结肠癌 z-bo 2020-12-17 295

　　Studies have shown that stem cell stimulation may increase the risk of cancer in obese patients. Obese mice, like obese humans, have a higher risk of colon cancer. A study recently published in the journal Nature revealed that the number of intestinal stem cells in overweight mice fed a high-fat diet increased. A protein called PPAR-δ is activated, which plays a role in regulating metabolism.

　　 If the experimental results are also applicable to humans, then it can explain a phenomenon in epidemiological research. "For quite some time, people believed that obesity would increase the risk of cancer in many tissues," said mer Yilmaz, a cancer biologist at the Center for Comprehensive Cancer Research at the Koch Institute at the Massachusetts Institute of Technology (MIT), who also contributed to the study. One of the leaders, "and we want to know the biological mechanism behind it."

　　 cell biologist P. Kay Lund believes that these molecular mechanisms may be important, and he holds positions at the University of North Carolina and the National Institutes of Health in Bethesda. Human tissue samples that have undergone colonoscopy can be used to verify whether this rule applies to humans. Eventually, the enhancement of PPAR-δ protein activity may become an effective cancer risk indicator. Lund said: "Therefore there is an opportunity to provide patients with early intervention treatment." Lund did not participate in the study.

　　 Yilmaz and David Sabatini collaborated to study the relationship between cancer and obesity, and David Sabatin studied metabolism at MIT and the Whitehead Institute. They fed mice a year of high-fat, high-calorie food, and then tested the effect of diet on the number and function of intestinal stem cells in mice.

　　 They found that 60% of the diet is fat, which will not only make mice overeating and become overweight, but also activate PPAR-δ protein and stimulate the proliferation of intestinal stem cells. Mice treated with drugs that can activate PAR-δ also produced the same cell proliferation. Compared to other types of cells, stem cells (proliferation) are considered more likely to cause tumors.

　　 It is not yet clear whether this change in mice was due to weight gain—the metabolism was changed—or because of high-fat food. The team also tested the response of intestinal cells in the three-dimensional culture of "organoids" to fatty acids in high-fat foods. The PPAR-δ protein in these cells is also activated, indicating that fatty acids may directly participate in the expression of PPAR-δ protein.

　　 If this is the case, it will be "a mechanism to find a connection that does not exist in humans," warns Walter Willett, professor of public health at Harvard Business School. He said that although there are many relevant studies that show that human body fat increases the risk of cancer, there is no conclusive evidence to prove the relationship between a high-fat diet and cancer.

　　 But Yilmaz mentioned that epidemiological research has become messy due to the mixing of many variables. He said: "The data on fat intake and cancer incidence is intricate." Yilmaz's research team hopes to use normal-weight mice on a high-fat diet in the next experiment to try to confirm the role of fatty acids in cancer risk.