FAT10基因,实验小鼠 z-bo 2020-08-17 444

　　A single gene seems to play an important role in regulating the immune system and metabolism. Deleting the FAT10 gene can reduce fat in mice and extend their lifespan. Related research results have been published in the PNAS journal. 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 Obing said: Turning off the FAT10 gene in mice has a variety of beneficial effects, including slowing down aging and reducing body fat, thereby extending the life of mice by 20%.

　　Generally, mice gain weight as their body weight increases. The authors observed that activation of the FAT10 gene in normal mice increases adipose tissue with aging. Rats lacking FAT10 will consume more food, but will burn fat faster. As a result, compared with normal old mice, its fat tissue is less than half. At the same time, skeletal muscle increases the production of immune molecules, thereby increasing the response of mice lacking FAT10 to insulin. This can reduce circulating insulin levels, prevent type 2 diabetes and extend life.

　　The author pointed out that eliminating FAT10 will not completely solve the problems of aging and weight gain. Experimental mice live in a sterile laboratory under ideal conditions. Mice without the FAT10 gene may be too thin to effectively resist infections outside the laboratory environment. How to achieve balance in mice requires further research.

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