An international team of scientists says it has identified an unsuspected mechanism impacting the development of obesity and type 2 diabetes in animals on a high fat diet. Patrice D. Cani, Ph.D., and her group from the Louvain Drug Research Institute, in collaboration with two French teams and Swedish researchers, report in Nature Communications an important discovery related to the essential role of the intestinal immune system regarding the control of energy metabolism.

Their work highlights a new therapeutic target for treatment of obesity and type 2 diabetes. More specifically, the team showed that when modifying the response of the immune system by disabling intestinal immune system protein MyD88, the development of diabetes induced by a high fat diet slowed down, adipose tissue creation was limited, and inflammation was reduced.

In addition, the researchers demonstrated that because of this immune system intervention, experimental animals still lost weight and showed metabolic improvement even when the animals were already obese and diabetic.

The scientists concluded the intestinal immune system, including intestinal bacteria, plays an important role in fat storage regulation by the body. They add that their discovery confirms the involvement of intestinal bacteria in the development of obesity, but even more importantly, their study provides new therapeutic possibilities by focusing on MyD88 for the treatment of obesity and type 2 diabetes.

“Targeting MyD88 after the onset of obesity reduces fat mass and inflammation,” wrote the investigators in an article entitled “Intestinal epithelial MyD88 is a sensor switching host metabolism towards obesity according to nutritional status”). “Our work thus identifies intestinal epithelial MyD88 as a sensor changing host metabolism according to the nutritional status and we show that targeting intestinal epithelial MyD88 constitutes a putative therapeutic target for obesity and related disorders.”

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