Luc Pellerin has long been interested in brain energy metabolism. In his research, the associate professor with the Department of Physiology at the University of Lausanne (UNIL) has focused his attention on nutrient transporters located within the brain, and other tissues and organs such as the liver and heart. That is how he discovered the MCT1 gene. By disrupting it in mice, he and his team realised that it plays an important role in the regulation of body weight. The genetically modified rodents displayed less obesity after being subjected to a high-fat and high-sugar diet, without experiencing hypoglycaemia or an increase in adipose tissue.
What would happen if the gene were to be disrupted in humans? “There are two main challenges,” says Luc Pellerin. “First, it’s technically difficult. The gene is found in different tissues and organs, which would have to be targeted one by one. And the gene also has useful functions. As a transporter, it contributes to the exchange of energy substrates. The gene is responsible for supplying some tissues with essential nutrients.”
Of course, we’re not saying that we can eat an unhealthy diet
One option could involve developing a pharmaceutical drug that partially inhibits the effects of the gene. In short, some of its activity would need to be reduced and some maintained. “Of course, we’re not saying that we can eat an unhealthy diet,” the scientist says. “What is interesting is that we were able to demonstrate that the development of obesity isnot linked to a series of genetic mutations but to a change in environment, which is now saturated in high-fat foods.”
MCT1 is actually a “normal” gene. It is there to promote the accumulation of fat, and has served this purpose since the time when human beings did not have abundant food and had to move more to get it. Bottom line: Instead of waiting for some miracle drug, we ought to watch what we ingest and get some exercise.