Authors

Robin K. Minor, National Institutes of Health
Joseph A. Baur, University of Pennsylvania
Ana P. Gomes, Harvard Medical School
Theresa M. Ward, National Institutes of Health
Anna Csiszar, University of Oklahoma Health Sciences Center
Evi M. Mercken, National Institutes of Health
Kotb Abdelmohsen, National Institutes of Health
Yu-Kyong Shin, National Institutes of Health
Carles Canto, Ecole Polytechnique Fédérale de Lausanne (EPFL), Switzerland
Morten Scheibye-Knudsen, National Institutes of Health
Melissa Krawczyk, National Institutes of Health
Pablo M. Irusta, National Institutes of Health
Alejandro Martín-Montalvo, National Institutes of Health
Basil P. Hubbard, Harvard Medical School
Yongqing Zhang, National Institutes of Health
Elin Lehrmann, National Institutes of Health
Alexa A. White, National Institutes of Health
Nathan L. Price, Harvard Medical School
William R. Swindell, Harvard Medical School
Kevin J. Pearson, University of KentuckyFollow
Kevin G. Becker, National Institutes of Health
Vilhelm A. Bohr, National Institutes of Health
Myriam Gorospe, National Institutes of Health
Josephine M. Egan, National Institutes of Health
Mark I. Talan, National Institutes of Health
Johan Auwerx, Ecole Polytechnique Fédérale de Lausanne (EPFL), Switzerland
Christoph H. Westphal, Sirtris
James L. Ellis, Sirtris
Zoltan Ungvari, University of Oklahoma Health Sciences Center
George P. Vlasuk, Sirtris
Peter J. Elliott, Sirtris
David A. Sinclair, Harvard Medical School
Rafael de Cabo, National Institutes of Health

Abstract

Sirt1 is an NAD(+)-dependent deacetylase that extends lifespan in lower organisms and improves metabolism and delays the onset of age-related diseases in mammals. Here we show that SRT1720, a synthetic compound that was identified for its ability to activate Sirt1 in vitro, extends both mean and maximum lifespan of adult mice fed a high-fat diet. This lifespan extension is accompanied by health benefits including reduced liver steatosis, increased insulin sensitivity, enhanced locomotor activity and normalization of gene expression profiles and markers of inflammation and apoptosis, all in the absence of any observable toxicity. Using a conditional SIRT1 knockout mouse and specific gene knockdowns we show SRT1720 affects mitochondrial respiration in a Sirt1- and PGC-1α-dependent manner. These findings indicate that SRT1720 has long-term benefits and demonstrate for the first time the feasibility of designing novel molecules that are safe and effective in promoting longevity and preventing multiple age-related diseases in mammals.

Document Type

Article

Publication Date

8-18-2011

Notes/Citation Information

Published in Scientific Reports, v. 1, 70.

This work is licensed under a Creative Commons Attribution-NonCommercial-No Derivative Works 3.0 Unported License. To view a copy of this license, visithttp://creativecommons.org/licenses/by-nc-nd/3.0/

Digital Object Identifier (DOI)

http://dx.doi.org/10.1038/srep00070

srep00070-s1.pdf (1311 kB)
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