The Prkar2a gene, when present and active, makes us eat a lot and conditions us not to exert ourselves. The goal would be to inhibit it so that we better control our urge to eat and are more inclined to play sports.
-1604931183.jpg "The same gene controls the urge to eat and exercise")
- The Prkar2a gene controls our desire to eat and exercise.
- When it is not activated and present, we would be more inclined to slow down on food and spend more time playing sports.
- This gene is managed by the hamidula, a structure in the brain that notably manages the reward system.
If we like to eat rich and lazy products to play sports, it is partly because of our genes. Researchers from the National Institute of Health (USA) have discovered the one that controls the craving for fatty and sweet foods as well as the desire to exercise. The study, published on November 3, 2020 in the journal JCI Insightsuggests that this gene present in rodents could also be present in us, and give similar results.
For their study, the researchers focused on 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 the habenula, a structure located towards the back of the brain, which is used in particular in the processes of depression, addiction, in the reward system and in motivation.
More sport and less fat in the diet
When present, Prkar2a can make two subunits of protein kinase A. These new enzymes speed up chemical reactions, either helping to combine small molecules to become larger, or breaking down large molecules they become small.
In a previous study on Prkar2a, the researchers had already noticed that mice that did not have a functional 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 had a blast, those lacking the Prkar2a gene ate and drank sparingly, observing regular exercise and fasting phases.
They concluded that the mice that did not have the Prkar2a gene had a lower fat diet than their counterparts, even when the food was unrestricted. Likewise, they were less tempted to consume the sugary drinks that scientists made available to them.
These mice were also more prone to exercise since they ran two to three times longer than the other mice in the experiment. Female mice that lacked Prkar2a ate less fat than males, while the latter showed a lower preference for sugary drinks than females. In fact, mice without this gene exercise more and are less obese than those with Prkar2a.
A gene also present in humans
Human beings also have the Prkar2a gene. His results could serve as a basis for future research to prevent obesity and the diabetes that can accompany it. Since habenula is responsible for the reward system, researchers believe that this gene is still activated in some of us because in evolution, food was considered a reward.
This reward system, which works for food as well as for drugs, would be “broken” with us. According to the researchers, this is due to a dysregulation of dopamine signaling in our brain, which does not know when to stop. Among our distant ancestors, it was necessary to hunt, and therefore to exert oneself, before having access to the reward that was food, which is no longer the case for us. If we could inhibit the Prkar2a gene, perhaps it would be possible to restore this reward system, which would encourage us to do more sports and eat less fatty foods.
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