The same gene controls the urge to eat and exercise

Part of the reason we like to eat rich, lazy foods for exercise is because of our genes. Researchers from the National Institute of Health (USA) have found that it controls the craving for fatty and sugary foods, as well as the desire to exercise. The study, published November 3, 2020 in the journal JCI Insight, suggests that this gene present in rodents could also be present in us and give similar results.

For their study, the researchers looked at mice, some of whose brains contain the Prkar2a gene, an enzyme from the protein kinase A family. This gene is expressed in a region of the brain called habenula, a structure located towards the back of the brain. brain, which is used in particular in the processes of depression, addiction, the reward system and motivation.

More sports and less fat in the diet

When present, Prkar2a can produce two subunits of protein kinase A. These new enzymes accelerate chemical reactions, helping to combine small molecules to become larger or by breaking down large molecules to become small.

In a previous study of Prkar2a, researchers already found that mice that did not have a working copy of Prkar2a in their genetic material were less likely to gain weight and become obese.

Based on this observation, they fed adult male and female mice high-fat foods and sugar water ad libitum for three weeks. While some rodents enjoyed it, those who did not have the Prkar2a gene ate and drank sparingly, observing exercise and fasting phases regularly.

They concluded that mice that did not have the Prkar2a gene had a lower-fat diet than their counterparts, even when the food had unrestricted access. Likewise, they were less tempted to consume the sugary drinks that scientists made available to them.

These mice were also more prone to exercise as they ran two to three times longer than the other mice in the experiment. Female mice lacking Prkar2a ate less fat than males, while males showed a lower preference for sugary drinks than females. In fact, mice lacking this gene exercise more and are less obese than those that have Prkar2a.

A gene also present in humans

Humans also have the Prkar2a gene. Its findings could serve as the basis for future research to prevent obesity and the diabetes that may accompany it. Since habenula is responsible for the reward system, researchers believe this gene is still activated in some of us because food was considered a reward in evolution.

This reward system, which works for both food and medication, is said to be “broken” with us. According to the researchers, this is due to a deregulation of dopamine signaling in our brain, which doesn’t know when to stop. With our distant ancestors, it was necessary to hunt, then spend, before we had access to the reward of food, which for us is no longer. If we were able to inhibit the Prkar2a gene, perhaps it would be possible to restore this reward system, which would push us to play more sports and eat less fatty foods.