Influence of different diets on development of DMH‐induced aberrant crypt foci and colon tumor incidence in Wistar rats

Abstract

The present study was undertaken to investigate certain dietary factors known to affect the development of colon cancer for their ability to modulate aberrant crypt foci (ACF). Male Wistar rats were initiated with oral doses of dimethylhydrazine dihydrochloride (DMH-2HCl, 20 mg/kg body wt) once a week for 10 or 20 weeks. Throughout the study the animals were fed 1) semisynthetic casein-based control diet, 2) control diet with 20% lard, 3) control diet with 20% lard and 20% dietary fiber, or 4) control diet where most of the carbohydrate pool was substituted with sucrose and dextrin. The composition of the different diets was designed to achieve equivalent intakes of essential nutrients. Animals were killed after 10, 20 and 31 weeks. The study showed a pronounced effect of dietary composition on the development of DMH-induced ACF. The diet high in sucrose and dextrin caused a statistically significant increase (p < or = 0.05) in the total number of ACF and number of small and medium ACF. Adding lard to the standard diet did not cause an increase in ACF, but if the dietary fiber was added to the high-fat diet, a statistically significant reduction (p < or = 0.05) in the total number of ACF and number of small and medium ACF was observed. The values of large and extra-large foci reflected the same effect of diets on ACF. The results indicate that tumors in the group fed the diet high in refined carbohydrates were more prominent and occurred with a higher incidence. However, the difference is based on few tumors and is not statistically significant.(ABSTRACT TRUNCATED AT 250 WORDS)

Prevention by natural food anthocyanins, purple sweet potato color and red cabbage color, of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP)-associated colorectal carcinogenesis in rats initiated with 1,2-dimethylhydrazine.

“…However, it must be borne in mind that the reliability of these lesions as a predictor of eventual tumor formation is not fully accepted (Kristiansen et al, 1995;Thorup, 1997). In this context, while our data for both ACF and tumors were in agreement, modified initiation/promotion bioassays using quantitative analysis of neoplasms as end-point lesions ) appear more appropriate for detection of inhibitors of colon tumor develop- ment.…”

High Sucrose Diets Promote Intestinal Epithelial Cell Proliferation and Tumorigenesis in APCMin Mice by Increasing Insulin and IGF-I Levels

“…Depending upon the source, dietary carbohydrates may differentially influence colonic luminal environment due to fermentation of undigested starch and production of short chain fatty acids (34). Previous research has demonstrated that colonic epithelial cell proliferation is significantly increased in rats fed sucrose compared to cornstarch (4)(5)(6)(7). Effects of carbohydrate source on colon proliferation were not associated with difference in luminal concentrations of short-chain fatty acids or cecal pH (34).…”

“…Epidemiological studies suggest that high dietary intakes of sucrose are associated with greater colon cancer risk (2,3). Most studies using carcinogen-induced colon cancer models have reported that feeding high-sucrose diets to rats promoted development of aberrant crypt foci (ACF) and increased epithelial cell proliferation in colon crypts compared with feeding high-cornstarch diets (4)(5)(6)(7). Colon adenocarcinomas in carcinogen-treated rats consuming high-sucrose diets were significantly larger and had more invasive potential compared with those in rats consuming cornstarch (8).…”

Colon cancer risk factors from nutrition

“…With this assay a sucroserich diet has repeatedly been observed to have co-carcinogenic action in the colon and liver of rats and to increase the number of aberrant crypt foci in rat colon [53,54,55,56]. Asbestos, an environmental mutagen, has also been found to induce aberrant crypt foci in the rat colon [57].…”