Effects of aging and methionine restriction on rat kidney metabolome

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dc.contributor.authorPradas Barriga, Irene
dc.contributor.authorJové Font, Mariona
dc.contributor.authorCabré Cucó, Rosanna
dc.contributor.authorAyala Jové, Ma. Victoria (Maria Victoria)
dc.contributor.authorMota Martorell, Natàlia
dc.contributor.authorPamplona Gras, Reinald
dc.date.accessioned2020-01-28T08:45:17Z
dc.date.available2020-01-28T08:45:17Z
dc.date.issued2019-11-14
dc.date.updated2020-01-28T08:45:17Z
dc.description.abstractMethionine restriction (MetR) in animal models extends maximum longevity and seems to promote renoprotection by attenuating kidney injury. MetR has also been proven to affect several metabolic pathways including lipid metabolism. However, there is a lack of studies about the effect of MetR at old age on the kidney metabolome. In view of this, a mass spectrometry-based high-throughput metabolomic and lipidomic profiling was undertaken of renal cortex samples of three groups of male rats—An 8-month-old Adult group, a 26-month-old Aged group, and a MetR group that also comprised of 26-month-old rats but were subjected to an 80% MetR diet for 7 weeks. Additionally, markers of mitochondrial stress and protein oxidative damage were analyzed by mass spectrometry. Our results showed minor changes during aging in the renal cortex metabolome, with less than 59 differential metabolites between the Adult and Aged groups, which represents about 4% of changes in the kidney metabolome. Among the compounds identified are glycerolipids and lipid species derived from arachidonic acid metabolism. MetR at old age preferentially induces lipid changes affecting glycerophospholipids, docosanoids, and eicosanoids. No significant differences were observed between the experimental groups in the markers of mitochondrial stress and tissue protein damage. More than rejuvenation, MetR seems to induce a metabolic reprogramming
dc.description.sponsorshipWe acknowledge funding from the Spanish Ministry of Science, Innovation and Universities (RTI2018-099200-B-I00), and the Generalitat of Catalonia, Agency for Management of University and Research Grants (2017SGR696) and Department of Health (SLT002/16/00250) to R.P. This study has been co-financed by FEDER funds from the European Union (“A way to build Europe”). I.P. was supported by a University of Lleida Predoctoral Fellowship. R.C. and N.M.M. were supported by a Generalitat of Catalonia Predoctoral Fellowship. M.J. is a Serra Húnter Fellow.
dc.format.mimetypeapplication/pdf
dc.identifier.doihttps://doi.org/10.3390/metabo9110280
dc.identifier.idgrec029379
dc.identifier.issn2218-1989
dc.identifier.urihttp://hdl.handle.net/10459.1/67892
dc.language.isoeng
dc.publisherMDPI
dc.relationinfo:eu-repo/grantAgreement/AEI/Plan Estatal de Investigación Científica y Técnica y de Innovación 2017-2020/RTI2018-099200-B-I00/ES/NEUROLIPIDOMICA DEL ENVEJECIMIENTO CEREBRAL HUMANO/
dc.relation.isformatofReproducció del document publicat a: https://doi.org/10.3390/metabo9110280
dc.relation.ispartofMetabolites, 2019, vol. 9, núm. 11: 280, p. 1-14
dc.rightscc-by (c) Pradas Barriga, Irene et al., 2019
dc.rights.accessRightsinfo:eu-repo/semantics/openAccess
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectAging
dc.subjectDietary restriction
dc.subjectMass spectrometry
dc.subjectLipidomics
dc.subjectProtein damage
dc.subjectRenal cortex
dc.titleEffects of aging and methionine restriction on rat kidney metabolome
dc.typeinfo:eu-repo/semantics/article
dc.type.versionpublishedVersion
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