Acetate reprograms gut microbiota during alcohol consumption

Cameron Martino, Livia S. Zaramela, Bei Gao, Mallory Embree, Janna Tarasova, Seth J. Parker, Yanhan Wang, Huikuan Chu, Peng Chen, Kuei-Chuan Lee, Daniela Domingos Galzerani, Jivani M. Gengatharan, Asama Lekbua, Maxwell Neal, Rob Knight, Hidekazu Tsukamoto, Christian M. Metallo, Bernd Schnabl () and Karsten Zengler ()
Additional contact information
Cameron Martino: University of California San Diego
Livia S. Zaramela: University of California San Diego
Bei Gao: University of California San Diego
Mallory Embree: University of California
Janna Tarasova: University of California San Diego
Seth J. Parker: University of California
Yanhan Wang: University of California San Diego
Huikuan Chu: University of California San Diego
Peng Chen: University of California San Diego
Kuei-Chuan Lee: University of California San Diego
Daniela Domingos Galzerani: University of California San Diego
Jivani M. Gengatharan: University of California
Asama Lekbua: University of California San Diego
Maxwell Neal: University of California San Diego
Rob Knight: University of California San Diego
Hidekazu Tsukamoto: Southern California Research Center for ALPD and Cirrhosis and Department of Pathology
Christian M. Metallo: University of California
Bernd Schnabl: University of California San Diego
Karsten Zengler: University of California San Diego

Nature Communications, 2022, vol. 13, issue 1, 1-11

Abstract: Abstract Liver damage due to chronic alcohol use is among the most prevalent liver diseases. Alcohol consumption frequency is a strong factor of microbiota variance. Here we use isotope labeled [1-13C] ethanol, metagenomics, and metatranscriptomics in ethanol-feeding and intragastric mouse models to investigate the metabolic impacts of alcohol consumption on the gut microbiota. First, we show that although stable isotope labeled [1-13C] ethanol contributes to fatty acid pools in the liver, plasma, and cecum contents of mice, there is no evidence of ethanol metabolism by gut microbiota ex vivo under anaerobic conditions. Next, we observe through metatranscriptomics that the gut microbiota responds to ethanol-feeding by activating acetate dissimilation, not by metabolizing ethanol directly. We demonstrate that blood acetate concentrations are elevated during ethanol consumption. Finally, by increasing systemic acetate levels with glyceryl triacetate supplementation, we do not observe any impact on liver disease, but do induce similar gut microbiota alterations as chronic ethanol-feeding in mice. Our results show that ethanol is not directly metabolized by the gut microbiota, and changes in the gut microbiota linked to ethanol are a side effect of elevated acetate levels. De-trending for these acetate effects may be critical for understanding gut microbiota changes that cause alcohol-related liver disease.

Date: 2022
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DOI: 10.1038/s41467-022-31973-2

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