Disease ⇒ Steatohepatitis ⇒ Non-alcoholic fatty liver disease {40000151}

Record Keys
Type:	Disease
Parent:	Steatohepatitis
Definition:	Non-alcoholic fatty liver disease

Details
Initialisation date:	2020-09-06
Other Terms:	NAFLD, NAFLD, Nonalcoholic Steatohepatitis, NASH

Links
Wickipedia Merck Manual

Meta Information
MedDra ID:	10082249
MedDra Level:	pt
ICD:	[ ]
Category:	Gastroenterology
Zone:	[ ]
Mechanism:	[ ]

Notes:

- Low levels of Parabacteroides distasonis lead to the development of NASH and increase cardiovascular risk. (1)
- Decreased levels of Prevotella might be detrimental for adults with NAFLD. (2)

Shared Reference Notes

[1.1]
- Metagenome-based gut microbiome panel can accurately diagnose advanced fibrosis
[1.2]
- Butyrate-producing bacteria were decreased and ethanol-producing bacteria were increased in patients with NAFLD.
[1.3] [#Exercise training]
-The exercise group showed improvements in the clinical indices of oral environment. Salivary component analysis revealed significant reductions in LPS, and lactoferrin during the exercise regimen. - Diversity analysis of oral bacterial flora revealed higher alpha- and beta-diversity after the exercise regimen. - Analysis of the microbial composition revealed that the numbers of Campylobacter, Corynebacterium, Actinomyces , and Lautropia were significantly higher, and that of Prevotella was significantly lower.
[1.4]
- Some #Bacteroides species have been reported to be protective against MAFLD
[1.5]
-The family #Ruminococcaceae has been consistently reported as less abundant in NAFLD
[1.6]
- Patients with NAFLD/NASH exhibit > increased numbers of Bacteroidetes and differences in the presence of Firmicutes > resulting in a decreased F/B ratio. - They also present an increased proportion of species belonging to Clostridium, Anaerobacter, Streptococcus, Escherichia, and Lactobacillus, whereas Oscillibacter, Flavonifaractor, Odoribacter, and Alistipes spp. are less prominent. - Patients with NASH show > a higher abundance of Proteobacteria, Enterobacteriaceae, and Escherichia spp., while Faecalibacterium prausnitzii and Akkermansia muciniphila are diminished. - Children with NAFLD/NASH have a > decreased proportion of Oscillospira spp. accompanied by an elevated proportion of Dorea, Blautia, Prevotella copri, and Ruminococcus spp. - Various metabolites may be involved in the pathogenesis of NAFLD, such as short-chain fatty acids, lipopolysaccharide, bile acids, choline and trimethylamine-N-oxide, and ammonia.
[1.7]
[1.8] [#Spinach consumption]
[1.9]
- NAFLD patients have the high abundance of Bradyrhizobium, Anaerococcus, Peptoniphilus, Propionibacterium acnes, Dorea, and Ruminococcus, with the low abundance of Oscillospira and Rikenellaceae. - In a Chinese cohort, the genera Lactobacillus, Oscillibacter, and Ruminiclostridium have been found to be decreased in obese NAFLD patients, while Faecalibacterium prausnitzii was the only species that presents a different abundance between those with and without NAFLD. - For the women cohort, the abundance of several different genera such as Subdoligranulum, Coprococcus, and Coprobacter were negatively correlated with hepatic steatosis
- Fatty Liver > increased N, N, N-trimethyl-#5-aminovaleric acid
[#Short Chain Fatty Acid] - SCFAs are considered to be able to alleviate the development of nonalcoholic fatty liver diseases (NAFLD), which may derive from their potential contribution to regulating fatty acid oxidation, inflammation, and insulin resistance.
[1.11]
- When translating these taxonomic shifts into predictive metabolic alterations, namely putative changes on microbial metabolic pathways, results suggested that the consortium was predicted to increase the biosynthesis of BCAA, and to decrease the biosynthesis of AAA and methionine. This is an interesting result, because a decreased BCAA/AAA ratio has been shown to correlate with liver dysfunction in cirrhotic patients. - BCAA treatment was shown to ameliorate liver fat accumulation in experimental animal models via increased production of acetic acid by gut microbes
[1.12] [#Non alcoholic steatohepatitis] [#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
[1.13]
- #Exiguobacterium acetylicum leads to increased lipid accumulation in the liver,
[1.14] [#Short Chain Fatty Acid]
- SCFA levels were observed to be decreased in non-obese non-alcoholic fatty liver disease. - SCFAs help to inhibit the progress of NAFLD in a variety of ways. - As histone deacetylase inhibitors, #Propionate, #Acetate, and #Butyrate play an important role in NAFLD by decreasing chromatin-bound acetyl groups
[1.15] [#Non alcoholic steatohepatitis]
[1.16]
- patients with NAFLD had higher rates of #Dementia and vascular #Dementia. - Comorbid NAFLD and either heart disease or stroke conferred a greater risk of #Dementia.
[1.17] [#Non alcoholic steatohepatitis]
- 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.
[1.18] [#Non alcoholic steatohepatitis]
[1.19]
- Via disturbing intestinal metabolic and immune pathways, #Porphyromonas gingivalis accelerates the progression of non-alcoholic fatty liver disease
[#Prevotella intermedia] - in mice experiments, oral administration of P. intermedia induces NAFLD

References Notes

[1.34]

↥ Microbiota

‐ Aanaerobacter Stool Human [1.20]

‐ Actinomycetaceae Stool Human [1.21]

‐ Akkermansia Stool Human [1.22]

‐ Anaerococcus Stool Human [1.23]

‐ Bacteroides Stool Human [1.24]

‐ Bradyrhizobium Stool Human [1.23]

‐ Caldithrix Blood Human [1.25]

‐ Citrobacter Stool Human [1.2]

‐ Clostridium group XI Stool Human [1.20]

‐ Coprococcus Stool Human [1.26]

‐ Deferribacteriales incertae cedis Blood Human [1.25]

‐ Dorea Stool Human [1.23]

‐ Enterobacteriaceae Stool Human [1.27]

‐ Enterococcus Stool Human [1.22]

‐ Escherichia Stool Human [1.20]

‐ Gallibacterium Stool Human [1.27]

‐ Klebsiella pneumoniae Stool Human [1.28]

‐ Kluyvera ascorbata Stool Human [1.28]

‐ Lachnospiraceae Stool Human [1.21]

‐ Lactobacillus mucosae Stool Human [1.29]

‐ Lactobacillus ruminis Stool Human [1.29]

‐ Lactobacillus Stool Human [1.20]

‐ Lactonifactor Stool Human [1.22]

‐ Oscillibacter Stool Human [1.22]

‐ Peptoniphilus Stool Human [1.23]

‐ Phascolarctobacterium succinatutens Stool Human [1.28]

‐ Propionibacterium acnes Stool Human [1.23]

‐ Proteobacteria Stool Human [1.2]

‐ Robinsoniella Stool Human [1.30]

‐ Roseburia Stool Human [1.30]

‐ Ruminococcus Stool Human [1.24]

‐ Streptococcus Stool Human [1.20]

‐ Veillonella Stool Human [1.26]

↧ Microbiota

‐ Acidaminococcus Stool Human [1.25]

‐ Alistipes Stool Human [1.20]

‐ Anaerosporobacter Stool Human [1.31]

‐ Anaerostipes Stool Human [1.32]

‐ Anaerotruncus Stool Human [1.31]

‐ Bacillus Stool Human [1.27]

‐ Bacteroidaceae Stool Human [1.21]

‐ Bacteroides dorei Stool Human [1.26]

‐ Bacteroides fragilis Stool Human [1.26]

‐ Bacteroides Stool Human [1.32]

‐ Beijerinckiaceae Blood Human [1.25]

‐ Bifidobacterium adolescentis Stool Human [1.29]

‐ Bifidobacterium bifidum Stool Human [1.29]

‐ Bifidobacterium longum Stool Human [1.29]

‐ Bilophila Stool Human [1.25]

‐ Blautia Stool Human [1.32]

‐ Catenibacterium Stool Human [1.27]

‐ Citrobacter Stool Human [1.25]

‐ Clostridium Blood Human [1.25]

‐ Coprococcus Stool Human [1.31]

‐ Deinococcus Blood Human [1.25]

‐ Desulfobacteraceae Blood Human [1.25]

‐ Desulfovibrionaceae Stool Human [1.25]

‐ Dorea Stool Human [1.32]

‐ Enterobacteriaceae Stool Human [1.25]

‐ Erysipelothrix Stool Human [1.25]

‐ Erysipelotrichaceae Stool Human [1.24]

‐ Faecalibacterium prausnitzii Stool Human [1.32]

‐ Faecalibacterium Stool Human [1.32]

‐ Fastidiospila Stool Human [1.25]

‐ Flavonifractor Stool Human [1.20]

‐ Lactobacillus Stool Human [1.31]

‐ Lactococcus Stool Human [1.27]

‐ Leuconostoc Blood Human [1.25]

‐ Mogibacterium Stool Human [1.27]

‐ Moryella Stool Human [1.31]

‐ Nocardioides Blood Human [1.25]

‐ Odoribacter Stool Human [1.20]

‐ Oscillibacter Stool Human [1.31]

‐ Oscillospira Stool Human [1.23]

‐ Parabacteroides distasonis Causal? Gut Lumen Human

‐ Parabacteroides johnsonii Stool Human [1.28]

‐ Parabacteroides merdae Stool Human [1.26]

‐ Parabacteroides Stool Human [1.32]

‐ Parasutterella Stool Human [1.25]

‐ Peptostreptococcaceae Stool Human [1.27]

‐ Prevotella copri Causal? Gut Lumen Human

‐ Prevotella copri Stool Human [1.33]

‐ Prevotella Stool Human [1.24]

‐ Pseudobutyrivibrio Stool Human [1.31]

‐ Pseudomonas Stool Human [1.27]

‐ Rikenellaceae Stool Human [1.23]

‐ Roseburia Stool Human [1.31]

‐ Ruminiclostridium Stool Human [1.28]

‐ Ruminococcaceae Stool Human [1.33]

‐ Ruminococcus gnavus Stool Human [1.26]

‐ Ruminococcus Stool Human [1.31]

‐ Turicibacter Stool Human [1.25]

Disease ⇒ Steatohepatitis ⇒ Non-alcoholic fatty liver disease {40000151}

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Notes:

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