动物实验,FAT10基因 z-bo 2020-08-31 385

　　A single gene seems to play a vital role in coordinating the immune system and metabolism. Deleting the FAT10 gene reduces body fat in mice and prolongs lifespan. The relevant research results were published in the journal PNAS.

　　Tufts University researchers initiated research on the role of FAT10 in adipose tissue and metabolism. Except that it is turned on by inflammation and seems to increase in gynecological and gastrointestinal cancers, no one really knows the role of FAT10 gene. Dr. Martin S. Obin said: Turning off the FAT10 gene in mice has a variety of beneficial effects, including reducing body fat, which will slow down aging and increase the life of mice by 20%.

　　Normally, mice gain weight as they grow. The author observed that the activation of the FAT10 gene in normal mice increases adipose tissue with age. Mice lacking FAT10 consume more food, but burn fat faster. As a result, they have less than half of adipose tissue compared to normal old mice. At the same time, skeletal muscle increases the production of an immune molecule that increases the response of mice lacking FAT10 to insulin, which leads to a decrease in circulating insulin levels, prevents type 2 diabetes, and leads to a longer lifespan.

　　The author pointed out that eliminating FAT10 cannot completely solve the dilemma of aging and weight gain, because laboratory mice live in a sterile laboratory under ideal conditions. Obin said: fighting infection requires energy, which can be provided by stored fat. Mice without the FAT10 gene may be too thin to effectively fight infection outside of the laboratory environment. How to balance this in mice needs more research.

　　Future research on FAT10 is exciting. Recent studies have reported that FAT10 interacts with hundreds of other proteins in cells. Now Tufts and Yale University researchers have shown that it affects immune response, lipid and sugar metabolism, and mitochondrial function.