French scientists have discovered elements of the gut microbiota in the brains of rodents. How did they get there and what role do they play? Especially for appetite regulation? The answer offers hope for better obesity management.
The gut microbiota, made up of billions of bacteria, is vital to our health. It acts on the digestive level, but also on the metabolic, immunological and neurological levels. During the course of study, the brain no longer appears as an independent organ, but is in communication with all other organs in our body. “In recent years we have realized that the answers in neuroscience are no longer just in the skull.“says Pierre-Marie Lledo, CNRS researcher and head of the Perception and Memory department at the Pasteur Institute. The one who had already highlighted the link between chronic stress, microbiota imbalance and depression, then became interested in inflammatory diseases such as Crohn’s disease, which are known to be associated with mood disorders.”In humans it is known that the mutation of the Nod2 receptor is a susceptibility factor for these specific chronic inflammatory diseases. Pierre-Marie Lledo. “It is known to be expressed by the immune system to allow the body to respond to invaders, invaders and bacteria“. With his team, however, he discovered that it is also expressed in the brain.
Bacteria migrate from the gut to the brain
Distributed in several areas, Nod2 was discovered in the hypothalamus of the rodents studied, a region that controls essential functions such as hunger, temperature, stress, social interactions…
Why do bacterial fragments ascend to the brain?
What justifies its presence, what information does it exchange with the brain? This is the question these researchers from INSERM, CNRS and the Institut Pasteur asked themselves. To find out, genetically modified mice without Nod2 were bred in the laboratory for over a year. If the males did not show any peculiarities in their development, then at 6 months the females began to grow abnormally. It turns out that the expression of the receptor in the neurons of the hypothalamus affects the feeling of satiety. So when we eat, we ingest bacteria that multiply in the gut before migrating to the brain (at least the muropeptides) where they inhibit satiety neurons when they interact with the Nod2 receptor. In the end, a bit like a short circuit, the neurons stop sending the signal “I ate too much, I’m fullsums up Pierre-Marie Lledo.
The saturation process is hindered
The microbiota therefore communicates directly with the brain, allowing it to control food intake. Could disorders like bulimia, diseases like obesity or diabetes be perceived differently in light of this discovery? At least that’s what the researcher thinks. “Here we realize that the expression of free will – have I eaten enough, I eat more cheese – depends not so much on our decision as on these fragments of bacteria that manage to reach our brain and inhibit the appetite center found in the hypothalamus . They act like a local anesthetic on the satiety phenomenon“.
As part of the study, Pierre-Marie Lledo and his colleagues will analyze the brains of deceased people to see if expression of the receptor varies from one individual to another. It is also possible that we may discover that the microbiota is sending the wrong signals due to an unbalanced diet, for example too low in fiber or too sweet. Also, perhaps, taking antibiotics disrupts the gut flora to the point of disrupting the proper functioning of the hypothalamus. So many paths still to be explored.