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. 2020 Jul 7;26(25):3577–3585. doi: 10.3748/wjg.v26.i25.3577

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©The Author(s) 2020. Published by Baishideng Publishing Group Inc. All rights reserved.

This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial.

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Monoacylglycerol lipase deletion impacts gut-liver axis via nuclear receptor and microbiome modulation. Monoacylglycerol lipase ablation ameliorates cholestatic liver disease induced by 3,5-diethoxycarbonyl-1,4-dihydrocollidine challenge diminishing fibrosis, inflammation, and fatty acid metabolism/oxidation in the liver. Accumulation of arachidonic acid binds nuclear receptors such as farnesoid X receptor, downregulating in turn fibroblast growth factor 15 and inducing bile acids synthesis and detoxification as shown by Cyp7a1/Cyp3a11. In addition, proinflammatory Proteobacteria were diminished in feces from Mgl^-/- mice. AA: Arachidonic acid; NRs: Nuclear receptors; FGF15: Fibroblast growth factor 15; BA: Bile acids.