Table 1.
Commonalities between CIH and CSF (with or without HFD-fed) related modification on lipid metabolism through gut microbiota-metabolite-liver/adipose axis.
| CIH, CSF and dietary modification on | Related mechanism of lipid metabolism disorders |
|---|---|
| Gut microbiota composition or properties | |
| Intestinal bacterial derivative metabolites | |
| Downregulation of Akkermansia mucinphlia | caused intestinal mucosal damage and increased intestinal permeability (21) |
| Upregulation of Firmicutes | activated PPAR-γ to promote β-oxidation of BAT (25) |
| induced insufficient BCAA | promoted IR (71) |
| Upregulation of Firmicures/Bacteroidetes | promoted TG deposition in WAT (40) |
| induced insufficient SCFAs | inhibited protective PPAR-α to induce hepatic steatosis (52) |
| insufficient BAs | inhibited TGR5 to induce IR through decreased endogenous GLP-1 secretion (70) |
| Upregulation of FFAs
due to CIH or CSF-decreased Clostridium spp. CIH-increased Bifidobacterium spp. or Lactobacillus spp. |
actived pro-inflammatory TLR2 and increased expression of pro-apoptotic gene Bax in liver, WAT and BAT (39); caused hepatic steatosis due to excessive synthesis of TG and cholesterol (58); actived c-JNK and NF-κB to induced ER stress and IR (72) |
| Downregulation of
Clostridium spp.
induced insufficient tryptophan and indoles |
inhibited AHR to promote IR through decreased endogenous GLP-1 secretion (32) |
| Downregulation of glutamate and glutathione
due to CIH-increased Enterorhabdus spp. CSF-decreased Bacteroides spp. |
induced excessive ROSs corelated with hepatic steatosis (50) |
| Upregulation of LPS
due to CIH-increased Desulfovibrio spp. CSF-increased Proteobacteria |
actived pro-inflammatory TLR4 and increased hepatic VLDL and lipoprotein levels (64) |
BAT, brown adipose tissue; WAT, white adipose tissue; BCAA, branched-chain amino acid; SCFA, short-chain fatty acid; BA, bile acid; LPS, lipopolysaccharide; TG, triglyceride; VLDL, very low-density lipoprotein; IR, insulin resistance; PPAR, peroxisome proliferator-activated receptor; TGR5, takeda G protein-coupled receptor; GLP-1, glucagon-like peptide-1; TLR, toll-like receptor; c-JNK, c-Jun N-terminal kinase; ER, endoplasmic reticulum; AHR, aryl hydrocarbon receptor; ROS, reactive oxygen species. The red color signified up-regulation, whereas the blue color signified down-regulation.