Researchers from Lausanne and the Salk Institute have been able to switch off a genetic regulator (NCoR1) and develop mice that can cover twice the distance run by mice which were not so treated. The mice also showed better cold resistance and were able to run faster. In an article in the journal Cell, they reported experiments done on mice and nematodes. By genetic manipulation, they were able to suppress the regulator NCoR1 that normally inhibits the buildup of muscle tissue. The regulator modulates the activity of specific genes, and in its absence, the mice and worms were able to grow muscle tissue which was much stronger than that of normal mice.
Researchers have already suggested that if these results are confirmed in humans, it is bound to attract interest from athletes as well as medical experts. “There are now ways to develop drugs for people who are unable to exercise due to obesity or other health complications, such as diabetes, immobility and frailty,” says Ronald M Evans, who led the Salk team. “We can now engineer specific gene networks in muscle to give the benefits of exercise to sedentary mice.”
According to a Salk press release, ‘The scientists have not yet detected any harmful side effects associated with eliminating the NCoR1 receptor from muscle and fat tissues. Although the experiments involved genetic manipulations, the researchers are already investigating potential drug molecules that could be used to reduce the receptor’s effectiveness. The researchers say their results are a milestone in our understanding of certain fundamental mechanisms of living organisms, in particular the little-studied role of corepressors—molecules that inhibit the expression of genes.’
“This could be used to combat muscle weakness in the elderly, which leads to falls and contributes to hospitalisations,” Johan Auwerx, the lead author from EPFL Lausanne, says. “In addition, we think that this could be used as a basis for developing a treatment for genetic muscular dystrophy.”