{"id":665,"date":"2025-08-19T17:31:10","date_gmt":"2025-08-19T15:31:10","guid":{"rendered":"https:\/\/www.nutrimedia.info\/?post_type=news&p=665"},"modified":"2025-08-12T11:53:44","modified_gmt":"2025-08-12T09:53:44","slug":"can-the-brain-modify-the-microbiota","status":"publish","type":"news","link":"https:\/\/www.nutrimedia.info\/en\/news\/le-cerveau-peut-il-modifier-le-microbiote\/","title":{"rendered":"Can the brain really change the microbiota in two hours? Interview with Prof. Patrice D. Cani"},"content":{"rendered":"

Yes, the activation of certain brain areas linked to hunger or satiety changes the composition of the intestinal microbiota in just two hours. This is one of the most astonishing discoveries of the NeuroGut project, led for more than 10 years by Prof. Patrice D. Cani, Dr Matthias Van Hul (UCLouvain), Dr Marc Claret (University of Barcelona) and Prof Rub\u00e9n Nogueras (University of Santiago de Compostela).<\/strong> In this exclusive interview, Patrice D. Cani talks about the origins of the project, the key results published in Nature Metabolism<\/em> and the implications of this breakthrough for our understanding of metabolic diseases.<\/strong><\/p>\n\n\n\n

Can you remind us of the framework and objective of this NeuroGut study?<\/strong><\/h2>\n\n\n\n

The project is part of the exploration of the intestine-brain and brain-gut axes. We have known for a long time that the microbiota<\/a> can send signals to the brain, in particular by influencing appetite. But we wanted to test the opposite hypothesis: Can the brain alone modify the composition of the microbiota? And the answer is yes.<\/strong><\/p>\n\n\n\n

Using several innovative animal models in which hypothalamic neurons regulating appetite (POMC, AGRP) can be activated or inhibited on demand, we have shown that these stimulations are sufficient to induce significant changes in the gut microbiota... in less than two hours.<\/strong><\/p>\n\n\n\n

It's a discovery that seems counter-intuitive. How were you funded?<\/strong><\/h2>\n\n\n\n

This is a long-term project. The first discussions date back to 2014, and the first results date back to 2017. But it took us some time to convince the scientific committees to fund this work. In 2019, the La Caixa Foundation finally backed the project to the tune of \u20ac900,000. At the time, the idea that a brain signal could rapidly modify the microbiota seemed far-fetched.<\/p>\n\n\n\n

What key results have you seen?<\/strong><\/h2>\n\n\n\n

When we activate the neurons of the satiety<\/a> (POMC pathway) or hunger (AGRP pathway), we observed statistically significant changes in the composition of the microbiota in the upper (duodenum) and lower (ileum, colon) parts of the intestine. More than 10 bacterial families are involved<\/strong>.<\/p>\n\n\n\n

We also carried out transcriptomic analyses on the duodenum. <\/p>\n\n\n\n

Result: brain activation massively modifies gene expression in the intestine<\/strong>, These include genes linked to immunity, neuronal signals and synapses. The same applies to metabolites: the brain also acts on the intestinal metabolome.<\/p>\n\n\n\n

Have you identified a stable \u00abbacterial signature\u00bb?<\/strong><\/h2>\n\n\n\n

Not really. It's not always the same bacterial family that is affected. The microbiota here acts like a dynamic ecosystem: some families increase, others decrease, and this varies according to the pathway activated. This makes any attempt at targeted intervention complex.<\/p>\n\n\n\n

But we have confirmed this, is that this brain-microbiota communication takes place via specific nerve pathways and not via changes in intestinal motility.<\/strong><\/p>\n\n\n\n

And in humans? Can we make the same observation?<\/strong><\/h2>\n\n\n\n

This is one of the challenges. Obviously, we can't inject leptin into the brains of human volunteers, nor can we take frequent duodenal samples. But certain clinical situations, such as gastric bypass<\/strong>, These studies suggest that a sudden change in microbiota is possible, with very rapid effects on metabolism.<\/p>\n\n\n\n

You also mention an altered phenomenon in obese or diabetic subjects...<\/strong><\/h2>\n\n\n\n

Yes, that's one of the major results.<\/strong> In obese and diabetic animals, this communication loop is disrupted. The brain no longer seems to be able to communicate properly with the microbiota. For example, central administration of leptin hardly induces any changes in the intestinal microbiota, unlike in control subjects.<\/p>\n\n\n\n

Is it linked to low-grade inflammation?<\/strong><\/h2>\n\n\n\n

This is a hypothesis<\/strong>. We know that these subjects have leptino-resistance, and that this may be linked to brain inflammation or to the accumulation of bioactive lipids. It is also possible that neuroinflammation disrupts this bidirectional communication loop. But this remains to be demonstrated in humans.<\/p>\n\n\n\n

What are the next steps?<\/strong><\/h2>\n\n\n\n

Many questions remain unanswered. <\/p>\n\n\n\n