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Comment
. 2020 Feb 4;31(2):213-214.
doi: 10.1016/j.cmet.2020.01.008.

Alcohol Makes Its Epigenetic Marks

Subhash C Pandey  1 , John Peyton Bohnsack  2
Affiliations
Comment

Alcohol Makes Its Epigenetic Marks

Subhash C Pandey et al. Cell Metab. .

Abstract

The toxic effects of alcohol consumption are dependent upon its metabolism in the liver to downstream metabolites: acetaldehyde, acetate, and acetyl-CoA. Recently, in Nature, Mews et al. (2019) have discovered that acetyl-CoA derived from alcohol plays an important epigenetic role in regulating ethanol's effects on the brain through histone acetylation.

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Figures

Figure 1:
Figure 1:
Alcohol metabolism in the liver and its impact on chromatin remodeling via transportation of acetate to the brain and its conversion to acetyl-CoA by ACSS2 leading to increased histone acetylation (Ac). Alcohol can also directly increase histone acetylation via inhibition of HDACs and activation of HATs. These epigenetic changes produced by ethanol or its metabolite, acetate, can produce relaxed chromatin leading to transcriptomic changes that regulate ethanol-related behavioral phenotypes.
See this image and copyright information in PMC

Comment on

  • Alcohol metabolism contributes to brain histone acetylation.
    Mews P, Egervari G, Nativio R, Sidoli S, Donahue G, Lombroso SI, Alexander DC, Riesche SL, Heller EA, Nestler EJ, Garcia BA, Berger SL. Mews P, et al. Nature. 2019 Oct;574(7780):717-721. doi: 10.1038/s41586-019-1700-7. Epub 2019 Oct 23. Nature. 2019. PMID: 31645761 Free PMC article.

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