Protein as well as
starch is fermented in the colon, but the interaction between
protein and
starch fermentation and the impact on colonic
oncogenesis is unknown.
High-protein diets increase delivery of
protein to the colon and might promote
oncogenesis through generation of toxic products. We investigated the interaction of
resistant starch (RS) with digestion-resistant potato
protein (PP) on colonic fermentation events and their relationship to intestinal tumourigenesis. Male Sprague-Dawley rats were fed an AIN-76A-based diet for 4 weeks and
intestinal neoplasms were induced by
azoxymethane. Experimental diets included the following: no added RS or PP, 10% high
amylose maize
starch (source of RS) replacing digestible
starch, 15% PP replacing
casein and 10% high
amylose maize starch+15% PP. Rats were maintained on diets until killed at 30 weeks. Feeding RS significantly increased
short-chain fatty acid (SCFA) levels (P<0.001) in the caecum and colon. Importantly,
butyrate concentration was significantly increased in the distal colon with RS (P<0.001). Feeding PP increased
protein fermentation products, but this effect was reduced by adding RS to the diet.
Intestinal neoplasms and colorectal
adenocarcinomas were reduced by feeding RS (P<0.01) regardless of whether PP was fed, whereas PP alone increased the incidence and number of small
intestinal neoplasms including the
adenocarcinomas (P<0.01). In conclusion, RS altered the colonic
luminal environment by increasing the concentration of SCFAs including
butyrate and lowering production of potentially toxic
protein fermentation products. These effects of RS not only protected against intestinal tumourigenesis but also ameliorated the tumour-enhancing effects of feeding indigestible
protein.