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SUMMARY:Mitochondrial Protein Hyperacetylation and Loss of SIRT3 Results i
 n Obesity and Metabolic Syndrome
DTSTART:20100820T104500
DTSTAMP:20260929T072216Z
UID:c8406fe44956948365dc29a783f69f30ee0e03a79cbdf29fa4c7ea03
CATEGORIES:Conferences - Seminars
DESCRIPTION:Dr. Matthew HIRSCHEY\, Ph.D.\, Gladstone Institute of Virology
  & Immunology\, University  California\, San Francisco (UCSF)\, CA\, USA\n
 In human liver\, virtually every metabolic pathway contains acetylated pro
 teins\, and acetylation is increasingly recognized as a regulatory post-tr
 anslational modification. Chronic high-fat diet feeding induces significan
 t mitochondrial protein hyperacetylation in mice. Mitochondrial sirtuin SI
 RT3 is a nicotinamide adenine dinucleotide (NAD+)-dependent protein deacet
 ylase that regulates mitochondrial protein acetylation and metabolism\, an
 d chronic high-fat diet feeding reduces hepatic SIRT3 levels in mice and h
 umans. To identify the metabolic consequence of unregulated protein hypera
 cetylation\, Sirt3-/- mice were fed a high-fat diet\, and we find these mi
 ce develop the metabolic syndrome. Mitochondrial protein acetylation is an
  important metabolic regulator\, and aberrant acetylation and impaired SIR
 T3 through high-fat diet feeding or genetic deletion results in multiple m
 etabolic abnormalities.
LOCATION:AI 1153 https://plan.epfl.ch/?room==AI%201153
STATUS:CONFIRMED
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