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dc.rights.licensehttp://creativecommons.org/licenses/by/4.0es_MX
dc.creatorDavid Frederick Fletcheres_MX
dc.creatorJames G. Davises_MX
dc.creatorAntonio Davilaes_MX
dc.creatorBeamon Agarwales_MX
dc.creatorSHADAY MICHAN AGUIRREes_MX
dc.creatorMichelle Puchowiczes_MX
dc.creatorEiko Nakamaru-Ogisoes_MX
dc.creatorJoseph Baures_MX
dc.date2015-
dc.date.accessioned2021-09-14T17:46:32Z-
dc.date.available2021-09-14T17:46:32Z-
dc.identifier.urihttp://repositorio.inger.gob.mx/jspui/handle/20.500.12100/17241-
dc.descriptionThe NAD biosynthetic precursors nicotinamide mononucleotide and nicotinamide riboside are reported to confer resistance to metabolic defects induced by high fat feeding in part by promoting oxidative metabolism in skeletal muscle. Similar effects are obtained by germ line deletion of major NAD-consuming enzymes, suggesting that the bioavailability of NAD is limiting for maximal oxidative capacity. However, because of their systemic nature, the degree to which these interventions exert cell- or tissue-autonomous effects is unclear. Here, we report a tissue-specific approach to increase NAD biosynthesis only in muscle by overexpressing nicotinamide phosphoribosyltransferase, the rate-limiting enzyme in the salvage pathway that converts nicotinamide to NAD (mNAMPT mice). These mice display a ∼50% increase in skeletal muscle NAD levels, comparable with the effects of dietary NAD precursors, exercise regimens, or loss of poly(ADP-ribose) polymerases yet surprisingly do not exhibit changes in muscle mitochondrial biogenesis or mitochondrial function and are equally susceptible to the metabolic consequences of high fat feeding. We further report that chronic elevation of muscle NAD in vivo does not perturb the NAD/NADH redox ratio. These studies reveal for the first time the metabolic effects of tissue-specific increases in NAD synthesis and suggest that critical sites of action for supplemental NAD precursors reside outside of the heart and skeletal muscle.es_MX
dc.formatAdobe PDFes_MX
dc.languageenges_MX
dc.publisherAmerican Society for Biochemistry and Molecular Biologyes_MX
dc.relationhttp://www.jbc.org/content/290/3/1546.longes_MX
dc.relation.requiresSies_MX
dc.rightsAcceso Abiertoes_MX
dc.sourceJournal of Biological Chemistry (1083-351X) vol. 290 (2015)es_MX
dc.subjectBIOLOGÍA Y QUÍMICAes_MX
dc.subjectMedicina y ciencias de la saludes_MX
dc.subjectBiología celulares_MX
dc.subjectCell biologyes_MX
dc.subjectMetabolismoes_MX
dc.subjectMetabolismes_MX
dc.subjectMitocondriaes_MX
dc.subjectMitochondriaes_MX
dc.subjectNicotinamidaes_MX
dc.subjectNicotinamidees_MX
dc.subjectNiacinamidaes_MX
dc.subjectNiacinamidees_MX
dc.subjectNicotinamide-Adenine Dinucleotide (NAD)es_MX
dc.subjectNicotinamida-Nucleótido Adenililtransferasaes_MX
dc.subjectNicotinamide-Nucleotide Adenylyltransferasees_MX
dc.subjectNicotinamida Fosforibosiltransferasaes_MX
dc.subjectNicotinamide Phosphoribosyltransferasees_MX
dc.subjectNMN Adenililtransferasaes_MX
dc.titleIncreasing NAD Synthesis in Muscle via Nicotinamide Phosphoribosyltransferase Is Not Sufficient to Promote Oxidative Metabolism.es_MX
dc.typeArtículoes_MX
dc.audienceResearcherses_MX
dc.creator.id0000-0003-2221-4192es_MX
dc.creator.idCA1242226es_MX
dc.creator.id0000-0002-8815-4201es_MX
dc.creator.idCA1242237es_MX
dc.creator.idMIAS721029MDFCGH04es_MX
dc.creator.idCA1242236es_MX
dc.creator.idCA1242230es_MX
dc.creator.id0000-0001-8262-6549es_MX
dc.creator.nameIdentifiercvues_MX
dc.creator.nameIdentifiercaes_MX
dc.creator.nameIdentifiercvues_MX
dc.creator.nameIdentifiercaes_MX
dc.creator.nameIdentifiercurpes_MX
dc.creator.nameIdentifiercaes_MX
dc.creator.nameIdentifiercaes_MX
dc.creator.nameIdentifiercvues_MX
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