Table 1.

The beneficial and harmful metabolic pathways of the gut microbiota and their impacts on the host.

		Consequence for Host
Source	Bacterial Group Involved	Derived Metabolites	Beneficial	Harmful
Dietary carbohydrates	Faecalibacterium, Bacteriodes, Ruminococcus, Blautia [32].	Fermentation to SCFAs (acetate, butyrate, propionate) [38].	Anti-inflammatory effect. Maintenance of intestinal barrier function. Motility regulation. Source of energy for epithelial cells [38,39].	Virulence factors of enteropathogen activation (e.g., Salmonella type III secretion system) [32].
Primary bile acids	In small animals, mainly C. hiranonis [34].	Transformation to secondary BAs in colon [34].	Anti-inflammatory effect. Growth inhibition (C. difficile, Clostridium perfringens, Escherichia coli). Modulation of glucose/insulin secretion [35].	Secretory diarrhoea caused by lack of C. hiranonis (e.g., chronic enteropathies). In humans, a diet rich in fat, due to increased secondary BAs, represents a high risk of colon cancer [34,36,37].
Dietary fat	C. perfringens, Bifidobacterium bifidum, Propiobacterium) [32].	Conversion to hydroxystearic acids [32].	None [32].	Fatty acid diarrhoea [32].
Dietary amino acid tryptophan	Various [32].	Indole metabolites [43].	Anti-inflammatory effect. Maintenance of intestinal function [43].	Cytotoxic and putrefactive, but only in high concentrations. Indoxyl sulfate acts as a uremic toxin [32].
Dietary amino acids tyrosine and phenylalanine	Various [32].	P-cresol [32].	None [32].	Progression of chronic kidney disease similar to uremic toxin [32].
Drug mycophenolate mofetil	Various [32].	MPA (mycophenil acids) and acyl glucuronide [32].	None [32].	Production of proinflammatory cytokines causing diarrhoea [32].