| Literature DB >> 29733330 |
Alberto Diaz-Ruiz1,2, Andrea Di Francesco1, Bethany A Carboneau1, Sophia R Levan1, Kevin J Pearson3, Nathan L Price4,5, Theresa M Ward1, Michel Bernier1, Rafael de Cabo1,2, Evi M Mercken1.
Abstract
Caloric restriction (CR) is the most potent nonpharmacological intervention known to both protect against carcinogenesis and delay aging in laboratory animals. There is a growing number of anticarcinogens and CR mimetics that activate NAD(P)H:quinone oxidoreductase 1 (NQO1). We have previously shown that NQO1, an antioxidant enzyme that acts as an energy sensor through modulation of intracellular redox and metabolic state, is upregulated by CR. Here, we used NQO1-knockout (KO) mice to investigate the role of NQO1 in both the aging process and tumor susceptibility, specifically in the context of CR. We found that NQO1 is not essential for the beneficial effects of CR on glucose homeostasis, physical performance, metabolic flexibility, life-span extension, and (unlike our previously observation with Nrf2) chemical-induced tumorigenesis.Entities:
Mesh：
Substances：
Year: 2019 PMID： 29733330 PMCID： PMC6599277 DOI： 10.1093/gerona/gly112
Source DB: PubMed Journal: J Gerontol A Biol Sci Med Sci ISSN： 1079-5006 Impact factor: 6.053