Carcinogenesis Advance Access published online on December 13, 2006
Carcinogenesis, doi:10.1093/carcin/bgl245
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Effect of Dietary Resistant Starch and Protein on Colonic Fermentation and Intestinal Tumourigenesis in Rats
Department of Medicine, Flinders University of South Australia, Bedford Park, 5042
1 National Starch & Chemical Company, Bridgewater, New Jersey, USA
2 School of Nursing and Midwifery, University of South Australia, 5000
3 Department of Applied Biological Chemistry, Faculty of Agriculture, Shizuoka University, Shizuoka 422-8529, Japan
* Author to whom correspondence should be addressed. Email: richard.leleu{at}flinders.edu.au Phone: 618 8204 5170 Fax: 618 8204 3943
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: no added RS or PP; 10% high-amylose maize starch (source of RS) replacing digestible starch; 15% PP replacing casein; 10% high-amylose maize starch + 15% PP. Rats were maintained on diets until sacrifice at 30 weeks. Feeding RS significantly increased 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, while 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 ameliorated the tumour-enhancing effects of feeding indigestible protein.
Key Words: colorectal cancer fermentation butyrate resistant starch indigestible protein
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