Diets high in fat can stimulate cancer by activating the subject tumor stem cells
Instead of eating a high fat diet can not only increase your size. You can also fill the stem cell populations in their gut cells that are likely to produce tumors.
After a year feeding mice with a diet of 60 percent fat, the researchers found that rodents have exceptionally high population susceptible to cancer cells and stem cells that act as intestinal stem cells. These cells were supercharged by a protein called PPAR-δ, which can be activated by the presence of fatty acids in the intestine, the researchers reported.
The findings, published in the journal Nature, could explain why the epidemiological evidence in humans has repeatedly linked to obesity risk driven from cancer, especially colon cancer. You can also give researchers a new target to strike again cancer risk in obese people.
In the gut, usually there is a small pocket of stem cells that work to restore the cells that line the intestine. These cells are maintained throughout life, providing additional opportunities to acquire mutations that might stimulate tumor.
Fat fed mice, which grew chubby, this small population of stem cells thrived unexpectedly. And specialized progenitor cell progeny of stem cells began to act more like their parents, too. They lived longer, increasing their chances of acquiring mutations and tumor potential spawning.
The researchers found that the PPAR-δ was behind the boom of stem and progenitor cells. Petri In experiments, the researchers found that the fatty acids of high fat diet increased amounts of PPAR-delta cells were doing.
This makes sense because the protein is known to activate the metabolic mechanism that helps to burn fat over carbohydrates. However, the protein also seems to cause specific genetic changes to light two populations of cells, the researchers suggest.
In fat mice, the researchers observed higher rates of spontaneous tumors in control mice.
Yet researchers must work harder to find out if stem cells and PPAR-O explain the relationship between cancer and obesity in humans.
Instead of eating a high fat diet can not only increase your size. You can also fill the stem cell populations in their gut cells that are likely to produce tumors.
After a year feeding mice with a diet of 60 percent fat, the researchers found that rodents have exceptionally high population susceptible to cancer cells and stem cells that act as intestinal stem cells. These cells were supercharged by a protein called PPAR-δ, which can be activated by the presence of fatty acids in the intestine, the researchers reported.
The findings, published in the journal Nature, could explain why the epidemiological evidence in humans has repeatedly linked to obesity risk driven from cancer, especially colon cancer. You can also give researchers a new target to strike again cancer risk in obese people.
In the gut, usually there is a small pocket of stem cells that work to restore the cells that line the intestine. These cells are maintained throughout life, providing additional opportunities to acquire mutations that might stimulate tumor.
Fat fed mice, which grew chubby, this small population of stem cells thrived unexpectedly. And specialized progenitor cell progeny of stem cells began to act more like their parents, too. They lived longer, increasing their chances of acquiring mutations and tumor potential spawning.
The researchers found that the PPAR-δ was behind the boom of stem and progenitor cells. Petri In experiments, the researchers found that the fatty acids of high fat diet increased amounts of PPAR-delta cells were doing.
This makes sense because the protein is known to activate the metabolic mechanism that helps to burn fat over carbohydrates. However, the protein also seems to cause specific genetic changes to light two populations of cells, the researchers suggest.
In fat mice, the researchers observed higher rates of spontaneous tumors in control mice.
Yet researchers must work harder to find out if stem cells and PPAR-O explain the relationship between cancer and obesity in humans.
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