ArticleAlcoholism, clinical and experimental research2022
Hepatic CYP2B10 is highly induced by binge ethanol and contributes to acute-on-chronic alcohol-induced liver injury.
Article in Alcoholism, clinical and experimental research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 13 citations in OpenAlex.
- Ya-Jie-Sha-Ba Decoction Regulates Arachidonic Acid Metabolism to Treat Alcohol-Associated Liver Disease by Activating PPARα-CYP4A14 Axis: Insights From Multi-Omics Analysis and Experimental Validations.Journal of cellular and molecular medicine · 2026Article
- Hydrogen gas (HFrontiers in immunology · 2026Article
- An Update on Animal Models of Alcohol-Associated Liver Disease.The American journal of pathology · 2026Review
- High-throughput quantitation of acetaldehyde and ethanol in mice using gas chromatography/mass spectrometry positive chemical ionization.Alcohol, clinical & experimental research · 2025Article
- Peripheral alcohol metabolism dictates ethanol consumption and drinking microstructure in mice.Alcohol, clinical & experimental research · 2025Article
- Hydrogen gas (HFrontiers in pharmacology · 2025Article
- Short-term high-fat diet feeding plus acute ethanol binge induced acute liver injury in mice via oxidative stress, inflammation and pyroptosis.Frontiers in pharmacology · 2025Article
- Chronic polypharmacy, monotherapy, and deprescribing: Understanding complex effects on the hepatic proteome of aging mice.Aging cell · 2025Article
- Molecular targets of PXR-dependent ethanol-induced hepatotoxicity in female mice.Biochemical pharmacology · 2024Article
- Diindoles produced from commensal microbiota metabolites function as endogenous CAR/Nr1i3 ligands.Nature communications · 2024Article
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10 authors at 2 institutions in 1 country.
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Abstract
backgroundThe chronic-plus-binge model of ethanol consumption, where chronically (8-week) ethanol-fed mice are gavaged a single dose of ethanol (E8G1), is known to induce steatohepatitis in mice. However, how chronically ethanol-fed mice respond to multiple binges of ethanol remains unknown.
methodsWe extended the E8G1 model to three gavages of ethanol (E8G3) spaced 24 h apart, sacrificed each group 9 h after the final gavage, analyzed liver injury, and examined gene expression changes using microarray analyses in each group to identify mechanisms contributing to liver responses to binge ethanol.
resultsSurprisingly, E8G3 treatment induced lower levels of liver injury, steatosis, inflammation, and fibrosis as compared to mice after E8G1 treatment. Microarray analyses identified several pathways that may contribute to the reduced liver injury after E8G3 treatment compared to E8G1 treatment. The gene encoding cytochrome P450 2B10 (Cyp2b10) was one of the top upregulated genes in the E8G1 group and was further upregulated in the E8G3 group, but only moderately induced after chronic ethanol consumption, as confirmed by RT-qPCR and western blot analyses. Genetic disruption of Cyp2b10 worsened liver injury in E8G1 and E8G3 mice with higher blood ethanol levels compared to wild-type control mice, while in vitro experiments revealed that CYP2b10 did not directly promote ethanol metabolism. Metabolomic analyses revealed significant differences in hepatic metabolites from E8G1-treated Cyp2b10 knockout and WT mice, and these metabolic alterations may contribute to the reduced liver injury in Cyp2b10 knockout mice.
conclusionHepatic Cyp2b10 expression is highly induced after ethanol binge, and such upregulation reduces acute-on-chronic ethanol-induced liver injury via the indirect modification of ethanol metabolism.
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