Blocking the expression of TRIP-Br2 gene in mice protects them against insulin resistance and obesity. This find of researchers could soon prove to be effective in humans by reducing obesity.
According to the study, the gene modulates fat storage. It does so by regulating energy expenditure and lipolysis, the process that produces energy by converting the fat. What the researchers found is that when blocked, the gene expression in mice, they increase lipolysis and energy expenditure, obesity reduces.
An alteration in the process that regulates food absorption and energy production usually leads to obesity. This causes fat storage. Researchers say that by understanding how factors control the fat storage can lead to new and effective therapies for obesity and obesity related illnesses (i.e. type 2 Diabetes).
Co-author of the study, Cristina Mallol, researcher at the Universitat Autònoma de Barcelona said: "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 study 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) and other research centres from Europe and USA.