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dc.contributor.authorMinois, Nadège
dc.contributor.authorRockenfeller, Patrick
dc.contributor.authorSmith, Terry K
dc.contributor.authorCarmona-Gutierrez, Didac
dc.date.accessioned2014-07-15T15:01:01Z
dc.date.available2014-07-15T15:01:01Z
dc.date.issued2014-07-10
dc.identifier132351710
dc.identifier5b8d1d52-620e-4ddd-a7a9-aa13fbed2879
dc.identifier25010732
dc.identifier000338763800100
dc.identifier84904213406
dc.identifier.citationMinois , N , Rockenfeller , P , Smith , T K & Carmona-Gutierrez , D 2014 , ' Spermidine feeding decreases age-related locomotor activity loss and induces changes in lipid composition ' , PLoS One , vol. 9 , no. 7 , e102435 . https://doi.org/10.1371/journal.pone.0102435en
dc.identifier.issn1932-6203
dc.identifier.urihttps://hdl.handle.net/10023/5018
dc.description.abstractSpermidine is a natural polyamine involved in many important cellular functions, whose supplementation in food or water increases life span and stress resistance in several model organisms. In this work, we expand spermidine's range of age-related beneficial effects by demonstrating that it is also able to improve locomotor performance in aged flies. Spermidine's mechanism of action on aging has been primarily related to general protein hypoacetylation that subsequently induces autophagy. Here, we suggest that the molecular targets of spermidine also include lipid metabolism: Spermidine-fed flies contain more triglycerides and show altered fatty acid and phospholipid profiles. We further determine that most of these metabolic changes are regulated through autophagy. Collectively, our data suggests an additional and novel lipid-mediated mechanism of action for spermidine-induced autophagy.
dc.format.extent11
dc.format.extent792652
dc.language.isoeng
dc.relation.ispartofPLoS Oneen
dc.subjectQH301 Biologyen
dc.subject.lccQH301en
dc.titleSpermidine feeding decreases age-related locomotor activity loss and induces changes in lipid compositionen
dc.typeJournal articleen
dc.contributor.institutionUniversity of St Andrews. School of Biologyen
dc.contributor.institutionUniversity of St Andrews. Biomedical Sciences Research Complexen
dc.identifier.doi10.1371/journal.pone.0102435
dc.description.statusPeer revieweden


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