The ketogenic diet, very high in fat and low in carbohydrates, could promote the growth of small intestine tumors. This is suggested by a study conducted on mice genetically predisposed to intestinal cancer.
The ketogenic diet pushes the body to use fats rather than glucose as its main source of energy. This transition produces molecules called ketone bodies. The diet was first designed in the 1920s to treat certain epilepsies, it is now also followed to lose weight or reduce carbohydrate intake.
The researchers from the MIT compared three groups of mice predisposed to intestinal tumors. Some received a ketogenic diet, others a control diet. A third group followed a high-fat and high-calorie diet. The mice on the ketogenic diet developed more small intestine tumors than those in the control group.
The ketone bodies do not seem to be responsible for the acceleration of tumors. The researchers instead identified the role of fatty acid oxidation, a cellular mechanism that transforms dietary lipids into energy. This pathway activates proteins named PPAR. These then stimulate the multiplication of intestinal stem cells.
These stem cells are essential for the renewal of the intestinal wall. They notably allow repairing tissue after an injury or infection. However, excessive activity increases the number of cell divisions. In animals already predisposed, this situation therefore increases the probability of tumor cells emerging.
The study also highlights a surprising contrast. The same ketogenic diet limited the development of tumors in the colon of the mice. The small intestine and colon, although neighbors, therefore do not respond the same way to a high-fat diet. The researchers now want to understand the origin of this difference between two segments of the digestive tract.