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Shared Reference Notes
- [1.1] [#Alcohol Consumption]
- gut microbiota responds to ethanol-feeding by activating #Acetate dissimilation, not by metabolizing ethanol directly. - 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.
- [1.2] [#Non alcoholic steatohepatitis, #Non-alcoholic fatty liver disease]
- median portal vein ethanol concentrations were 187 (interquartile range (IQR), 17–516) times higher and increased with disease progression from 2.1 mM in individuals without steatosis to 8.0 mM in NAFL 21.0 mM in nonalcoholic steatohepatitis. - Inhibition of ADH induced a 15-fold (IQR,1.6- to 20-fold) increase in peripheral blood ethanol concentrations in individuals with NAFLD, although this effect was abolished after antibiotic treatment. - #Lactobacillaceae correlated with postprandial peripheral ethanol concentrations.
- [1.3] [#Alcoholic Hepatitis, #Alcoholism] [#Glutamine]
- Gln supplementation attenuated ethanol-induced mucosal permeability and disruption of tight junctions and adherens junctions in a dose-dependent manner
- - Ethanol feeding caused a significant increase in #Inulin permeability in distal colon. - Elevated permeability was associated with a redistribution of tight junction and adherens junction proteins and depletion of detergent-insoluble fractions of these proteins, suggesting that ethanol disrupts apical junctional complexes in colonic epithelium and increases paracellular permeability.