Obesity and eating fatty food are significant risk factors for many types of cancer. A new study has revealed that a high-fat diet makes the cells of the intestinal lining in the gut more likely to become cancerous.
"We wanted to understand how a long-term high-fat diet influences the biology of stem cells and how such diet-induced changes that occur in stem cells impact tumour initiation in the intestine," said Omer Yilmaz from the Massachusetts Institute of Technology's (MIT) Koch Institute for Integrative Cancer.
To investigate a possible link between these stem cells and obesity-linked cancer, researchers fed healthy mice a diet made up of 60 percent fat for nine to 12 months.
This diet, according to the scientists, is much higher in fat than the typical American diet, which is usually about 20 to 40 percent fat.
During this period, the mice on the high-fat diet gained 30 to 50 percent more body mass than mice fed a normal diet and they developed more intestinal tumours than mice on a normal diet.
These mice also showed some distinctive changes in their intestinal stem cells.
The study suggests that a high-fat diet drives a population boom of intestinal stem cells and also generates a pool of other cells that behave like stem cells that is, they can reproduce themselves indefinitely and differentiate into other cell types.
First, the team found that the mice on a high-fat diet had many more intestinal stem cells than mice on a normal diet. These stem cells were also able to operate without input from neighbouring cells.
"Not only does the high-fat diet change the biology of stem cells, it also changes the biology of non-stem-cell populations, which collectively leads to an increase in tumour formation," explained Yilmaz in the paper published in the journal Nature.
"These stem cells and "stem-like" cells are more likely to give rise to intestinal tumours, Yilmaz added.
Not only do you have more of the traditional stem cells (on a high-fat diet), but now you have non-stem-cell populations that have the ability to acquire mutations that give rise to tumours, the authors noted. IANS
