Mitochondrial Protein Hyperacetylation and Loss of SIRT3 Results in Obesity and Metabolic Syndrome
Event details
| Date | 20.08.2010 |
| Hour | 10:45 |
| Speaker | Dr. Matthew HIRSCHEY, Ph.D., Gladstone Institute of Virology & Immunology, University California, San Francisco (UCSF), CA, USA |
| Location | |
| Category | Conferences - Seminars |
In human liver, virtually every metabolic pathway contains acetylated proteins, and acetylation is increasingly recognized as a regulatory post-translational modification. Chronic high-fat diet feeding induces significant mitochondrial protein hyperacetylation in mice. Mitochondrial sirtuin SIRT3 is a nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylase that regulates mitochondrial protein acetylation and metabolism, and chronic high-fat diet feeding reduces hepatic SIRT3 levels in mice and humans. To identify the metabolic consequence of unregulated protein hyperacetylation, Sirt3-/- mice were fed a high-fat diet, and we find these mice develop the metabolic syndrome. Mitochondrial protein acetylation is an important metabolic regulator, and aberrant acetylation and impaired SIRT3 through high-fat diet feeding or genetic deletion results in multiple metabolic abnormalities.
Practical information
- General public
- Free