We have known for a long time that there is an association between the saturated fats we take in our diet and the risk of getting colorectal cancer: we have epidemiological and observational evidence. But we know less about how we move from fat molecules to the onset of disease. Now a study published on Cell Report sheds some light on the precise molecular mechanisms that link fat to cancer, adding a piece of knowledge about this dangerous relationship.
The secret in the crypts
Things, simplifying a bit, go like this. When food travels through the digestive system, it comes into contact with intestinal stem cells (or ISCs, from the English Intestinal Stem Cell) distributed throughout the digestive tract within structures called crypts. SSIs, which are responsible for the renewal of the inner wall of the intestine, i.e. the mucosa, contain sensor molecules that detect fat molecules and react to their presence. SSIs, therefore, adapt to the fats they come in contact with.
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A bad program
This sensor molecule is PPAR (an acronym for Peroxisomal Proliferator Activated Receptors). There are several PPARs and scientists have tried to define the roles that two of them – PPAR alpha and PPAR delta – play in the development of colorectal cancer using a population of laboratory mice undergoing a study as a model. excessively high fat diet. They thus discovered that the two PPARs interact in turn with another protein, Cpt1a, which has the function of importing the fat molecules into the mitochondria, that is, in the power plants where the energy needed by the cells is produced – and therefore also to the ISCs – to proliferate, that is, to increase in number. Now, the more SSIs increase in number, the more likely it is that mutations will accumulate in their DNA. And when mutations accumulate, the risk that some cells will lose control of themselves, so to speak, and start the processes that lead to a tumor also increases.
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By blocking the gene that codes for Cpt1a, it is possible to think of blocking the uncontrolled proliferation of ISCs, and therefore of reducing the risk of colorectal cancer in those who follow a very high fat diet. “One of the surprising things we are discovering – said Miyeko D. Mana, researcher at MIT and at the University of Arizona and first author of the study – is that fatty acids can have a direct effect on stem cells. But also that targeting PPARs or CPT1a could protect the gut from cancer. We are making progress using our study model (on laboratory animals, ed.), But the ultimate goal is to prevent or treat human bowel cancer ”.
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No miracle medicine: we have to intervene on the diet
“We have known for a long time that a high-fat diet is associated with the risk of bowel and other cancers as well. Now, it is true that this study adds a piece to the knowledge of fat metabolism, but it must be clear that we are talking about animals and that we are very far from applying these results in the clinic, “he says. Giordano Beretta, president of AIOM, the Italian Association of Medical Oncology: “We absolutely must not expect that one day a pill will allow us to eat as we want. It could be that in the future we will discover that in some individuals the metabolic mechanism just identified is activated even in the absence of excess fat ingested. Well, in that case it might make sense to intervene (pharmacologically, ed.). But it must be very clear that the point is diet: it is on what we can and must act “.
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