Alcohol metabolism contributes to brain histone acetylation.

ABSTRACT: Emerging evidence suggests that epigenetic regulation is dependent on metabolic state, and implicates specific metabolic factors in neural functions that drive behaviour¹. In neurons, acetylation of histones relies on the metabolite acetyl-CoA, which is produced from acetate by chromatin-bound acetyl-CoA synthetase 2 (ACSS2)². Notably, the breakdown of alcohol in the liver leads to a rapid increase in levels of blood acetate³, and alcohol is therefore a major source of acetate in the body. Histone acetylation in neurons may thus be under the influence of acetate that is derived from alcohol⁴, with potential effects on alcohol-induced gene expression in the brain, and on behaviour⁵. Here, using in vivo stable-isotope labelling in mice,

SUBMITTER: Mews P 

PROVIDER: S-EPMC6907081 | biostudies-literature | 2019 Oct

REPOSITORIES: biostudies-literature