The intestinal immune system is linked to obesity and diabetes. A Belgian team, by deactivating a protein, was able to make mice lose weight and slow down the progression of their diabetes.
Reducing inflammation linked to obesity, slowing down the development of type 2 diabetes, is what a team from the Catholic University of Louvain (Belgium) has achieved in mice. Led by Prof. Patrice Cani and Dr Amandine Everard, work has identified a mechanism involved in the development of obesity and type 2 diabetes in the context of a high fat diet. The results appeared in Nature Communications.
Deactivate a key protein
The researchers made mice obese and diabetic on a diet very high in fat. Then they induced a mutation so as to deactivate the protein MyD88, over-stimulated by this diet, in the rodent intestine. Several phenomena result from this. The immune system’s response changes, and inflammation is reduced. “We see that if we reduce the over-stimulation, the body is better and starts spending energy again”, explains Patrice Cani, contacted by why actor.
The MyD88 protein is also present in humans. It is part of the innate immune system, the one we are born with, and is extremely important. “Imagine a room in which you have different sockets, to which you can plug your devices”, illustrates the Pr Patrice Cani. “One device detects a virus, another gram negative bacteria, another gram positive bacteria… All the information comes to one switch, called MyD88. It was this “switch” that the team turned off.
Transfer intestinal bacteria
The researchers also transferred the gut microbiota from mice protected from obesity to other mice without gut flora. The intestinal microbiota is all the microorganisms (bacteria, viruses, etc.) living in the intestine. And this transfer made it possible to confer protection on the mice. “The fact of modifying the ability of bacteria to interact with our own cells will slow down the development of obesity, limit the development of T2DM”, specifies Patrice Cani. “What we have observed, and what we might have expected, is that by changing the innate immune system of animals in the intestine, we observe that the intestinal microbiota of these animals is also different. We have been able to demonstrate that the innate immune system of the intestine is capable of controlling energy expenditure, ”concludes the Belgian researcher.
This is an exciting first step, because the results can be translated in humans and opens up a therapeutic avenue. But it will still take years of research, because many bacteria involved in the phenomenon have not yet been identified. “We have a genetic signature of the intestinal microbiota that we are trying to understand, since the key may be found within this modification of the microbiota”, explains the Prof Cani. “Analyzing the composition of the intestinal microbiota of animals that were protected, the metabolites or the products that these bacteria can produce would probably make it possible to arrive at new therapeutic targets. ”
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