Dietary Resistant Starch Alters the Characteristics of Colonic Mucosa and Exerts a Protective Effect on Trinitrobenzene Sulfonic Acid-induced Colitis in Rats

Abstract

The protective effect of a dietary high-amylose cornstarch (HAS) against trinitrobenzene sulfonic acid (TNBS)-induced colitis was examined in rats. Rats were fed a HAS-free basal diet or, a 15% or 30% HAS supplemented diet for 10 d, and then received intracolonic TNBS to induce colitis and fed the respective diets for a further 8 d. HAS ingestion significantly protected colonic injuries as evidenced by lower colonic myeloperoxidase activity. Rats fed the HAS diet showed greater cecal short-chain fatty acid (SCFA) production than those fed the basal diet. Further, just before TNBS administration, HAS ingestion dose-dependently increased fecal and cecal mucin contents, and protein and nucleic acid contents in the colonic mucosa. HAS ingestion also reduced colonic permeability. The protective effect of HAS ingestion on TNBS-induced colitis is perhaps exerted through alterations in colonic mucosa, possibly due to cecal SCFA production.Key words: high-amylose cornstarch; trinitrobenzene sulfonic acid; short-chain fatty acids; mucin; ratsThe etiology of inflammatory bowel disease, encompassing Crohn's disease and ulcerative colitis, remains unknown, but studies in animal models suggest that disruption of mucosal barrier function may induce abnormal immune responses to luminal bacteria, resulting in acute and chronic inflammation in the large bowel.1) Mucosal barrier function has been ascribed to colonic epithelial cells based on mucus production and shedding of surface cells, which are replenished by renewal from crypt cells.2) In this regard, short-chain fatty acids (SCFA: mainly acetate, propionate, and butyrate), products of large bowel fermentation by bacteria, have been reported to be major fuels for colonic epithelial cells and to accelerate epithelial cell proliferation. 3,4) Earlier studies indicated that SCFA irrigation stimulated the mucosal repair process and decreased inflammation in human patients 5) and rats injected with trinitrobenzene sulfonic acid 6) (TNBS). Also, Barcelo et al. 7) found that a physiological concentration of butyrate and acetate caused a significant increase in mucus secretion in the lumen of isolated perfused rat colon. Greater mucin production might contribute to the lower incidence of bacterial translocation across the gut barrier reported in studies that fed dietary fiber. 8) Clearly, SCFAs are considered to be of benefit in the treatment of inflammatory bowel disease.Although SCFA delivery to the colon might be accomplished with an enteric-coated capsule or a rectal infusion of SCFA, the nutritional approach is more physiological, consistent, and cost-effective, and less stressful. One potential route is to increase the consumption of foods high in resistant starch, because studies in experimental animals have shown that the feeding of resistant starch, such as high-amylose cornstarch (HAS), increases the large bowel digesta SCFA level in rats [9][10][11] and pigs. 12) Previously we found that ingestion of HAS prevented endotoxin influx from the intestinal tract into the portal ...

The intestinal microbiota in aged mice is modulated by dietary resistant starch and correlated with improvements in host responses

“…Enrichment in A. mucinphila was also recently reported for genetically obese ( ob/ob ) mice fed prebiotic carbohydrates (Everard et al ., ). These bacteria might have benefited from increases in cecal mucin production induced by the dietary carbohydrates (Morita et al ., ). Moreover, different Bifidobacterium species were found in mice fed HAM‐RS2.…”

Crosstalk between Microbiota-Derived Short-Chain Fatty Acids and Intestinal Epithelial HIF Augments Tissue Barrier Function

“…The protection afforded by fiber and resistant starch in experimental colitis are thought to be dependent on SCFA production (Ito et al, 2009; Morita et al, 2004; Videla et al, 2001), and administration of exogenous butyrate promotes resistance to experimental colitis (Cresci et al, 2013; Leonel et al, 2013). Studies investigating dysbiosis in inflammatory bowel disease identified reduced abundance of butyrate-producing organisms (e.g., certain Roseburia and Faecalibacterium genera) and lower concentrations of butyrate associated with disease (Machiels et al, 2013; Eeckhaut et al, 2013; Sokol et al, 2009).…”

Dietary Cycloinulooligosaccharides Enhance Intestinal Immunoglobulin A Production in Mice

“…Ichikawa et al 15) have demonstrated that an oral or rectal administration of SCFA (a mixture of acetic acid, propionic acid and butyric acid) stimulated gut epithelial cell proliferation. Morita et al 16) have reported that mucin production in the gut may be stimulated by SCFA. Butyrate has been found to enhance the cytotoxic activity of natural killer cells and to increase the density of splenic T-helper cells.…”