Using animal modeling technology to reveal why obesity causes colon cancer

  Animal experiments have shown that stem cell stimulation may increase the risk of cancer in obese patients.

  Obese mice, like obese humans, 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. This is a protein called PPAR-. . When δ is activated, the protein plays a role in regulating metabolism.

  If the results of this experiment are applicable to humans, we can explain the phenomenon in epidemiological research. A cancer biologist at the Koch Institute of the Massachusetts Institute of Technology (MIT) National Cancer Center said: "For a long time, it has been thought that obesity increases the risk of cancer in many tissues." A Mel Yilmaz Say. He is also a research leader. "And I want to know the biological mechanism behind it."

  cell biologist P. Kay Lund believes that these molecular mechanisms may be important. He works at the University of North Carolina. The National Institutes of Health in Bethesda. A sample of human tissue that has undergone colonoscopy can be used to see if this rule applies to humans. Ultimately, enhanced PPAR-δ protein activity may be an effective cancer risk indicator. "Therefore, there is an opportunity to provide early intervention treatment for patients," Lund said. Lund was not involved in this research.

  Yilmaz and David Sabatini study the relationship between cancer and obesity. David Sabatin will be at the Massachusetts Institute of Technology and the Whitehead Institute. They fed mice with a high-fat, high-calorie diet for one year, and tested the effect of this diet on the number and function of intestinal stem cells in mice.

  They found out that they were 60 years old? Fat in the diet. The mice not only overeated and became overweight, but also activated the PPAR-δ protein and stimulated the proliferation of intestinal stem cells. PAR mice treated with agents capable of activating -δ also developed the same cell proliferation. Compared with other types of cells, stem cells (proliferation) are thought to be more likely to cause tumors.

  It is unclear whether the changes in this mouse are due to weight gain, metabolic changes, or a high-fat diet. The team also performed "organoids" on fatty acids in high-fat foods. We tested intestinal cells cultured in three-dimensions. The PPAR-δ protein in these cells was also activated, indicating that fatty acids may directly participate in the expression of PPAR-δ protein. I'm.

  If this is the case, it is "a mechanism for finding connections that do not exist in humans," warned Walter Willett, a professor of public health at Harvard Business School. He has increased body fat. Although there are many related studies showing that it increases the risk of cancer, there is no conclusive evidence to prove the relationship between a high-fat diet and cancer.

  However, Yurumaz said that many variables are mixed. Epidemiological research is very confusing because it fits. "The data on fat intake and cancer incidence is complex," Irmas's research team said in the next experiment, high-fat diet and normal body weight. It is hoped that mice will prove the role of fatty acids in cancer risk.