动物造模 z-bo 2020-09-26 365

　　A single gene seems to play an important role in regulating the immune system and metabolism. Removal of the FAT10 gene can reduce body fat and extend the life of mice. Related research results have been published in the PNAS journal. Tufts University

　　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 is turned on by inflammation, and it seems to increase in gynecological and gastrointestinal cancers. Dr. Martin Orbin said: Turning off the FAT10 gene in mice has many beneficial effects, including reducing body fat. This can slow down aging and extend the life of the mouse by 20%.

　　Normally, mice will gain weight when they grow up. The authors observed that activation of the FAT10 gene in normal mice increases adipose tissue with age. Mice lacking FAT10 will consume more food, but will burn fat faster. As a result, compared with normal aging mice, the adipose tissue is less than half. At the same time, skeletal muscle increases the production of immune molecules, increases the response of FAT10-deficient mice to insulin, reduces circulating insulin levels, prevents type 2 diabetes and prolongs lifespan. The author pointed out that eliminating FAT10 will not completely solve the problems of aging and weight gain, because laboratory mice live in sterile laboratories under ideal conditions. Mr. Obin said: Mice lacking the FAT10 gene may be too thin to effectively resist infection outside the laboratory environment. How to achieve balance in mice requires further research.

　　The future research of FAT10 is exciting. Recent studies have reported that FAT10 interacts with hundreds of other proteins in cells. Researchers at Tufts University and Yale University have shown that it affects the immune response, lipid and sugar metabolism, and mitochondrial function.