Table 1.
Signal | Target organ | Effect | Reference |
---|---|---|---|
Bile acids (BAs) | Adipose tissue, intestine, liver | Hepatic metabolism, bacterial regulation, lipid metabolism | (36, 38) |
Short chain fatty acids (SCFAs) | Adipose tissue, brain, intestine, liver, muscle | Lipid metabolism, regulation of appetite | (40–42) |
Neuroactive molecules [g-aminobutyric acid (GABA), serotonine] | Central and peripheral nervous system | Regulation of appetite | (43, 44) |
Lipopolysaccharide (LPS) | Adipose tissue, liver, brain | Systemic inflammation, hepatic glucose metabolism, adipose tissue fibrosis | (45–47) |
Trimethylamine N-oxide | Adipose tissue, liver, kidney | Higher atherosclerosis risk, reduced beige fat | (48, 49) |
Branched-chain amino acids (BCAAs) | Adipose tissue, endothelium, skeletal muscle | Adipogenesis, lipid trafficking, lipogenesis, and insulin resistance | (12, 13, 26, 27, 50, 51) |
LPS, BAs, SCFAs, BCAAs, trimethylamine N-oxide, and neuroactive molecules are major known signals of microbial origin that can affect different metabolic organs listed together with the proposed model of action.