MIT researchers find ketogenic diet increases small-intestinal tumours in cancer-prone mice via fat metabolism in stem cells

Researchers at the Massachusetts Institute of Technology have published findings showing that a ketogenic diet produced markedly different outcomes in neighbouring regions of the gut in cancer-prone mice. Small-intestinal tumours increased on the diet, while colonic tumours were reduced — a divergence the team traced to the way intestinal stem cells processed the diet's high fat content.

The investigators found that the elevated fat availability prompted intestinal stem cells to upregulate fat-oxidation pathways, which in turn drove more rapid cell proliferation. Increased stem cell division raises the probability of replication-associated mutations accumulating, which may underlie the higher tumour burden observed in the small intestine. Importantly, the team identified fat metabolism — rather than circulating ketone bodies — as the mechanistic driver, a distinction that has implications for how dietary interventions interact with cancer risk biology.

The findings are reported from a mouse model and have not been tested in humans. Cancer-prone mouse models carry germline or somatic alterations that accelerate tumour formation at rates not directly translatable to human populations. The study does not provide a basis for dietary recommendations. From a research perspective, the work adds to a growing literature on how metabolic state influences stem cell behaviour and cancer risk, with relevance to researchers studying the intersection of diet, metabolism, and intestinal biology.