FIGURE 2 Boxplots showing ef- fects of including different sources of starch in Western diets moder- ate in protein and fat on colonic gene expression of Mdm2 (A), Top1 (B), Msh3 (C), Ung (D), Rere (E), Cebpa (F), Gmnn (G), and Parg (H) in rats. Standard gene symbols are used (32,33). The limits of the boxes represent the lower and upper quartile range, and the solid line within the box represents the median value. Whiskers extend to the lowest and highest values within 1.5 times the quartile range and values outside this range are shown as circles. C-LAMS, control diet containing low amylose maize starch (n = 5); W-HAMS, Western diet containing high amylose maize starch (n = 8); W-HAMSB, West- ern diet containing butyrylated high amylose maize starch (n = 9); W- HAW, Western diet containing high amylose wheat flour (n = 8); W-LAMS, Western diet containing low amylose maize starch (n = 7); W-LAW, Western diet containing low amylose wheat flour (n = 6). LAMS treatments, suggesting relatively little effect of increasing the fat and protein content of the diet on the large bowel micro- biota. The proﬁles of the W-HAMS– and W-HAMSB–treated rats also clustered together, indicating little effect of the extra butyrate delivered by HAMSB relative to HAMS. The micro- biota proﬁles of rats receiving the wheat treatments comprised the third grouping. These groupings suggest the feeding of RS alters the relative proportions of the gut microbiota but also that the further addition of mixed forms of NSP from a whole meal ﬂour leads to other changes in the microbiota proﬁles. Our an- alyses also revealed a common feature of the microbial proﬁles 838 Conlon et al. associated with the RS diets: the high abundance of clostridial cluster IV bacteria (except Faecalibacterium prausnitzii). The butyrate-producing ability of many bacteria in this cluster is expected to have contributed to the increased butyrate and SCFA produced in response to RS diets. There has been debate around the potential for greater SCFA production through fermentation to induce a colonic epithelial hyperproliferation and, hence, contribute to CRC. This propo- sition is supported by the greater incidence of polyps in mutant CRC-prone mice when fed fermentable NSP as apple pomace (52). However, .90% of those tumors were in the small intestine