A diet high in fat from specific sources is uniquely responsible for contributing to intestinal cancer through promoting inflammation, scientists found during a recent study in mice models.
From the Perelman School of Medicine at the University of Pennsylvania, in collaboration with Case Western Reserve University and the Pacific Northwest Research Institute, scientists studied a mice model of familial adenomatous polyposis, an inherited disease where individuals have an 80 percent increased risk of developing colorectal cancer due to a mutation in a tumor suppressor gene called Apc.
For people who inherit this disease, benign cancer growths that appear in the colon during teenage years transform into malignant growths if they are not removed. People usually develop cancer when they are around 39 years old.
“Diet, but not necessarily obesity, can promote intestinal cancer," said co-author Edimara Reis, PhD. The team of research saw an immune reaction induced by a high-fat diet based on corn and coconut oils specifically that increased the risk of intestinal cancer in the mice. However, when they fed the mice olive oil as a source of fat instead, intestinal growths did not develop even in the obese mice.
Edimara and the other researchers from the study believe that their findings indicate that a high fat diet, not simply metabolic status, along with the chemical composition of the diet are the most important factors for determining cancer risk. But how does a high fat diet promote inflammation?
They found that the corn- and coconut-based diets induced inflammation that led to tumor formation through the activation of specific proteins within the complement system, a complicated network of proteins that’s equally involved in eradicating invading pathogens and acute and chronic inflammatory diseases like sepsis, acute lung injury, ischemia-reperfusion injury, and asthma.
Specifically, the mice fed high fat diets from corn- and coconut-based oils showed an increase in intestinal and system complement protein C5a, a pro-inflammatory molecule and strong chemoattractant involved with the recruitment of inflammatory cells like neutrophils, eosinophils, monocytes, and T lymphocytes as well as the activation of phagocytic cells, release of granule-based enzymes and generation of oxidants.
Additionally, mice given C5a inhibitors were protected from the development of intestinal tumors, indicating diet changes for humans could help reduce risk of cancer.
The recent study was published in the journal
Molecular Cancer Research.
Sources:
Perelman School of Medicine at the University of Pennsylvania,
U.S. National Library of Medicine,
Annual Review of Immunology
