Ketogenic diet, double metabolic effect on tumors, one organ slows down and another accelerates

The research, performed on mouse models genetically predisposed, reveals that the ketogenic diet produces diametrically opposed biological responses within the gastrointestinal tract, stimulating tumor growth in the small intestine while reducing it in the colon. From a purely molecular point of view, the most relevant aspect of study led by Omer Yilmaz, director of the MIT Stem Cell Initiative, lies in the fact that ketone bodies, such as beta-hydroxybutyrate, do not play an active role in this processpartially disproving previous hypotheses that saw them as the main drivers of these cellular dynamics.

Omer Yilmaz, director of the MIT Stem Cell Initiative

“Ketone bodies are essentially metabolic bystanders, while the real surprise is that tumor acceleration is driven entirely by how stem cells process and burn the massive influx of dietary fat“, explains Yilmazhighlighting how the entire phenomenon is governed by the oxidation of fatty acids. This specific metabolic pathway activates the family of proteins called PPAR, which sends signals to intestinal stem cells causing them to multiply more rapidly. Although accelerated proliferation is useful for repairing intestinal tissues after injury or disease, the excess of this stimulus increases the probability that the cells undergo oncogenic mutations.

The discrepancy in behavior between two adjacent tracts of the digestive system therefore imposes extreme caution in the clinical adoption of these diets, since a regime that proves protective for one organ can prove harmful for another. The conclusions of the MIT research team open new scenarios also on the supplement market, since the exclusion of ketone bodies from tumor activation or suppression processes suggests that commercial ketone-based supplements are unable to replicate either the protective benefits found in the colon or the risks identified in the small intestinefocusing clinical attention exclusively on the complex metabolic biochemistry of individual tissue districts.