Neurons in the brain that make us hungry can be turned off by a compound created by gut bacteria, researchers have found. Further understanding this gut-brain conversation could one day help treat obesity and metabolic diseases, such as diabetes.
The gut microbiome is the collection of bacteria, fungi and other microbes that live within our gastrointestinal tract. There are trillions of organisms to be found in our gut, some good and some bad. They help us get nutrients from our food, repair and replace the cell linings of our gut and our skin, and they even aid our immune system in the fight against invading pathogens.
Previous studies have found links between the make up of our microbiome and psychological factors like our mood. But the exact pathway by which our gut bacteria and our brain communicate hasn't been identified.
This study suggests one possible answer – that bacteria in our gut can manipulate our feeding behaviour by releasing fragments that act as a message to the hypothalamus, the area of the brain that makes us feel hungry. These fragments, called muropeptides, are part of the bacteria's cell wall. If the bacteria is dying, or growing, these pieces will break away and travel through our bloodstream.
"The hypothalamus is the brain centre for controlling hunger, thirst, body temperature, hormone release, among many things,” said Prof Gerard Eberl, one of the co-authors of the new study, of the French National Institute of Health and Medical Research.
There are neurons within the hypothalamus that make us hungry and there are those that block the feeling of hunger after eating. Previous studies have shown that the latter have a sensor that can detect bacterial fragments, but the team wanted to find out just how much influence the microbes could have on the brain.
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To test this, scientists gave food containing these bacterial muropeptides to two groups of mice – one that had the neurons to detect the compound, and the other without.
Those that lacked the receptor were found to eat much more than the normal mice, gaining more weight. Their brain was not receiving the signal to stop.Then, when the researchers gave the normal mice a different compound that can also trigger the sensor, they noticed the mice were feeding less.
"It could be that this is a way for the gut bacteria to tell the brain: 'stop eating that stuff, it makes us die' or 'it makes this bad bug proliferate over us'. My interpretation, however, is that these bacterial fragments reaching the brain is an indication that bacteria are growing or dying excessively in the gut, which is a health risk for the gut, for the individual [and thus for the bacteria living there]," said Eberl. "So, then the brain can make an association between this risk and that food, and give the order to eat less and make you feel full."
When the gut microbiome is well-balanced, the individual and the bacteria thrive. But if this balance is upset by one species growing excessively, it could be dangerous for all involved, said Eberl.
Next, the team will need to test the same pathway in humans, research that could go on to aid the development of new treatments. In theory, obesity could be treated by changing the food that someone is eating, to change the bacteria's reaction.
"In human studies, these bacterial fragments have been associated with sleeping disorders. Mutations [to the receptors] are associated with mood disorder and neurodegenerative diseases like Alzheimer's," said Eberl. While there is still more to uncover about how our gut communicates with our brain, the new research shows just how influential our microbial hitchhikers can be.
