WASHINGTON — A new study has found that high-fat diets can trigger a molecular cascade of events that leads to intestinal and colon cancer.
The findings of the study were published in the journal “Cell Reports“.
According to the Centers for Disease Control and Prevention, dietary components high in saturated fats such as red meat are thought to be risk factors for colon cancer. Diet is thought to influence the risk of colorectal cancer strongly, and changes in food habits might reduce up to 70 percent of this cancer burden.
Of all the risk factors that elevate colon cancer risk, diet is the one environmental and lifestyle factor that may be the easiest to control, simply by changing people’s behavior and eating habits.
“There’s epidemiological evidence for a strong link between obesity and increased tumor risk,” Miyeko Mana, Assistant professor, School of Life Sciences, said.
“And in the intestine, the stem cells are the likely cell of origin for cancer. So diet is something that feeds into that cycle of obesity and colorectal cancer,” she said.
The new Arizona State University study led by Mana and her team has shown in greater detail than ever before how high-fat diets can trigger a molecular cascade of events that leads to intestinal and colon cancer.
As foods are broken down and make their way through the gut, they interact with intestinal stem cells that lie along the inside surfaces of the gut, which reside in a series of regularly folded valleys called crypts.
Intestinal stem cells are thought to be the gateway that coordinates intestinal tumor formation when they adapt to high-fat diets and elevate cancer risk.
“We were following up on mechanisms that might be required for stem cells to adapt to the high-fat diet — and that’s where we came across the PPARs (peroxisome proliferator-activated receptors),” said Mana.
These PPARs trigger a cellular program that elevates cancer risk, but the exact mechanisms were unclear because there are multiple types of PPARs, and complexities in teasing out their roles.
From their studies, Mana’s team could trace the development of cancer from the data, right from the diet to tumor formation.
The group also found that feeding a high-fat diet dramatically accelerated mortality in this model compared with the control condition by accelerating tumorigenesis.
“The levels of these fats that you can get through your diet are going to impact your stem cells, probably in a fairly direct way,” said Mana.
The new study evidence gives hope to apply their work to human colon cancers one day.
“These studies have all been in these mouse models to date,” said Mana.
“We are making progress with the high-fat diet model. Ultimately though, the goal is to eliminate or prevent colorectal cancer in humans.”
(With inputs from ANI)
(Edited by Anindita Ghosh and Nikita Nikhil)
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