In a latest research, scientists have identified a gene which synchronizes the immune system and metabolism of the body. And the study conducted on mice shows that eliminating the gene results in increased longevity and less body mass.
The research was led by a team of scientists from the Jean Mayer USDA Human Nutrition Research Center (USDA HNRCA) on Aging at Tufts University and Yale University School of Medicine which carefully studied the link between the gene expression and fat tissue.
Depending upon the study of gene expression of fat tissue, the scientists at the Tufts University examined the effect of FAT10 gene in adipose tissue and metabolism. So far the role of FAT10 gene was not understood, however the scientists observed that inflammation, turned on the gene and during gynecological and gastrointestinal cancers, the proportion of the gene gets increased. As per an adjunct scientist in the Functional Genomics Core Unit at the USDA HNRCA at Tufts University and co-author of the study Martin S. Obin, turning off the FAT10 gene yielded favorable results in the mice such as a reduction in the body fat, which in turn delays ageing and also increased the average life by 20 percent.
The researchers, examining the influence FAT10 gene on metabolism and fat tissue, used two sets of mice for the experiment. The scientists stimulated the FAT10 gene in one set of mice and observed an increase in fat tissues and aged normally. The FAT10 gene was eliminated from the other set of mice. These mice were lean and ageing slowing, though they were seen to consume more food. They were lean because they were capable of burning the fat tissues much faster. These mice showed an enhanced response to insulin, which decreased the insulin levels and diminished the danger of type 2 diabetes and postponed ageing.
Though, noticing the positive result of deleting FAT10 gene, the researchers were not convinced that the same positive results can be achieved in the real world. Obin says, that the experiment on mice were conducted in a germ free environment of the laboratory. But in the real world, the body needs to battle different kinds of infections, which requires energy that are stored in the fat tissues of the body. And the mice which lacked the FAT10 gene, burned the fat tissue and were not capable of fighting infections in the world outside the laboratory environment. Therefore, more in depth study is required to manage that balance in mice, before something similar can be thought to be achieved in humans.
But one cannot deny that the research seems promising and in the future scientists will be able to solve the problem of obesity by controlling the expression of the FAT10 gene. If the human variant of FAT10 behaves the same way as the mouse gene does, drugs that meddle with it could cure obesity and diabetes and could delay ailments associated with ageing.
