TY - JOUR
T1 - Benefits of Caloric Restriction in Longevity and Chemical-Induced Tumorigenesis Are Transmitted Independent of NQO1
AU - Diaz-Ruiz, Alberto
AU - Di Francesco, Andrea
AU - Carboneau, Bethany A.
AU - Levan, Sophia R.
AU - Pearson, Kevin J.
AU - Price, Nathan L.
AU - Ward, Theresa M.
AU - Bernier, Michel
AU - De Cabo, Rafael
AU - Mercken, Evi M.
N1 - Publisher Copyright:
© 2018. Published by Oxford University Press on behalf of The Gerontological Society of America. All rights reserved.
PY - 2019/1/16
Y1 - 2019/1/16
N2 - 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.
AB - 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.
KW - Aging
KW - Carcinogenesis
KW - Liver
KW - Mitochondrial dysfunction
KW - Oxidative stress
KW - Whole-body metabolism
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U2 - 10.1093/gerona/gly112
DO - 10.1093/gerona/gly112
M3 - Article
C2 - 29733330
AN - SCOPUS:85060055073
SN - 1079-5006
VL - 74
SP - 155
EP - 162
JO - Journals of Gerontology - Series A Biological Sciences and Medical Sciences
JF - Journals of Gerontology - Series A Biological Sciences and Medical Sciences
IS - 2
ER -