结肠癌 z-bo 2020-10-21 274

　　Studies have shown that stem cell stimulation may increase the risk of cancer in obese patients. Like obese humans, obese mice have an increased risk of colon cancer. A recent study published in the journal Nature found that overweight mice fed a high-fat diet increased the number of intestinal stem cells. , A protein called PPAR-δ is activated and plays a role in the regulation of metabolism. If the experimental results are also applicable to humans, we can explain the epidemiological research phenomenon. Mar-Ilmaz (Mar-Ilmaz), a cancer biologist and head of research at the Cancer Research Center at the Koch Institute of MIT, said: “For a long time, obesity has become a cancer in many tissues. Risk.” It is believed that this situation will increase. Someone said: "I want to know the biological mechanism behind it. "

　　cell biologist P. Kay Lund believes that these molecular mechanisms may be important. He worked at the University of North Carolina and the National Institutes of Health in Bethesda. A sample of human tissue that has undergone colonoscopy can be used to verify whether the rule applies to humans. Ultimately, enhanced PPAR-delta protein activity may be an effective cancer risk indicator. Lund said: "Therefore, there is an opportunity to provide early intervention treatment for patients." Lund did not participate in this study.

　　Yilmaz and David Sabatini collaborated to study the relationship between cancer and obesity, and David Sabatin studied metabolism at the Massachusetts Institute of Technology and the Whitehead Institute. They fed mice high-fat, high-calorie foods for one year, and then tested the effects of the diet on the number and function of intestinal stem cells in mice.

　　They noticed that 60% of their diet is fat. It not only made mice overeating and overweight, but also activated PPAR-δ protein and stimulated the growth of intestinal stem cells. Mice treated with agents capable of activating PAR-δ caused the same cell proliferation. Compared with other types of cells, stem cells (proliferation) are considered more likely to cause tumors. still not clear

　　This change in mice is due to weight gain, changes in metabolism or high-fat food. The team also tested the response of intestinal cells to fatty acids in high-fat foods through the three-dimensional organism "organic matter". The PPAR-δ protein in these cells was also activated, indicating that fatty acids may directly participate in the expression of PPAR-δ protein.

　　If this were the case, it would be a “mechanism for finding connections that do not exist in humans,” warned Walter Willett, a professor of public health at Harvard Business School. He said that many related studies have shown that body fat increases the risk of cancer, but there is no conclusive evidence that there is a link between a high-fat diet and cancer.

　　But Yilmaz said that epidemiological studies are very confusing due to the mixture of many variables. "The data on fat intake and cancer incidence is complicated." Yilmaz's research team decided to use normal-weight mice on a high-fat diet in the next experiment to confirm the role of fatty acids in cancer risk.