Mounting epidemiological and experimental evidence consistently indicates that obesity is a robust risk factor, with 50~100% increase in risk for CRC. As obesity has reached an epidemic level and increases in the scope of the problem are projected, it is critical to understand the mechanism(s) responsible for the link and thereby to develop preventive strategies. The ultimate goal is, through the completion of this project, to facilitate the development of preventive approaches to diminish dietary obesity associated CRC. The primary objective of this project is to determine the role of Turicibacter and SCFAs, particularly butyrate in this project, in the mediation of intestinal tumorigenesis exclusively associated with a high fat diet-induced obesity. We aim a) to determine how the microbial metabolite butyrate mediates the short-chain fatty acid receptor pathway and to what extent it can attenuate intestinal tumorigenesis associated with the consumption of a high fat diet; b) to define whether the administration of Turicibacter improves the production of short-chain fatty acids and suppresses the tumorigenesis in the Apc1638N mice fed with a high fat diet.