dc.creatorGhiraldini, FG
dc.creatorCrispim, ACV
dc.creatorMello, MLS
dc.date2013
dc.dateAUG 1
dc.date2014-07-30T17:21:32Z
dc.date2015-11-26T16:33:03Z
dc.date2014-07-30T17:21:32Z
dc.date2015-11-26T16:33:03Z
dc.date.accessioned2018-03-28T23:14:43Z
dc.date.available2018-03-28T23:14:43Z
dc.identifierMolecular Biology Of The Cell. Amer Soc Cell Biology, v. 24, n. 15, n. 2467, n. 2476, 2013.
dc.identifier1059-1524
dc.identifierWOS:000322736800017
dc.identifier10.1091/mbc.E13-04-0186
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/64978
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/64978
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1270709
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.descriptionHyperglycemia, like aging, induces chromatin remodeling in mouse hepatocytes in comparison to normoglycemia and younger age, respectively. Changes in glucose metabolism also affect the action and expression of sirtuins, promoting changes in chromatin conformation and dynamics. Here we investigate the abundance and activity of the nuclear sirtuins Sirt1, Sirt6, and Sirt7 in mouse hepatocytes in association with specific histone acetylation, DNA damage, and the activation of nucleolar organizing regions (NORs) in hyperglycemic nonobese diabetic (NOD) and old normoglycemic BALB/c mouse strains. Higher levels of Sirt1 and PGC-1 alpha and increased expression of gluconeogenesis pathway genes are found in the hyperglycemic NOD mice. Increased Sirt6 abundance is found in the hyperglycemic NOD mice, which might increase DNA damage repair. With aging, lower Sirt1 abundance and activity, increased acetylated histone modifications and Sirt7 levels, and NOR methylation are found. Thus, whereas in normal aging cell metabolism is reduced, in the diabetic mice a compensatory mechanism may elevate Sirt1 and Sirt6 levels, increasing gluconeogenesis and DNA repair from the oxidative damage caused by hyperglycemia. Therefore understanding the regulation of epigenetic factors in diabetes and aging is crucial for the development of new therapeutic approaches that could prevent diseases and improve quality of life.
dc.description24
dc.description15
dc.description2467
dc.description2476
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.descriptionConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.descriptionFAPESP [2010/50015-6, 2008/58067-5]
dc.descriptionCNPq [471303/2009-7, 301943/2009-5]
dc.languageen
dc.publisherAmer Soc Cell Biology
dc.publisherBethesda
dc.publisherEUA
dc.relationMolecular Biology Of The Cell
dc.relationMol. Biol. Cell
dc.rightsaberto
dc.sourceWeb of Science
dc.subjectPolymerase-i Transcription
dc.subjectCalorie Restriction
dc.subjectImage-analysis
dc.subjectSirt6
dc.subjectChromatin
dc.subjectCells
dc.subjectLiver
dc.subjectMice
dc.subjectSenescence
dc.subjectRepair
dc.titleEffects of hyperglycemia and aging on nuclear sirtuins and DNA damage of mouse hepatocytes
dc.typeArtículos de revistas


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