A high-fat diet and NAD+ activate sirt1 to rescue premature aging in cockayne syndrome

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

A high-fat diet and NAD+ activate sirt1 to rescue premature aging in cockayne syndrome. / Scheibye-Knudsen, Morten; Mitchell, Sarah J.; Fang, Evandro F.; Iyama, Teruaki; Ward, Theresa; Wang, James; Dunn, Christopher A.; Singh, Nagendra; Veith, Sebastian; Hasan-Olive, Md Mahdi; Mangerich, Aswin; Wilson, Mark A.; Mattson, Mark P.; Bergersen, Linda H.; Cogger, Victoria C.; Warren, Alessandra; Le Couteur, David G.; Moaddel, Ruin; Wilson, David M.; Croteau, Deborah L.; De Cabo, Rafael; Bohr, Vilhelm A.

In: Cell Metabolism, Vol. 20, No. 5, 04.11.2014, p. 840-855.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Scheibye-Knudsen, M, Mitchell, SJ, Fang, EF, Iyama, T, Ward, T, Wang, J, Dunn, CA, Singh, N, Veith, S, Hasan-Olive, MM, Mangerich, A, Wilson, MA, Mattson, MP, Bergersen, LH, Cogger, VC, Warren, A, Le Couteur, DG, Moaddel, R, Wilson, DM, Croteau, DL, De Cabo, R & Bohr, VA 2014, 'A high-fat diet and NAD+ activate sirt1 to rescue premature aging in cockayne syndrome', Cell Metabolism, vol. 20, no. 5, pp. 840-855. https://doi.org/10.1016/j.cmet.2014.10.005

APA

Scheibye-Knudsen, M., Mitchell, S. J., Fang, E. F., Iyama, T., Ward, T., Wang, J., Dunn, C. A., Singh, N., Veith, S., Hasan-Olive, M. M., Mangerich, A., Wilson, M. A., Mattson, M. P., Bergersen, L. H., Cogger, V. C., Warren, A., Le Couteur, D. G., Moaddel, R., Wilson, D. M., ... Bohr, V. A. (2014). A high-fat diet and NAD+ activate sirt1 to rescue premature aging in cockayne syndrome. Cell Metabolism, 20(5), 840-855. https://doi.org/10.1016/j.cmet.2014.10.005

Vancouver

Scheibye-Knudsen M, Mitchell SJ, Fang EF, Iyama T, Ward T, Wang J et al. A high-fat diet and NAD+ activate sirt1 to rescue premature aging in cockayne syndrome. Cell Metabolism. 2014 Nov 4;20(5):840-855. https://doi.org/10.1016/j.cmet.2014.10.005

Author

Scheibye-Knudsen, Morten ; Mitchell, Sarah J. ; Fang, Evandro F. ; Iyama, Teruaki ; Ward, Theresa ; Wang, James ; Dunn, Christopher A. ; Singh, Nagendra ; Veith, Sebastian ; Hasan-Olive, Md Mahdi ; Mangerich, Aswin ; Wilson, Mark A. ; Mattson, Mark P. ; Bergersen, Linda H. ; Cogger, Victoria C. ; Warren, Alessandra ; Le Couteur, David G. ; Moaddel, Ruin ; Wilson, David M. ; Croteau, Deborah L. ; De Cabo, Rafael ; Bohr, Vilhelm A. / A high-fat diet and NAD+ activate sirt1 to rescue premature aging in cockayne syndrome. In: Cell Metabolism. 2014 ; Vol. 20, No. 5. pp. 840-855.

Bibtex

@article{d61458e6ad5b4baca35ceecb00d0ffb4,
title = "A high-fat diet and NAD+ activate sirt1 to rescue premature aging in cockayne syndrome",
abstract = "Cockayne syndrome (CS) is an accelerated aging disorder characterized by progressive neurodegeneration caused by mutations in genes encoding the DNA repair proteins CS group A or B (CSA or CSB). Since dietary interventions can alter neurodegenerative processes, Csbm/m mice were given a high-fat, caloric-restricted, or resveratrol-supplemented diet. High-fat feeding rescued the metabolic, transcriptomic, and behavioral phenotypes of Csbm/m mice. Furthermore, premature aging in CS mice, nematodes, and human cells results from aberrant PARP activation due to deficient DNA repair leading to decreased SIRT1 activity and mitochondrial dysfunction. Notably, β-hydroxybutyrate levels are increased by the high-fat diet, and β-hydroxybutyrate, PARP inhibition, or NAD+ supplementation can activate SIRT1 and rescue CS-associated phenotypes. Mechanistically, CSB can displace activated PARP1 from damaged DNA to limit its activity. This study connects two emerging longevity metabolites, β-hydroxybutyrate and NAD+, through the deacetylase SIRT1 and suggests possible interventions for CS.",
author = "Morten Scheibye-Knudsen and Mitchell, {Sarah J.} and Fang, {Evandro F.} and Teruaki Iyama and Theresa Ward and James Wang and Dunn, {Christopher A.} and Nagendra Singh and Sebastian Veith and Hasan-Olive, {Md Mahdi} and Aswin Mangerich and Wilson, {Mark A.} and Mattson, {Mark P.} and Bergersen, {Linda H.} and Cogger, {Victoria C.} and Alessandra Warren and {Le Couteur}, {David G.} and Ruin Moaddel and Wilson, {David M.} and Croteau, {Deborah L.} and {De Cabo}, Rafael and Bohr, {Vilhelm A.}",
year = "2014",
month = nov,
day = "4",
doi = "10.1016/j.cmet.2014.10.005",
language = "English",
volume = "20",
pages = "840--855",
journal = "Cell Metabolism",
issn = "1550-4131",
publisher = "Cell Press",
number = "5",

}

RIS

TY - JOUR

T1 - A high-fat diet and NAD+ activate sirt1 to rescue premature aging in cockayne syndrome

AU - Scheibye-Knudsen, Morten

AU - Mitchell, Sarah J.

AU - Fang, Evandro F.

AU - Iyama, Teruaki

AU - Ward, Theresa

AU - Wang, James

AU - Dunn, Christopher A.

AU - Singh, Nagendra

AU - Veith, Sebastian

AU - Hasan-Olive, Md Mahdi

AU - Mangerich, Aswin

AU - Wilson, Mark A.

AU - Mattson, Mark P.

AU - Bergersen, Linda H.

AU - Cogger, Victoria C.

AU - Warren, Alessandra

AU - Le Couteur, David G.

AU - Moaddel, Ruin

AU - Wilson, David M.

AU - Croteau, Deborah L.

AU - De Cabo, Rafael

AU - Bohr, Vilhelm A.

PY - 2014/11/4

Y1 - 2014/11/4

N2 - Cockayne syndrome (CS) is an accelerated aging disorder characterized by progressive neurodegeneration caused by mutations in genes encoding the DNA repair proteins CS group A or B (CSA or CSB). Since dietary interventions can alter neurodegenerative processes, Csbm/m mice were given a high-fat, caloric-restricted, or resveratrol-supplemented diet. High-fat feeding rescued the metabolic, transcriptomic, and behavioral phenotypes of Csbm/m mice. Furthermore, premature aging in CS mice, nematodes, and human cells results from aberrant PARP activation due to deficient DNA repair leading to decreased SIRT1 activity and mitochondrial dysfunction. Notably, β-hydroxybutyrate levels are increased by the high-fat diet, and β-hydroxybutyrate, PARP inhibition, or NAD+ supplementation can activate SIRT1 and rescue CS-associated phenotypes. Mechanistically, CSB can displace activated PARP1 from damaged DNA to limit its activity. This study connects two emerging longevity metabolites, β-hydroxybutyrate and NAD+, through the deacetylase SIRT1 and suggests possible interventions for CS.

AB - Cockayne syndrome (CS) is an accelerated aging disorder characterized by progressive neurodegeneration caused by mutations in genes encoding the DNA repair proteins CS group A or B (CSA or CSB). Since dietary interventions can alter neurodegenerative processes, Csbm/m mice were given a high-fat, caloric-restricted, or resveratrol-supplemented diet. High-fat feeding rescued the metabolic, transcriptomic, and behavioral phenotypes of Csbm/m mice. Furthermore, premature aging in CS mice, nematodes, and human cells results from aberrant PARP activation due to deficient DNA repair leading to decreased SIRT1 activity and mitochondrial dysfunction. Notably, β-hydroxybutyrate levels are increased by the high-fat diet, and β-hydroxybutyrate, PARP inhibition, or NAD+ supplementation can activate SIRT1 and rescue CS-associated phenotypes. Mechanistically, CSB can displace activated PARP1 from damaged DNA to limit its activity. This study connects two emerging longevity metabolites, β-hydroxybutyrate and NAD+, through the deacetylase SIRT1 and suggests possible interventions for CS.

UR - http://www.scopus.com/inward/record.url?scp=84910132320&partnerID=8YFLogxK

U2 - 10.1016/j.cmet.2014.10.005

DO - 10.1016/j.cmet.2014.10.005

M3 - Journal article

C2 - 25440059

AN - SCOPUS:84910132320

VL - 20

SP - 840

EP - 855

JO - Cell Metabolism

JF - Cell Metabolism

SN - 1550-4131

IS - 5

ER -

ID: 172128793