| Literature DB >> 27304511 |
Juliana Camacho-Pereira1, Mariana G Tarragó2, Claudia C S Chini2, Veronica Nin2, Carlos Escande2, Gina M Warner2, Amrutesh S Puranik2, Renee A Schoon3, Joel M Reid3, Antonio Galina4, Eduardo N Chini5.
Abstract
Nicotinamide adenine dinucleotide (NAD) levels decrease during aging and are involved in age-related metabolic decline. To date, the mechanism responsible for the age-related reduction in NAD has not been elucidated. Here we demonstrate that expression and activity of the NADase CD38 increase with aging and that CD38 is required for the age-related NAD decline and mitochondrial dysfunction via a pathway mediated at least in part by regulation of SIRT3 activity. We also identified CD38 as the main enzyme involved in the degradation of the NAD precursor nicotinamide mononucleotide (NMN) in vivo, indicating that CD38 has a key role in the modulation of NAD-replacement therapy for aging and metabolic diseases.Entities:
Keywords: CD38; NAD(+); aging; glucose intolerance; mitochondrial function
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Year: 2016 PMID： 27304511 PMCID： PMC4911708 DOI： 10.1016/j.cmet.2016.05.006
Source DB: PubMed Journal: Cell Metab ISSN： 1550-4131 Impact factor: 27.287