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Article: Molecular Links between Caloric Restriction and Sir2/SIRT1 Activation.

TitleMolecular Links between Caloric Restriction and Sir2/SIRT1 Activation.
Authors
Issue Date2014
PublisherKorean Diabetes Association. The Journal's web site is located at http://e-dmj.org/
Citation
Diabetes & Metabolism Journal, 2014, v. 38 n. 5, p. 321-329 How to Cite?
AbstractAgeing is the most significant risk factor for a range of prevalent diseases, including cancer, cardiovascular disease, and diabetes. Accordingly, interventions are needed for delaying or preventing disorders associated with the ageing process, i.e., promotion of healthy ageing. Calorie restriction is the only nongenetic and the most robust approach to slow the process of ageing in evolutionarily divergent species, ranging from yeasts, worms, and flies to mammals. Although it has been known for more than 80 years that calorie restriction increases lifespan, a mechanistic understanding of this phenomenon remains elusive. Yeast silent information regulator 2 (Sir2), the founding member of the sirtuin family of protein deacetylases, and its mammalian homologue Sir2-like protein 1 (SIRT1), have been suggested to promote survival and longevity of organisms. SIRT1 exerts protective effects against a number of age-associated disorders. Caloric restriction increases both Sir2 and SIRT1 activity. This review focuses on the mechanistic insights between caloric restriction and Sir2/SIRT1 activation. A number of molecular links, including nicotinamide adenine dinucleotide, nicotinamide, biotin, and related metabolites, are suggested to be the most important conduits mediating caloric restriction-induced Sir2/SIRT1 activation and lifespan extension.
Persistent Identifierhttp://hdl.handle.net/10722/200776
ISSN
2015 SCImago Journal Rankings: 1.430
PubMed Central ID

 

DC FieldValueLanguage
dc.contributor.authorWang, Yen_US
dc.date.accessioned2014-08-21T07:01:00Z-
dc.date.available2014-08-21T07:01:00Z-
dc.date.issued2014en_US
dc.identifier.citationDiabetes & Metabolism Journal, 2014, v. 38 n. 5, p. 321-329en_US
dc.identifier.issn2233-6079-
dc.identifier.urihttp://hdl.handle.net/10722/200776-
dc.description.abstractAgeing is the most significant risk factor for a range of prevalent diseases, including cancer, cardiovascular disease, and diabetes. Accordingly, interventions are needed for delaying or preventing disorders associated with the ageing process, i.e., promotion of healthy ageing. Calorie restriction is the only nongenetic and the most robust approach to slow the process of ageing in evolutionarily divergent species, ranging from yeasts, worms, and flies to mammals. Although it has been known for more than 80 years that calorie restriction increases lifespan, a mechanistic understanding of this phenomenon remains elusive. Yeast silent information regulator 2 (Sir2), the founding member of the sirtuin family of protein deacetylases, and its mammalian homologue Sir2-like protein 1 (SIRT1), have been suggested to promote survival and longevity of organisms. SIRT1 exerts protective effects against a number of age-associated disorders. Caloric restriction increases both Sir2 and SIRT1 activity. This review focuses on the mechanistic insights between caloric restriction and Sir2/SIRT1 activation. A number of molecular links, including nicotinamide adenine dinucleotide, nicotinamide, biotin, and related metabolites, are suggested to be the most important conduits mediating caloric restriction-induced Sir2/SIRT1 activation and lifespan extension.-
dc.languageengen_US
dc.publisherKorean Diabetes Association. The Journal's web site is located at http://e-dmj.org/-
dc.relation.ispartofDiabetes & Metabolism Journalen_US
dc.titleMolecular Links between Caloric Restriction and Sir2/SIRT1 Activation.en_US
dc.typeArticleen_US
dc.identifier.emailWang, Y: yuwanghk@hku.hken_US
dc.identifier.authorityWang, Y=rp00239en_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.4093/dmj.2014.38.5.321-
dc.identifier.pmid25349818-
dc.identifier.pmcidPMC4209345-
dc.identifier.hkuros232282en_US
dc.identifier.volume38en_US
dc.identifier.issue5-
dc.identifier.spage321-
dc.identifier.epage329-
dc.publisher.placeRepublic of Korea-

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