Deactivating This Gene Reduces Craving for Food and Increases the Desire for Exercise

A team of researchers managed to reduce the joy of eating in mice and increase physical activity by disabling a specific gene in the brain.

Obesity is a complex disease, the onset of which is caused by many factors: genetic, hormonal, environmental, life changes, and so on. That is why there is not a single strategy that can overcome this pathology. However, we can imagine several combined treatments, some of which are directed to genetics, as in this study, others to psychology, or to the structural food environment of our cities.

In this study, conducted by Maryland researchers affiliated with the National Institute of Health, the deactivation of a particular gene allowed a drastic change in the eating and physical behavior of rodents. In mice whose gene had been deactivated, there was a decrease in the attraction and consumption of appetizing and rewarding foods (in the sense that they particularly stimulate our reward cycle) and an increase in the “willingness” to exercise. Could such treatment be considered in humans?

Under the influence of our brain

the habenula is a brain structure that is part of the epithalamus. It refers to the dorsal part of the diencephalon, which is formed by the epiphysis, habenula, and medullar striations. It is a region whose functions are still little known. But the habenular neural circuit is of growing interest to scientists due to its possible effects on dependence, depression, motivation, and the rewarding process.

This circuit is under the influence of the action of one gene in particular: Prkar2a. Previous experiences have shown that the alteration of the neural circuits prevents mice from becoming obese, even when they are on a diet that leads to obesity. In this new experiment, changing this circuit reduces the attraction of mice to “reward” food and encourages them to do more exercise, which can be a good thing in obese patients.

A way to treat obesity?

As we said, obesity is a complex disease that one single strategy is unlikely to treat it. However, it is conceivable that therapies aimed at this brain circuit could be tested a little further in animal models to measure potential long-term side effects before human studies are done.

In the vast majority of cases, obesity is the result of an inadequate environment. It would be good to focus on structural variables, such as our nutritional environment. For example, healthy foods should become more readily available in supermarkets than processed foods. In the 21st century, the challenge of nutrition is a challenge in many ways. We need to rethink our food systems, both for the obese and the hungry around the world.