Table 2.
Metabolite | Source | Involved Bacteria | Effect | Reference |
---|---|---|---|---|
Secondary bile acids LCA and DCA | Primary bile Acids |
Clostridium sp. Lactobacillus Enterococcus Bifidobacterium Bacteroides |
More hydrophobic/toxic molecules? Easier reabsorption, reduction of gut bile salt concentration? Less FXR activation than CDCAHigher TGR5 activation than CDCA and CA |
[57] |
Short chain fatty acids: butyrate, propionate, acetate | Polysaccharides |
Lachnospiriaceae fam. Ruminococcacecae fam. Eubacterium rectale Faecalibacterium prausnitzii Roseburia sp. Anaerostipes |
gut inflammation gut barrier GLP-1 production steatosis |
[26] |
Indole | Dietary tryptophan |
Escherichia coli |
liver macrophage activation gut endotoxin |
[58,59,60] |
Ethanol | Polysaccharides |
Klebsiella pneumoniae
Escherichia |
Alcohol in the (portal) blood, oxidative stress and liver damage | [40,61] |
Phenylacetate | Phenylalanine | Proteobacteria | steatosis | [39] |
Trimethyl-5-aminovaleric acid (TMAVA) | Trimethyllysine |
Enterococcus faecalis
Pseudomonas aeruginosa |
steatosis | [62] |
Succinate | Polysaccharides | Prevotellaceae Veillonellaceae |
Controversial data | [63] |
LCA: lithocholic acid; DCA: deoxycholic acid; CDCA: chenodeoxycholic acid; CA: cholic acid; FXR: farnesoid X receptor; TGR5: Takeda G-coupled receptor 5.