Please use this identifier to cite or link to this item: http://hdl.handle.net/1893/22898
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dc.contributor.authorWhite, Amanda Ten_UK
dc.contributor.authorPhilp, Andrewen_UK
dc.contributor.authorFridolfsson, Heidi Nen_UK
dc.contributor.authorSchilling, Jan Men_UK
dc.contributor.authorMurphy, Anne Nen_UK
dc.contributor.authorHamilton, David Leeen_UK
dc.contributor.authorMcCurdy, Carrie Een_UK
dc.contributor.authorPatel, Hemal Hen_UK
dc.contributor.authorSchenk, Simonen_UK
dc.date.accessioned2016-09-14T22:39:33Z-
dc.date.available2016-09-14T22:39:33Z-
dc.date.issued2014-11-01en_UK
dc.identifier.urihttp://hdl.handle.net/1893/22898-
dc.description.abstractSkeletal muscle sirtuin 1 (SIRT1) expression is reduced under insulin-resistant conditions, such as those resulting from high-fat diet (HFD) feeding and obesity. Herein, we investigated whether constitutive activation of SIRT1 in skeletal muscle prevents HFD-induced muscle insulin resistance. To address this, mice with muscle-specific overexpression of SIRT1 (mOX) and wild-type (WT) littermates were fed a control diet (10% calories from fat) or HFD (60% of calories from fat) for 12 wk. Magnetic resonance imaging and indirect calorimetry were used to measure body composition and energy expenditure, respectively. Whole body glucose metabolism was assessed by oral glucose tolerance test, and insulin-stimulated glucose uptake was measured at a physiological insulin concentration in isolated soleus and extensor digitorum longus muscles. Although SIRT1 was significantly overexpressed in muscle of mOX vs. WT mice, body weight and percent body fat were similarly increased by HFD for both genotypes, and energy expenditure was unaffected by diet or genotype. Importantly, impairments in glucose tolerance and insulin-mediated activation of glucose uptake in skeletal muscle that occurred with HFD feeding were not prevented in mOX mice. In contrast, mOX mice showed enhanced postischemic cardiac functional recovery compared with WT mice, confirming the physiological functionality of the SIRT1 transgene in this mouse model. Together, these results demonstrate that activation of SIRT1 in skeletal muscle alone does not prevent HFD-induced glucose intolerance, weight gain, or insulin resistance.en_UK
dc.language.isoenen_UK
dc.publisherAmerican Physiological Societyen_UK
dc.relationWhite AT, Philp A, Fridolfsson HN, Schilling JM, Murphy AN, Hamilton DL, McCurdy CE, Patel HH & Schenk S (2014) High-fat diet-induced impairment of skeletal muscle insulin sensitivity is not prevented by SIRT1 overexpression. American Journal of Physiology - Endocrinology and Metabolism, 307 (9), pp. E764-E772. https://doi.org/10.1152/ajpendo.00001.2014en_UK
dc.rightsThe publisher does not allow this work to be made publicly available in this Repository. Please use the Request a Copy feature at the foot of the Repository record to request a copy directly from the author. You can only request a copy if you wish to use this work for your own research or private study.en_UK
dc.rights.urihttp://www.rioxx.net/licenses/under-embargo-all-rights-reserveden_UK
dc.titleHigh-fat diet-induced impairment of skeletal muscle insulin sensitivity is not prevented by SIRT1 overexpressionen_UK
dc.typeJournal Articleen_UK
dc.rights.embargodate2999-12-27en_UK
dc.rights.embargoreason[White et al_Am J Physiol Endocrinol Metab_2014.pdf] The publisher does not allow this work to be made publicly available in this Repository therefore there is an embargo on the full text of the work.en_UK
dc.identifier.doi10.1152/ajpendo.00001.2014en_UK
dc.identifier.pmid25159328en_UK
dc.citation.jtitleAmerican journal of physiology. Endocrinology and metabolismen_UK
dc.citation.issn1522-1555en_UK
dc.citation.issn0193-1849en_UK
dc.citation.volume307en_UK
dc.citation.issue9en_UK
dc.citation.spageE764en_UK
dc.citation.epageE772en_UK
dc.citation.publicationstatusPublisheden_UK
dc.citation.peerreviewedRefereeden_UK
dc.type.statusVoR - Version of Recorden_UK
dc.author.emaild.l.hamilton@stir.ac.uken_UK
dc.citation.date26/08/2014en_UK
dc.contributor.affiliationUniversity of California, San Diegoen_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.affiliationSporten_UK
dc.contributor.affiliationUniversity of Oregonen_UK
dc.contributor.affiliationUniversity of California, San Diegoen_UK
dc.contributor.affiliationUniversity of California, San Diegoen_UK
dc.identifier.isiWOS:000344989400004en_UK
dc.identifier.scopusid2-s2.0-84908360911en_UK
dc.identifier.wtid576965en_UK
dc.contributor.orcid0000-0002-5620-4788en_UK
dc.date.accepted2014-08-20en_UK
dcterms.dateAccepted2014-08-20en_UK
dc.date.filedepositdate2016-03-03en_UK
rioxxterms.apcnot requireden_UK
rioxxterms.typeJournal Article/Reviewen_UK
rioxxterms.versionVoRen_UK
local.rioxx.authorWhite, Amanda T|en_UK
local.rioxx.authorPhilp, Andrew|en_UK
local.rioxx.authorFridolfsson, Heidi N|en_UK
local.rioxx.authorSchilling, Jan M|en_UK
local.rioxx.authorMurphy, Anne N|en_UK
local.rioxx.authorHamilton, David Lee|0000-0002-5620-4788en_UK
local.rioxx.authorMcCurdy, Carrie E|en_UK
local.rioxx.authorPatel, Hemal H|en_UK
local.rioxx.authorSchenk, Simon|en_UK
local.rioxx.projectInternal Project|University of Stirling|https://isni.org/isni/0000000122484331en_UK
local.rioxx.freetoreaddate2999-12-27en_UK
local.rioxx.licencehttp://www.rioxx.net/licenses/under-embargo-all-rights-reserved||en_UK
local.rioxx.filenameWhite et al_Am J Physiol Endocrinol Metab_2014.pdfen_UK
local.rioxx.filecount1en_UK
local.rioxx.source0193-1849en_UK
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