Disease ⇒ Non alcoholic steatohepatitis {40000296}

Shared Reference Notes

• [1.1] 
  - Following administration of a high-fructose, high-fat diet, mice that received the human NAFL microbiota (NAFLR) gained more weight and had a higher liver triglycerides level and higher plasma LDL cholesterol than mice that received the human healthy microbiota (HR). - Metabolomic analyses revealed that it was associated with lower and higher plasma levels of glycine and 3-Indolepropionic acid in NAFLR mice, respectively. Moreover, several bacterial genera and OTUs were identified as differently represented in the NAFLR and HR microbiota and therefore potentially responsible for the different phenotypes observed.
• [1.2] [#Non-alcoholic fatty liver disease] [#Lipopolysaccharide, #TMA] 
  - A shift in the metabolic function of intestinal bacteria is predominantly caused by dysbiosis. In the intestine, it leads to an increase in the permeability of intestinal mucosa for LPS and ultimately causes chronic inflammation. Concentration of bacterial metabolites in the blood, such as trimethylamine which is metabolized in the liver to trimethylamine-N-oxide (#TMAO) correlates with the severity of #Steatohepatitis
• [1.3] [#Non-alcoholic fatty liver disease] 
• [1.4] [#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.
• [1.5] [#Non-alcoholic fatty liver disease] 

References Notes