Obesity-Enhanced Colon Cancer: Functional Food Compounds and their Mechanisms of Action
Christopher C. Tarver,
Peter S. Murano.
Obesity is rapidly becoming a global phenomenon. This is more than a cosmetic issue as obesity is associated with several life-threatening diseases, including colon cancer. Insulin resistance and inflammation, underlying factors in obesity-related diseases, promote colonocyte proliferation and suppress programmed cell death, or apoptosis, by activating the insulin-like growth factor (IGF) and prostaglandin pathways. These pathways converge on the Wnt pathway, which is implicated in colon carcinogenesis. Despite tremendous advances in our understanding of the molecular mechanisms involved in colon carcinogenesis, mortality due to colon cancer world-wide is unacceptably high. Even though conventional therapies can prolong a patients life-span a few years, they cause serious side effects. Thus, there is growing interest in functional foods and dietary bioactive compounds with chemopreventive properties. This search is fueled by the epidemiological studies indicating that plant-based diets are protective against several types of cancers. This review provides a brief summary of the IGF and prostaglandin pathways, which are implicated in obesity-enhanced colon cancer, and some of the functional foods/dietary compounds that target these pathways. It is essential to understand the molecular mechanisms involved in chemoprevention before providing appropriate science-based dietary recommendations to prevent colon cancer in both obese and non-obese individuals.
Keywords: Colon cancer, functional foods, obesity, Wnt, prostaglandin, IGF, insulin, inflammation
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