The Role of Sirtuins in the Control of Metabolic Homeostasis
Authors:
- 16 September 2009
- journal article
- review article
- Published by Wiley in Annals of the New York Academy of Sciences
- Vol. 1173 (s1) , E10-E19
Abstract
Recently the function of the sirtuin family, named after their homology to the Saccharomyces cerevisiae gene silent information regulator 2 (Sir2), has received a lot of attention, as their beneficial impact on longevity was linked to their effects on metabolic control. All sirtuins require nicotinamide adenine dinucleotide (NAD+) for their deacetylase or ADP‐ribosyl transferase activity, linking their function tightly to cellular energy levels. SIRT1, the founding member of the sirtuin family, modulates many aspects of glucose and lipid homeostasis in almost all key metabolic tissues. Other members including SIRT2, SIRT3, and SIRT4 are also implicated in various metabolic processes. Here, we review the recent data related to the role of sirtuins in the control of metabolic homeostasis and possible underlying molecular mechanisms.Keywords
This publication has 72 references indexed in Scilit:
- Glucose Restriction Inhibits Skeletal Myoblast Differentiation by Activating SIRT1 through AMPK-Mediated Regulation of NamptDevelopmental Cell, 2008
- SIRT6 is a histone H3 lysine 9 deacetylase that modulates telomeric chromatinNature, 2008
- Negative regulation of the deacetylase SIRT1 by DBC1Nature, 2008
- Metabolic adaptations through the PGC‐1α and SIRT1 pathwaysFEBS Letters, 2007
- SIRT1 sumoylation regulates its deacetylase activity and cellular response to genotoxic stressNature Cell Biology, 2007
- Nutrient-Sensitive Mitochondrial NAD+ Levels Dictate Cell SurvivalCell, 2007
- SIRT2 Regulates Adipocyte Differentiation through FoxO1 Acetylation/DeacetylationCell Metabolism, 2007
- Transcriptional Control of Brown Fat Determination by PRDM16Cell Metabolism, 2007
- Resveratrol improves health and survival of mice on a high-calorie dietNature, 2006
- Sirt1 promotes fat mobilization in white adipocytes by repressing PPAR-γNature, 2004