In a study published in Nature Communications, the research team of Patrice D. Cani, WELBIO investigator at UCL, has identified a novel mechanism involved in the development of obesity and type 2 diabetes following a high-fat diet feeding. This work identifies a novel therapeutic target for the treatment of obesity and type 2 diabetes.
The researchers found for the first time that upon a fat rich diet, inactivating a specific target of the innate immune system from intestinal cells (i.e., the protein MyD88) induces body weight loss and improves type 2 diabetes associated with obesity.The team shows that modifying the response of the immune system by deactivating this protein MyD88 in the intestinal cells delay the development of type 2 diabetes induced by a high fat diet, reduces the development of fat mass, reduces the deleterious inflammation observed during obesity and reinforced the gut barrier thereby preventing the leakage of unsuitable bacterial compounds from the intestine to the organism.
More importantly, the researchers show that it is experimentally possible, through this modification of the immune system, to induce body weight loss and therefore to have a therapeutic effect despite the fact that the animals were already obese and diabetic.
Among the mechanisms discovered, the WELBIO team from UCL identifies that on top of the partial protection against inflammation and type 2 diabetes, the mice that lack this MyD88 protein in the intestine are protected against the development of obesity because they spend more energy than their obese counterpart. In addition, they have a different gut microbiota. Surprisingly, the team found that it is possible to partially protects against obesity and diabetes by transferring (i.e., grafting) the gut microbiota from these mice to axenic mice (i.e., germ free).
This work published in Nature communications suggest that during high-fat diet feeding the intestinal immune system plays a major role on the regulation of fat storage and is literally capable to modify the composition of intestinal bacteria (among which some are not yet identified).
Everard A et al. Intestinal epithelial MyD88 is a sensor switching host metabolism towards obesity according to nutritional status. Nature Communications (2014) doi:10.1038/ncomms6648
CONTACT: Prof. Dr. Patrice D. Cani, Université Catholique de Louvain, WELBIO, LDRI, Tel: +32-474-900-562 e-mail: firstname.lastname@example.org