Inulin Modulates Gut Microbiota and Increases Short-Chain Fatty Acids Levels to Inhibit Colon Tumorigenesis in Rat Models: A Systematic Review and Meta-Analysis.
- 2025-05
- Journal of food science 90(5)
- Yangyang Yu
- Jinling He
- Haiqi Fu
- Yong Mi
- Hao Wu
- Yuan Gao
- Minhui Li
- PubMed: 40331741
- DOI: 10.1111/1750-3841.70250
Study Design
- Type
- Meta-Analysis
- Methods
- Systematic review and meta-analysis; search of nine databases; selection of 12 studies; standardized meta-analyses
- Rigorous Journal
- Animal Study
Colorectal cancer (CRC) incidence rises with age, driven by factors such as diet. Inulin, a soluble fiber found in plants like Jerusalem artichoke and chicory, may influence CRC risk by modulating gut microbiota and improving metabolic profiles. This systematic review and meta-analysis evaluate the effects of inulin on CRC in animal models and explore its underlying mechanisms. A comprehensive search of nine databases led to the selection of 12 studies from an initial pool of 114 articles, based on predefined inclusion criteria. Standardized meta-analyses were performed for eligible studies. Results indicate that inulin supplementation significantly reduced aberrant crypt foci count in rats (SMD = -3.805, 95% CI, -7.348 to -0.262, p < 0.001), increased cecal weight (SMD = 6.723, 95% CI, 3.395-10.051, p = 0.000), enhanced colonic lactobacillus counts (SMD = 1.307, 95% CI, 0.644-1.970, p = 0.000), decreased coliform bacteria (SMD = -1.659, 95% CI, -2.147 to -1.171, p = 0.000), and elevated colonic short-chain fatty acids (SCFAs) levels, including acetate (SMD = 3.50, 95% CI, 1.111-5.890, p < 0.001), propionate (SMD = 3.081, 95% CI, 1.416-4.746, p < 0.001), and butyrate (SMD = 4.471, 95% CI, 2.464-6.478, p < 0.001). This systematic review demonstrates inulin's chemopreventive effects against CRC in animal models by enhancing beneficial gut bacteria (e.g., lactobacillus) and boosting SCFAs. Findings advocate integrating inulin-rich foods/supplements into prevention strategies for precision prebiotic development via SCFA-mediated epigenetic and antitumor mechanisms.