Scientists observed that blocking the expression of the gene TRIP-Br2 in mice protects them against obesity and insulin resistance. The study shows that the gene modulates fat storage by regulating energy expenditure and lipolysis, the process which transforms fat into lipids for the body’s energy consumption. If the gene expression is blocked, the mice increase their lipolysis and their energy expenditure, thus reducing their obesity.
Obesity is the result of an alteration in the processes that regulate food absorption and energy production. This alteration tips the balance towards excessive storage of fat. According to the researchers, understanding the regulation of the factors that control the storage, mobilisation and use of excess energy in fat cells (the adipocytes) can lead to the development of therapies for obesity and its related illnesses, such as type 2 diabetes.
In the words of Cristina Mallol, a researcher at the Universitat Autònoma de Barcelona and co-author of the study: “The protection of mice with no expression of the gene TRIP-Br2, and its selective elevation in the visceral fat of humans point the way to a future gene therapy to counteract obesity, insulin resistance and excess lipids in the blood”.
The research, the findings of which were published this week in the online edition of the journal Nature Medicine, was led by researchers from the Joslin Diabetes Center, of the Harvard Medical School in Boston, Massachusetts (USA), with the participation of the University of Singapore (Singapore); the Centre for Animal Biotechnology and Gene Therapy (CBATEG) at the Universitat Autònoma de Barcelona (Spain); INSERM, Toulouse (France); the University of California, at Berkeley (USA); the University of Leipzig (Germany); and the University of Florida (USA); the University of Illinois, at Chicago (USA).