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Modulation of Intracellular Second Messengers by Dietary Fat during Colonic Tumor Development

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Dietary Fat and Cancer

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 422))

Abstract

Marked differences in the incidence of colon cancer in populations migrating from low to high risk areas suggest that environmental factors, specifically dietary factors, play an important role in the etiology of colon cancer.1,2 Dietary fat has received considerable attention as a possible risk factor in the etiology of colon cancer. A proposed hypothesis regarding the induction of colon cancer suggests that fats increase the amount of bile acids in the colon, which in turn are metabolized to secondary carcinogens to promote the growth of adenomas and subsequently invasive cancer.3 Moreover, the amount and type of fat in the diet directly affects the concentration of free fatty acids, eicosanoids and diacylglycerols in the colonic lumen which can influence colonic intracellular second messengers and modify the risk of colon cancer development.4,5,26,93 In comparison, dietary fiber is postulated to reduce the adverse effects of certain fats through several mechanisms, including dilution of carcinogens, decrease in transit time, reduction in fecal pH, chemical binding, and alteration in microflora metabolism6,7. However, experiments in animal models using a variety of fats and fibers have produced conflicting results. In some studies, fiber failed to protect,8,9 and in others, fat failed to promote colon carcinogenesis.10 The interpretation of this data is made even more complicated by the fact that different types of dietary fiber and fat may affect colon carcinogenesis in an interactive site-specific manner.11

This work was supported in part by the American Institute for Cancer Research and NIH CA59034.

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Chapkin, R.S., Jiang, YH., Davidson, L.A., Lupton, J.R. (1997). Modulation of Intracellular Second Messengers by Dietary Fat during Colonic Tumor Development. In: Dietary Fat and Cancer. Advances in Experimental Medicine and Biology, vol 422. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-2670-1_7

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