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dc.contributor.authorJacobson, Jake
dc.contributor.authorLambert, Adrian J.
dc.contributor.authorPortero Otín, Manuel
dc.contributor.authorPamplona Gras, Reinald
dc.contributor.authorMagwere, Tapiwanashe
dc.contributor.authorMiwa, Satomi
dc.contributor.authorDriege, Yasmine
dc.contributor.authorBrand, Martin D.
dc.contributor.authorPartridge, Linda
dc.date.accessioned2016-11-28T10:24:18Z
dc.date.available2016-11-28T10:24:18Z
dc.date.issued2010
dc.identifier.issn1474-9718
dc.identifier.urihttp://hdl.handle.net/10459.1/58663
dc.description.abstractLow environmental temperature and dietary restriction (DR) extend lifespan in diverse organisms. In the fruit fly Drosophila, switching flies between temperatures alters the rate at which mortality subsequently increases with age but does not reverse mortality rate. In contrast, DR acts acutely to lower mortality risk; flies switched between control feeding and DR show a rapid reversal of mortality rate. Dietary restriction thus does not slow accumulation of aging-related damage. Molecular species that track the effects of temperatures on mortality but are unaltered with switches in diet are therefore potential biomarkers of aging-related damage. However, molecular species that switch upon instigation or withdrawal of DR are thus potential biomarkers of mechanisms underlying risk of mortality, but not of aging-related damage. Using this approach, we assessed several commonly used biomarkers of aging-related damage. Accumulation of fluorescent advanced glycation end products (AGEs) correlated strongly with mortality rate of flies at different temperatures but was independent of diet. Hence, fluorescent AGEs are biomarkers of aging-related damage in flies. In contrast, five oxidized and glycated protein adducts accumulated with age, but were reversible with both temperature and diet, and are therefore not markers either of acute risk of dying or of aging-related damage. Our approach provides a powerful method for identification of biomarkers of aging.ca_ES
dc.description.sponsorshipThis work was supported by the Wellcome Trust and in part by I+D grants from the Spanish Ministry of Education and Science (BFU2006-14495 ⁄ BFI), the Spanish Ministry of Health (ISCIII, Red de Envejecimiento y Fragilidad, RD06 ⁄ 0013 ⁄ 0012), and the Generalitat of Catalunya (2005SGR00101) to R.P; the Spanish Ministry of Health (FIS PI081843), Spanish Ministry of Education and Science (AGL2006-12433), and ‘‘La Caixa’’ Foundation to M.P.O. Also supported by the Max Planck Society (J.J. and L.P), COST B-35 Action; Research into Ageing (A.J.L.) and the Medical Research Council and National Institutes of Health (P01 AG025901, PL1 AG032118 and P30 AG025708) (M.D.B.).ca_ES
dc.language.isoengca_ES
dc.publisherWileyca_ES
dc.relationMIECI/PN2004-2007/BFU2006-14495/BFI
dc.relationMIECI/PN2004-2007/AGL2006-12433
dc.relation.isformatofReproducció del document publicat a https://doi.org/10.1111/j.1474-9726.2010.00573.xca_ES
dc.relation.ispartofAging Cell, 2010, vol. 9, núm. 4, p. 466-477ca_ES
dc.rightscc-by-n (c) Jacobson, Jake et al., 2010ca_ES
dc.rights.urihttp://creativecommons.org/licenses/by-nc/3.0/es/*
dc.subjectBiomarkers of agingca_ES
dc.subjectDemography of agingca_ES
dc.subjectDrosophilaca_ES
dc.titleBiomarkers of aging in Drosophilaca_ES
dc.typearticleca_ES
dc.identifier.idgrec015604
dc.type.versionpublishedVersionca_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccessca_ES
dc.identifier.doihttps://doi.org/10.1111/j.1474-9726.2010.00573.x


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