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] 
• [1.6] [#Non-alcoholic fatty liver disease] 
• [1.7] [#Non-alcoholic fatty liver disease] 
• [1.8] [#Short Chain Fatty Acid] 
  - #Alistipes, which are potential SCFA-producing bacteria that reduce hepatic fibrotic conditions through cytokine modulation, have been found at lower levels in the guts of NASH and NASH-#Cirrhosis patients
• [#Non-alcoholic fatty liver disease] [#Lipopolysaccharide] - The elevated localization of LPS in hepatocytes has been reported in NAFLD and may cause liver inflammation via a TLR4-related pathway. - LPS is a risk factor for inducing hepatic inflammation and NASH. - The upregulation of the LPS-TLR4 pathway leads to NF-κB activation and inflammatory cytokine production, which play key roles in NASH progression and development
• [#Ginger] - GEO reduced the relative abundance of NASH-associated bacteria, including #Blautia and #Tyzzerella, which are considered harmful.
• [#Lipopolysaccharide] - #Blautia abundance increased in NASH patients and was positively correlated with LPS levels
• - #Ginger essential oil (GEO) supplementation substantially lower hepatic CYP2E1 protein expression and significantly enhanced the hepatic antioxidant enzyme capacity, including CAT, GRd, and GSH. - GEO alleviates hepatic #Oxidative stress in mice with PL-induced NASH. - GEO alleviated the NASH phenotype and pro-inflammatory cytokines TNF-α, IL-6, and IL-1β. - NASH patients and animal models have exhibited increases in the activation of the NLRP3 inflammasome - GEO exhibited anti-inflammatory activity by reducing NLRP3 inflammasome activation, which may be caused by #Citral and its isomers.
• [1.9] [#Lipopolysaccharide] 
  - LPS-mediated inflammatory signaling has been shown to accelerate the progression of NASH with liver inflammation and #Fibrosis.
• [#Non-alcoholic fatty liver disease] - The reduction or loss of the resident Killer Cells (tissue-resident macrophages, called KCs) population has been observed in a series of liver diseases, including NAFLD and NASH, partly because of the increased lipotoxicity.
• [#Non-alcoholic fatty liver disease] [#Escherichia coli] [#Lipopolysaccharide] -#Small intestinal bacterial overgrowth is frequently observed in patients with NAFLD/NASH and is often associated with increased serum LPS levels due to the increased growth of E. coli, which serve as a source of LPS
• [#Non-alcoholic fatty liver disease] [#Branched-chain amino acids] [#Resistant starch] - 4-month RS intervention in humans could significantly reduce the serum levels of BCAAs. - serum BCAAs were positively correlated with IHTC, ALT, AST, and GGT > direct influence of BCAAs on hepatic steatosis and thus NAFLD pathogenesis.
• [1.11] [#Non-alcoholic fatty liver disease] [#Coffee, #High fibre diet, #Mediterranean diet] 
• [#Probiotic] - Probiotics, such as #Bifidobacterium and #Lactobacillus strains, have been shown to reduce oxidative and inflammatory liver damage while also decreasing hepatic triglycerides (TG) and hepatic steatosis.
• [1.12] [#Xanthohumol] 
  - XN and even more so, TXN, attenuates hepatosteatosis by acting as antagonists of PPARγ

References Notes