Abstract
High red meat intake is associated with the risk of colorectal cancer (CRC), whereas dietary fibers, such as resistant starch (RS) seemed to protect against CRC. The aim of this study was to determine whether high-amylose potato starch (HAPS), high-amylose maize starch (HAMS), and butyrylated high-amylose maize starch (HAMSB)—produced by an organocatalytic route—could oppose the negative effects of a high-protein meat diet (HPM), in terms of fermentation pattern, cecal microbial composition, and colonic biomarkers of CRC. Rats were fed a HPM diet or an HPM diet where 10% of the maize starch was substituted with either HAPS, HAMS, or HAMSB, for 4 weeks. Feces, cecum digesta, and colonic tissue were obtained for biochemical, microbial, gene expression (oncogenic microRNA), and immuno-histochemical (O6-methyl-2-deoxyguanosine (O6MeG) adduct) analysis. The HAMS and HAMSB diets shifted the fecal fermentation pattern from protein towards carbohydrate metabolism. The HAMSB diet also substantially increased fecal butyrate concentration and the pool, compared with the other diets. All three RS treatments altered the cecal microbial composition in a diet specific manner. HAPS and HAMSB showed CRC preventive effects, based on the reduced colonic oncogenic miR17-92 cluster miRNA expression, but there was no significant diet-induced differences in the colonic O6MeG adduct levels. Overall, HAMSB consumption showed the most potential for limiting the negative effects of a high-meat diet.
Highlights
Intake of red and processed meat is positively associated with the risk of colorectal cancer (CRC) [1]
N-nitroso compounds are alkylating agents that generate DNA-adducts in colonocytes [7], one of them being the pro-mutagenic O6-methyl-2-deoxyguanosine (O6MeG) adduct that is increased in both murine [8] and human [9] colonocytes, following consumption of a high red meat diet
The aim of this study was to determine whether high-amylose potato starch (HAPS), high-amylose maize starch (HAMS), and HAMSB, the latter synthesized by a simple organocatalytic route [25,26], could oppose the negative effects of a high red meat diet, in terms of microbial metabolism in the large intestine, intestinal microbial composition, and biomarkers of CRC in rats
Summary
Intake of red and processed meat is positively associated with the risk of colorectal cancer (CRC) [1]. Human studies indicate that diets high in dietary fibers (DF), such as resistant starch (RS) reduce the CRC risk [1]. Several mechanisms to explain the association between red meat consumption and CRC risk have been suggested These mechanisms implicate metabolites produced by the gut microbiota from undigested dietary proteins, heme iron, heterocyclic aromatic amines, synthesized upon cooking and an endogenous formation of N-nitroso compounds, which might all negatively impact the colonic epithelial cell physiology [6]. It has been suggested that high quantities of red meat intake can increase the expression of oncogenic microRNA’s (miRNA), such as the miR17-92 cluster (miR17, miR18a, miR19a, miR20a, miR19b and miR92a) and miR21 in human rectal epithelial cells [10]. Butyrate has its strong anti-tumorigenic properties [14] and was shown to modulate oncogenic miRNA expression [15]
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