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dc.contributor.authorPhilp, Andrewen_UK
dc.contributor.authorPerez-Schindler, Joaquinen_UK
dc.contributor.authorGreen, Charlotteen_UK
dc.contributor.authorHamilton, David Leeen_UK
dc.contributor.authorBaar, Keithen_UK
dc.description.abstractSodium pyruvate can increase mitochondrial biogenesis in C2C12 myoblasts in a peroxisome proliferator-activated receptor-γ coactivator-1α (PGC1α)-independent manner. The present study examined the effect of 72-h treatment with sodium pyruvate (5-50 mM) or sodium chloride (50 mM) as an osmotic control on the regulation of mitochondrial substrate metabolism and biogenesis in C2C12 myotubes. Pyruvate (50 mM) increased the levels of fatty acid oxidation enzymes (CD36, 61%, and β-oxidative enzyme 3-hydroxyacyl-CoA dehydrogenase, 54%) and the expression of cytochrome-c oxidase subunit I (220%) and cytochrome c (228%), consistent with its previous described role as a promoter of mitochondrial biogenesis. However, in contrast, pyruvate treatment reduced glucose transporter 4 (42%), phosphofructokinase (57%), and PGC1α (72%) protein content as well as PGC1α (48%) and PGC1β (122%) mRNA. The decrease in PGC1α was compensated for by an increase in the PGC1α-related coactivator (PRC; 187%). Pyruvate treatment reduced basal and insulin-stimulated glucose uptake (41% and 31%, respectively) and palmitate uptake and oxidation (24% and 31%, respectively). The addition of the pyruvate dehydrogenase activator dichloroacetate (DCA) and the TCA precursor glutamine increased PGC1α expression (368%) and returned PRC expression to basal. Glucose uptake increased by 4.2-fold with DCA and glutamine and palmitate uptake increased by 18%. Coupled to this adaptation was an 80% increase in oxygen consumption. The data suggest that supraphysiological doses of pyruvate decrease mitochondrial function despite limited biogenesis and that anaplerotic agents can reverse this effect.en_UK
dc.publisherAmerican Physiological Societyen_UK
dc.relationPhilp A, Perez-Schindler J, Green C, Hamilton DL & Baar K (2010) Pyruvate suppresses PGC1 alpha expression and substrate utilization despite increased respiratory chain content in C2C12 myotubes. American Journal of Physiology - Cell Physiology, 299 (2), pp. C240-C250.
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.subjectglucose metabolismen_UK
dc.subjectType 2 diabetesen_UK
dc.subjectperoxisome proliferator-activated receptor-gamma coactivator-1 alphaen_UK
dc.subjectDiabetes Mellitus, Type 2 therapyen_UK
dc.subjectEvidence-Based Medicineen_UK
dc.titlePyruvate suppresses PGC1 alpha expression and substrate utilization despite increased respiratory chain content in C2C12 myotubesen_UK
dc.typeJournal Articleen_UK
dc.rights.embargoreason[Hamilton_2010_Pyruvate_suppresses_PGC1alpha_expression.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.citation.jtitleAmerican Journal of Physiology - Cell Physiologyen_UK
dc.type.statusVoR - Version of Recorden_UK
dc.contributor.affiliationUniversity of Dundeeen_UK
dc.contributor.affiliationUniversity of Dundeeen_UK
dc.contributor.affiliationUniversity of Dundeeen_UK
dc.contributor.affiliationUniversity of Dundeeen_UK
rioxxterms.typeJournal Article/Reviewen_UK
local.rioxx.authorPhilp, Andrew|en_UK
local.rioxx.authorPerez-Schindler, Joaquin|en_UK
local.rioxx.authorGreen, Charlotte|en_UK
local.rioxx.authorHamilton, David Lee|0000-0002-5620-4788en_UK
local.rioxx.authorBaar, Keith|en_UK
local.rioxx.projectInternal Project|University of Stirling|
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