动物造模,剔除FAT10基因 z-bio 2021-09-28 559

　　A gene seems to play an important role in regulating the immune system and metabolism. Deleting the FAT10 gene can reduce body fat in mice and prolong lifespan. Related research results were published in PNAS magazine.

　　Researchers at Tufts University have begun to study the role of FAT10 in adipose tissue and metabolism. No one really knows the role of the FAT10 gene, except that it seems to be activated by inflammation and is increased in gynecological cancer and gastrointestinal cancer. Dr. Martin S. Obin said: Statement. Turning off the FAT10 gene in mice has many beneficial effects, including reducing body fat, delaying aging, and extending the life of mice by 20 ?.

　　Normally, rats will gain weight when they grow up. The authors observed that the activation of the FAT10 gene in normal mice caused adipose tissue to increase with age. Mice lacking FAT10 ate more food, but increased their fat burning rate. Therefore, compared with normal old mice, its adipose tissue is less than half. At the same time, skeletal muscle will increase the production of immune molecules, thereby enhancing the response of FAT10-deficient mice to insulin, thereby reducing circulating insulin levels, preventing type 2 diabetes and prolonging lifespan.

　　Laboratory mice live in a sterile laboratory under ideal conditions, so eliminating FAT10 will not completely solve the dilemma of aging and weight gain. Mice without the FAT10 gene may be too thin to effectively fight infection outside the laboratory environment. Further research is needed on how to balance this in mice. Future pair

　　FAT10 research is very interesting. Recent research reports that FAT10 interacts with hundreds of other proteins in cells. Researchers at Tufts University and Yale University have discovered that it is immune. It has been shown to affect response, lipid and sugar metabolism, and mitochondrial function.