Benefits of Caloric Restriction in Longevity and Chemical-Induced Tumorigenesis Are Transmitted Independent of NQO1

Alberto Diaz-Ruiz; Andrea Di Francesco; Bethany A. Carboneau; Sophia R. Levan; Kevin J. Pearson; Nathan L. Price; Theresa M. Ward; Michel Bernier; Rafael De Cabo; Evi M. Mercken

doi:10.1093/gerona/gly112

Benefits of Caloric Restriction in Longevity and Chemical-Induced Tumorigenesis Are Transmitted Independent of NQO1

Alberto Diaz-Ruiz, Andrea Di Francesco, Bethany A. Carboneau, Sophia R. Levan, Kevin J. Pearson, Nathan L. Price, Theresa M. Ward, Michel Bernier, Rafael De Cabo, Evi M. Mercken

Research output: Contribution to journal › Article › peer-review

15 Scopus citations

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.

Original language	English
Pages (from-to)	155-162
Number of pages	8
Journal	Journals of Gerontology - Series A Biological Sciences and Medical Sciences
Volume	74
Issue number	2
DOIs	https://doi.org/10.1093/gerona/gly112
State	Published - Jan 16 2019

Bibliographical note

Publisher Copyright:
© 2018. Published by Oxford University Press on behalf of The Gerontological Society of America. All rights reserved.

Funding

This work was supported in part by the Intramural Research Program of the National Institute on Aging/National Institutes of Health, and by a postdoctoral grant of the Research Foundation—Flanders (FWO/12R2415N) to E.M.M. This work was supported in part by the Intramural Research Program of the National Institute on Aging/National Institutes of Health, and by a postdoctoral grant of the Research Foundation-Flanders (FWO/12R2415N) to E.M.M.

Funders	Funder number
National Institutes of Health National Institute on Aging
Research Foundation—Flanders	FWO/12R2415N
National Institutes of Health (NIH)
National Institute on Aging	ZIAAG000368

Keywords

Aging
Carcinogenesis
Liver
Mitochondrial dysfunction
Oxidative stress
Whole-body metabolism

ASJC Scopus subject areas

General Medicine

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10.1093/gerona/gly112

Cite this

Diaz-Ruiz, A., Di Francesco, A., Carboneau, B. A., Levan, S. R., Pearson, K. J., Price, N. L., Ward, T. M., Bernier, M., De Cabo, R., & Mercken, E. M. (2019). Benefits of Caloric Restriction in Longevity and Chemical-Induced Tumorigenesis Are Transmitted Independent of NQO1. Journals of Gerontology - Series A Biological Sciences and Medical Sciences, 74(2), 155-162. https://doi.org/10.1093/gerona/gly112

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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.",

keywords = "Aging, Carcinogenesis, Liver, Mitochondrial dysfunction, Oxidative stress, Whole-body metabolism",

author = "Alberto Diaz-Ruiz and {Di Francesco}, Andrea and Carboneau, {Bethany A.} and Levan, {Sophia R.} and Pearson, {Kevin J.} and Price, {Nathan L.} and Ward, {Theresa M.} and Michel Bernier and {De Cabo}, Rafael and Mercken, {Evi M.}",

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Diaz-Ruiz, A, Di Francesco, A, Carboneau, BA, Levan, SR, Pearson, KJ, Price, NL, Ward, TM, Bernier, M, De Cabo, R & Mercken, EM 2019, 'Benefits of Caloric Restriction in Longevity and Chemical-Induced Tumorigenesis Are Transmitted Independent of NQO1', Journals of Gerontology - Series A Biological Sciences and Medical Sciences, vol. 74, no. 2, pp. 155-162. https://doi.org/10.1093/gerona/gly112

Benefits of Caloric Restriction in Longevity and Chemical-Induced Tumorigenesis Are Transmitted Independent of NQO1. / Diaz-Ruiz, Alberto; Di Francesco, Andrea; Carboneau, Bethany A. et al.
In: Journals of Gerontology - Series A Biological Sciences and Medical Sciences, Vol. 74, No. 2, 16.01.2019, p. 155-162.

Research output: Contribution to journal › Article › peer-review

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AU - Di Francesco, Andrea

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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.

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Benefits of Caloric Restriction in Longevity and Chemical-Induced Tumorigenesis Are Transmitted Independent of NQO1

Abstract

Bibliographical note

Funding

Keywords

ASJC Scopus subject areas

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