Colon cancer incidence is strongly linked to dietary and lifestyle factors such as consumption of Western diets and refined sugars, specifically sucrose. The mechanistic pathways are not clear, yet there is evidence that carbohydrates may act on circulating glucose, insulin levels, and insulin-like growth factors (IGFs). The aim of this study is to determine the effects of feeding APCMin as well as normal C57BL6/J mice diets containing corn starch (control), sucrose, glucose, fructose, or a 1:1 ratio of glucose:fructose (G:F) as the sole carbohydrate source. The G:F treatment is meant to mimic the composition of high fructose corn syrup (HFCS). Overall, mice fed sucrose diets for 10 weeks gained the most weight and body fat. Fructose- and starch-fed mice had the lowest body weights. Percent body fat was the same for mice fed starch, fructose, or G:F. In the small intestine (SI), the fructose-fed mice developed the most tumors. Sucrose-fed mice had fewer tumors in the distal third of the SI, yet were not different than the starch control overall. Sucrose-fed mice also tended to have higher plasma glucose and insulin while starch-fed mice had the lowest, yet these trends were not significant. There was no effect of dietary treatment on colonic tumors or plasma IGF-1 concentrations. Sucrose feeding resulted in higher body weights, body fat, and a shift towards insulin resistance, while fructose feeding resulted in an increased number of SI tumors. These results do not strongly support the hypothesis that intestinal tumorigenesis is driven by circulating glucose or insulin at 10 weeks. Also, G:F-fed mice tended to be more similar to those fed glucose rather than sucrose. This suggests that glucose is mediating some of the effects that are seen with fructose feeding.
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