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Butyrate, a short-chain fatty acid, may suppress colon cancer growth.

Colon cancer is one of the leading causes of death in developed nations. Health experts attribute much of the risks associated with colon cancer to dietary patterns, especially those that are high in red meat and low in fruits, vegetables, and fiber. Findings from a 2009 study suggest that butyrate, a short-chain fatty acid, activates a protein called GPR109A in the colon to suppress colon cancer.

Short-chain fatty acids are produced by the gut microbiota during the fermentation of dietary fiber. In turn, these fatty acids provide energy to cells in the colon and play key roles in maintaining gut health. Butyrate, in particular, functions as a tumor suppressor by inhibiting enzymes called histone deacetylases, which drive tumor growth.

The investigators assessed the production of GPR109A in the colon tissues of mice and humans (with and without colon cancer) using monoclonal antibodies that targeted the protein. Then they determined whether butyrate bound to GPR109A and how the fatty acid influenced tumor growth. Finally, they gauged the effects of butyrate on cancer cell growth and progression.

They found that GPR109A was present on the surface of cells in the colons of both mice and humans, where it recognized and bound with butyrate. In the setting of cancer, GPR109A activity was silenced, effectively shutting down its activity. Supplying butyrate switched on the activity of GPR109A, which in turn promoted the death of cancer cells and suppressed the activity of nuclear factor-κB, a transcription factor that drives inflammation and tumor growth.

These findings suggest that GPR109A mediates the tumor-suppressive effects of butyrate in the colon. Interestingly, evidence indicates that beta-hydroxybutyrate, a type of ketone, also binds with GPR109A, suggesting that the compound exerts anticancer properties in the colon. Learn more about the beneficial health effects of butyrate and beta-hydroxybutyrate in our overview articles.

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