Table 1.

Studies demonstrating the role of the gut microbiota and its metabolites in obesity and CRC models.

Disease Model	Outcomes	References
OB-CRC patients	Decrease in butyrate-producing bacteria. Overabundance of opportunistic pathogens. Increased levels of proinflammatory cytokine IL-1β, the deleterious bacterial metabolite TMAO, and gut permeability.	[48]
OB-CRC patients	The α-diversity was higher in patients with colorectal cancer versus controls. The relative abundance of the genera Enterococcus, Capnocytophaga, and Polaribacter was significantly altered with reduced presence of E. faecalis.	[49]
HFD mouse model	HFD promotes CRC by inducing gut microbial dysbiosis, metabolomic dysregulation with elevated lysophosphatidic acid, and gut barrier dysfunction.	[50]
CRC patients	Decrease in butyrate-producing bacteria Eubacterium rectale, Faecalibacterium prausnitzii.	[51]
CRC patients	Enrichment of potential pathogens. Decrease in butyrate-producing members Faecalibacterium and Roseburia.	[52]
CRC patients	Increase in Enterococcus, Escherichia/Shigella, Klebsiella, Streptococcus, and Peptostreptococcus. Decrease in Genus Roseburia and other butyrate-producing bacteria of the family Lachnospiraceae.	[53]
CRC and colorectal adenomas patients	Altered gut metabolites and microbiota interactions are implicated in colorectal carcinogenesis and can be non-invasive diagnostic biomarkers.	[54]
CRC cellular model	Microbial metabolite deoxycholic acid promoted vasculogenic mimicry formation and EMT through VEGFR2 activation, which further exacerbated intestinal carcinogenesis.	[55]
Mouse model of CRC associated with colitis	Combined dosing of SCFAs (67.5 mM acetate, 40 mM butyrate, 25.9 mM propionate) inhibited tumor formation and reduced colon inflammation.	[56]
CRC mouse and cellular models	Faecalibaculum rodentium and its human homologue, Holdemanella biformis, produced SCFAs that contributed to control protein acetylation and tumor cell proliferation by inhibiting calcineurin and NFATc3 activation in mouse and human settings.	[57]
CRC cellular model	Greater inhibitory efficacy of butyrate over propionate and acetate against human colon cancer cell proliferation via cell cycle arrest and apoptosis.	[58]
HFD-induced intestinal tumor development in Apcmin/+ mice.	Butyrate-producing C. butyricum exhibited decreased proliferation, increased apoptosis, and suppressed the Wnt/β-catenin signaling pathway. Positively modulated the gut microbiota composition, by decreasing some pathogenic bacteria and bile acid (BA)-biotransforming bacteria and increasing some beneficial bacteria, including SCFA-producing bacteria.	[59]
CRC cellular models	BAs decreased activation of functional farnesoid X receptor (FXR) signaling in CRC cells, promoting colonic carcinogenesis and CRC risk.	[60,61]
CRC cellular models	Fusobacterium nucleatum promotes colorectal carcinogenesis by modulating E-cadherin/β-catenin signaling via its FadA adhesin.	[62]
CRC mouse model	Fusobacteria generate a proinflammatory microenvironment through recruitment of tumor-infiltrating immune cells, which is conducive for colorectal neoplasia progression.	[63]
Obese humans	Gut microbiota is enriched in Lactobacillus reuteri and depleted in Bifidobacterium animalis and Methanobrevibacter smithii.	[64]
Obese mice model	Obese microbiome has an increased capacity to harvest energy from the diet. Colonization of germ-free mice with an ‘obese microbiota’ results in a significantly greater increase in total body fat than colonization with a ‘lean microbiota’.	[44]
Mouse models	Exercise and butyrate supplement increase butyrate-producing bacteria in the gut microbiota, and increases the production of butyrate, thereby improving lipid metabolism through the butyrate-SESN2/CRTC2 pathway and protecting against obesity.	[65]
Cellular and murine models	L. paracasei and E. coli, impacted host lipid metabolism in a diet-dependent manner. L. paracasei resisted HFD-induced obesity.	[66]
HFD-induced obese mouse model	Decreased fat storage by regulating levels of angiopoietin-like 4 protein (ANGPTL4).	[67]
HFD-induced obese mouse model	Gut microbiome is a critical factor for the anti-obesity effects of Capsaicin (CAP). CAP increased levels of butyrate-producing Ruminococcaceae and Lachnospiraceae, while it caused lower levels of members of the LPS-producing family S24_7. CAP prevented HFD-induced intestinal barrier dysfunction by inhibiting cannabinoid receptor type 1.	[68]
HFD-induced obese mouse model	SCFA butyrate is effective in alleviating diet-induced obesity through activation of the ARβ3-mediated lipolysis in the epididymal white adipose tissue. SCFA acetate reduces appetite via a central homeostatic mechanism.	[69,70]