Mitochondrial protein acylation and intermediary metabolism: regulation by sirtuins and implications for metabolic disease

J Biol Chem. 2012 Dec 14;287(51):42436-43. doi: 10.1074/jbc.R112.404863. Epub 2012 Oct 18.

Abstract

The sirtuins are a family of NAD(+)-dependent protein deacetylases that regulate cell survival, metabolism, and longevity. Three sirtuins, SIRT3-5, localize to mitochondria. Expression of SIRT3 is selectively activated during fasting and calorie restriction. SIRT3 regulates the acetylation level and enzymatic activity of key metabolic enzymes, such as acetyl-CoA synthetase, long-chain acyl-CoA dehydrogenase, and 3-hydroxy-3-methylglutaryl-CoA synthase 2, and enhances fat metabolism during fasting. SIRT5 exhibits demalonylase/desuccinylase activity, and lysine succinylation and malonylation are abundant mitochondrial protein modifications. No convincing enzymatic activity has been reported for SIRT4. Here, we review the emerging role of mitochondrial sirtuins as metabolic sensors that respond to changes in the energy status of the cell and modulate the activities of key metabolic enzymes via protein deacylation.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Acylation
  • Coenzyme A / metabolism
  • Humans
  • Metabolic Diseases / metabolism*
  • Mitochondrial Proteins / metabolism*
  • Sirtuins / metabolism*
  • Substrate Specificity

Substances

  • Mitochondrial Proteins
  • Sirtuins
  • Coenzyme A