Table 1.
Characteristics of the animal studies that investigated the role of HAMSB in modulating colorectal disturbances.
| First author, year | Animal, animal model | Control group (backbone) | HAMSB: dosage, duration | Key findings |
|---|---|---|---|---|
| Bajka et al. (2006) (89) | Rat, high protein diet-induced CRC | HAMS (RS backbone) | 10% diet, 10 days | ↑ cecal digesta weight, ↑ cecal and distal colon acetate, propionate and butyrate concentrations. ↑ portal plasma propionate and butyrate concentrations. ↓ high protein-induced colonocyte genetic damage. ↓ cecal, proximal and distal colon pH. Affected cecal ammonia. |
| Clarke et al. (2008) (84) | Rat, AOM-induced CRC | LAMS; LAMS +3% tributyrin; HAMS (N/R). |
10% diet, 4 weeks | HAMSB ↑ cecal tissue and digesta weight. HAMSB ↑ cecal, proximal, and distal colon butyrate; HAMSB ↑ portal plasma butyrate. HAMS, HAMSB ↓ tumor incidence compared with LAMS, HAMSB ↓ tumor number compared with LAMS. Cecal butyrate pools and concentrations were significantly and negatively correlated with the number of large bowel tumors. |
| Abell et al. (2011) (82) | Rat, AOM-induced CRC | HAMS (N/R) | 10% diet, 31 weeks | ↑ distal colon butyrate, did not change acetate, propionate concentrations. Did not change distal colon pH. Colon cancer incidence, tumor number and surface area were similar. ↑ Lactobacillus gasseri, Phascolarctobacterium and Parabacteroides distasonis. |
| Clarke et al. (2012) (85) | Rat, AOM-induced CRC | HAMS (N/R) | 10% diet, 4 weeks | ↑ SCFAs in large bowel digesta and plasma. ↑ apoptotic rates in the proliferate zone of distal colon (↑caspase-3), cellular proliferation did not change. |
| Conlon et al. (2012) (86) | Rat, Western diet-induced CRC | HAMS (Hi-Maize® 260) | 28% diet, 11 weeks | ↑ cecal tissue and digesta weight, ↑ cecal SCFA pool and portal vein propionate and butyrate ↓ western diet-induced weight and fat gain ↓ cecal and colon ammonia and phenols concentrations ↓ colonocyte genetic damage. ↑ Ung, Gmnn, Cebpa mRNA, ↓Rere mRNA. |
| Furusawa et al. (2013) (100) | Mouse, genetic modification-induced colitis | HAMS (N/R) | 15% diet, 4 weeks | ↓ colitis Induced Treg cells independent of TLR-MyD88 pathway ↑ histone H3 acetylation in the promoter and conserved non-coding sequence regions of the Foxp3 locus. |
| Toden et al. (2014) (87) | Rat, AOM-induced colon cancer | LAMS (AIN-93G) | 5, 10, 20, 40%, 4 weeks | ↑ Gut total SCFA, acetate and butyrate pools; ↑ hepatic portal venous plasma total SCFA, acetate, butyrate pools, ↓cecal ammonia pools. ↑ distal colonic epithelial apoptotic index, mucus thickness. ↓ Genetic damage dose-dependently; ↑ apoptotic rates, not affect colonocyte proliferation. |
| Le Leu et al. (2016) (102) | Rat, AOM-induced CRC | LAMS (AIN-93G) | 20% diet, 4 weeks | ↓ AOM-induced O6MeG adducts, especially in the lower third of the crypts. Crypt column height did not change. ↑ apoptotic rates |
| Nielsen et al. (2019) (99) | Rat, high protein diet-induced CRC | HAMS (Hi-Maize® 260) | 10% diet, 4 weeks | ↓ cecal acetate, not affect propionate, ↑ cecal butyrate, ↓ branched-chain fatty acids, ↑ fecal output. ↓ Diversity, ↑ Proteobacteria Sutterella, Proteobacteria Bilophila, Parabacteroides. ↓ miR19b and miR92a, ↓ O6MeG formation (not statistically significant). |
| Isobe et al. (2019) (101) | Mouse, DSS-induced colitis | HAMS (N/R) | 15% diet, 4 weeks | ↓ the translocation of luminal bacteria to the liver. ↑ IgA production in the colonic lamina propria by ↑ the T-cell independent response, which was mediated by GPR41 and GRP109a/HCA2, and the inhibition of HDAC. ↑ colonic barrier function; ↓ systemic bacterial dissemination under inflammatory conditions. |
| Yap et al. (2021) (103) | Mouse, Citrobacter rodentium infection- induced colitis | HAMS (N/R) | 15% diet, 3 weeks | Did not change infection-induced weight loss. ↑ epithelial damage of distal colon, ↓ neutrophils at lamina propria. |
AOM, Azoxymethane; DSS, dextran sulfate sodium; GPR: G protein-coupled receptor; HAMS, high-amylose maize starch; HAMSB, Butyrylated high-amylose maize starch; HDAC, histone deacetylase; O6MeG, O6-methyl guanine; N/R, not reported; SCFA: short-chain fatty acid.