Metabolic Characterization of a Sirt5 deficient mouse model

Authors

Jiujiu Yu, Ecole Polytechnique Federale de LausanneFollow
Sushabhan Sadhukhan, Cornell University
Lilia G. Noriega, Ecole Polytechnique Federale de Lausanne
Norman Moullan, Ecole Polytechnique Federale de Lausanne
Bin He, Cornell University
Robert S. Weiss, Cornell University
Hening Lin, Cornell University
Kristina Schoonjans, Ecole Polytechnique Federale de Lausanne
Johan Auwerx, Ecole Polytechnique Federale de LausanneFollow

Document Type

Article

Date of this Version

9-30-2013

Citation

Yu, J. et al. Metabolic Characterization of a Sirt5 deficient mouse model. Sci. Rep. 3, 2806; DOI:10.1038/srep02806 (2013)

Comments

SCIENTIFIC REPORTS | 3 : 2806 | DOI: 10.1038/srep02806

Abstract

Sirt5, localized in the mitochondria, is a member of sirtuin family of NAD1-dependent deacetylases. Sirt5 was shown to deacetylate and activate carbamoyl phosphate synthase 1. Most recently, Sirt5 was reported to be the predominant protein desuccinylase and demalonylase in the mitochondria because the ablation of Sirt5 enhanced the global succinylation and malonylation of mitochondrial proteins, including many metabolic enzymes. In order to determine the physiological role of Sirt5 in metabolic homeostasis, we generated a germline Sirt5 deficient (Sirt52/2) mouse model and performed a thorough metabolic characterization of this mouse line. Although a global protein hypersuccinylation and elevated serum ammonia during fasting were observed in our Sirt52/2 mouse model, Sirt5 deficiency did not lead to any overt metabolic abnormalities under either chow or high fat diet conditions. These observations suggest that Sirt5 is likely to be dispensable for the metabolic homeostasis under the basal conditions.