevieren_UK
dc.relationDent JR, Martins VF, Svensson K, LaBarge SA, Schlenk NC, Esparza MC, Buckner EH, Meyer GA, Hamilton DL, Schenk S & Philp A (2017) Muscle-specific knockout of general control of amino acid synthesis 5 (GCN5) does not enhance basal or endurance exercise-induced mitochondrial adaptation. Molecular Metabolism, 6 (12), pp. 1574-1584. https://doi.org/10.1016/j.molmet.2017.10.004en_UK
dc.rightsCopyright 2017 The Authors. Published by Elsevier GmbH. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by- nc-nd/4.0/).en_UK
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/en_UK
dc.subjectAcetylationen_UK
dc.subjectGCN5en_UK
dc.subjectMitochondriaen_UK
dc.subjectSIRT1en_UK
dc.subjectDeacetylaseen_UK
dc.subjectPGC-1αen_UK
dc.titleMuscle-specific knockout of general control of amino acid synthesis 5 (GCN5) does not enhance basal or endurance exercise-induced mitochondrial adaptationen_UK
dc.typeJournal Articleen_UK
dc.identifier.doi10.1016/j.molmet.2017.10.004en_UK
dc.identifier.pmid29111103en_UK
dc.citation.jtitleMolecular Metabolismen_UK
dc.citation.issn2212-8778en_UK
dc.citation.volume6en_UK
dc.citation.issue12en_UK
dc.citation.spage1574en_UK
dc.citation.epage1584en_UK
dc.citation.publicationstatusPublisheden_UK
dc.citation.peerreviewedRefereeden_UK
dc.type.statusVoR - Version of Recorden_UK
dc.citation.date16/10/2017en_UK
dc.contributor.affiliationUniversity of Birminghamen_UK
dc.contributor.affiliationUniversity of California, San Diegoen_UK
dc.contributor.affiliationUniversity of California, San Diegoen_UK
dc.contributor.affiliationUniversity of California, San Diegoen_UK
dc.contributor.affiliationUniversity of California, San Diegoen_UK
dc.contributor.affiliationUniversity of California, San Diegoen_UK
dc.contributor.affiliationUniversity of California, San Diegoen_UK
dc.contributor.affiliationWashington University In Saint Louisen_UK
dc.contributor.affiliationSporten_UK
dc.contributor.affiliationUniversity of California, San Diegoen_UK
dc.contributor.affiliationUniversity of Birminghamen_UK
dc.identifier.isiWOS:000419084300002en_UK
dc.identifier.scopusid2-s2.0-85032193041en_UK
dc.identifier.wtid511725en_UK
dc.contributor.orcid0000-0002-5620-4788en_UK
dc.date.accepted2017-10-10en_UK
dcterms.dateAccepted2017-10-10en_UK
dc.date.filedepositdate2017-11-16en_UK
rioxxterms.apcnot requireden_UK
rioxxterms.typeJournal Article/Reviewen_UK
rioxxterms.versionVoRen_UK
local.rioxx.authorDent, Jessica R|en_UK
local.rioxx.authorMartins, Vitor F|en_UK
local.rioxx.authorSvensson, Kristoffer|en_UK
local.rioxx.authorLaBarge, Samuel A|en_UK
local.rioxx.authorSchlenk, Noah C|en_UK
local.rioxx.authorEsparza, Mary C|en_UK
local.rioxx.authorBuckner, Elisa H|en_UK
local.rioxx.authorMeyer, Gretchen A|en_UK
local.rioxx.authorHamilton, David Lee|0000-0002-5620-4788en_UK
local.rioxx.authorSchenk, Simon|en_UK
local.rioxx.authorPhilp, Andrew|en_UK
local.rioxx.projectInternal Project|University of Stirling|https://isni.org/isni/0000000122484331en_UK
local.rioxx.freetoreaddate2017-11-16en_UK
local.rioxx.licencehttp://creativecommons.org/licenses/by-nc-nd/4.0/|2017-11-16|en_UK
local.rioxx.filename1-s2.0-S2212877817306968-main.pdfen_UK
local.rioxx.filecount1en_UK
Appears in Collections:Faculty of Health Sciences and Sport Journal Articles

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