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dc.contributor.authorPedraza González, Neus
dc.contributor.authorRosell, Meritxell
dc.contributor.authorVillarroya, Joan
dc.contributor.authorIglesias, Roser
dc.contributor.authorGonzalez, Frank J.
dc.contributor.authorSolanes, Gemma
dc.contributor.authorVillarroya, Francesc
dc.date.accessioned2017-01-18T11:15:58Z
dc.date.issued2006
dc.identifier.issn0013-7227
dc.identifier.urihttp://hdl.handle.net/10459.1/59021
dc.description.abstractUncoupling protein-3 (UCP3) is a member of the mitochondrial carrier family expressed preferentially in skeletal muscle and heart. It appears to be involved in metabolic handling of fatty acids in a way that minimizes excessive production of reactive oxygen species. Fatty acids are powerful regulators of UCP3 gene transcription. We have found that the role of peroxisome proliferator-activated receptor- (PPAR ) on the control of UCP3 gene expression depends on the tissue and developmental stage. In adults, UCP3 mRNA expression is unaltered in skeletal muscle from PPAR -null mice both in basal conditions and under the stimulus of starvation. In contrast, UCP3mRNAis down-regulated in adult heart both in fed and fasted PPAR -null mice. This occurs despite the increased levels of free fatty acids caused by fasting in PPAR - null mice. In neonates, PPAR -null mice show impaired UCP3 mRNA expression in skeletal muscle in response to milk intake, and this is not a result of reduced free fatty acid levels. The murineUCP3promoter is activated by fatty acids through either PPAR or PPAR but not by PPAR or retinoid X receptor alone. PPAR -dependent activation could be a potential compensatory mechanism to ensure appropriate expression of UCP3 gene in adult skeletal muscle in the absence of PPAR . However, among transcripts from other PPAR and PPAR target genes, only those acutely induced by milk intake in wild-type neonates were altered in muscle or heart from PPAR -null neonates. Thus, PPAR -dependent regulation is required for appropriate gene regulation of UCP3 as part of the subset of fatty-acid-responsive genes in neonatal muscle and heart.ca_ES
dc.description.sponsorshipWe thank Drs. S. Green, P. Grimaldi, R. Evans, and L. Fajas for kindly supplying expression vectors and Dr. Chandraratna for AGN 194204. Address all correspondence and requests for reprints to: Dr. G. Solanes, Departament de Bioquı´mica i Biologia Molecular, Universitat de Barcelona, Avda Diagonal 645, E-08028 Barcelona, Spain. E mail: gsolanes@ub.edu. This work was supported by Grants SAF2002-03648 and SAF2005- 01722 from Ministerio de Educacio´n y Ciencia and Grant C03/08 from Instituto de Salud Carlos III, Ministerio de Sanidad y Consumo, Spain. Disclosure of potential conflicts of interest: N.P., M.R., J.V., R.I., F.J.G., G.S., and F.V. have nothing to declareca_ES
dc.language.isoengca_ES
dc.publisherEndocrine Societyca_ES
dc.relationMICYT/PN2000-2003/SAF2002-03648ca_ES
dc.relationMIECI/PN2004-2007/SAF2005-01722ca_ES
dc.relation.isformatofReproducció del document publicat a https://doi.org/10.1210/en.2006-0226ca_ES
dc.relation.ispartofEndocrinology, 2006, vol. 147, núm. 10, p. 4695-4704ca_ES
dc.rights(c) The Endocrine Society, 2006ca_ES
dc.titleDevelopmental and Tissue-Specific Involvement of Peroxisome Proliferator-Activated Receptor-α in the Control of Mouse Uncoupling Protein-3 Gene Expressionca_ES
dc.typearticleca_ES
dc.type.versionpublishedVersionca_ES
dc.rights.accessRightsinfo:eu-repo/semantics/restrictedAccessca_ES
dc.identifier.doihttps://doi.org/10.1210/en.2006-0226
dc.date.embargoEndDate2025-01-01


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