A new target for the treatment of type 2 diabetes
Previous studies have implicated the transcription factor Rev-erba in adipogenesis and in muscle mitochondrial function. With the support from FFRD, we have been able to start a project to better delineate the functions of Rev-erba in muscle and adipose tissue, and their contribution to whole body insulin sensitivity and glucose utilisation. Interesting preliminary results have already been obtained that support a prominent role of Rev-erba in skeletal muscle. Future studies will unravel the molecular mechanisms behind and help design new therapeutic strategies for the treatment of type 2 diabetes.
The non-coding RNAs: new regulators of β cells
Most forms of diabetes mellitus are caused by the dysfunction or the loss of pancreatic ß-cells producing insulin. The human genome was recently discovered to generate thousands of RNA molecules that are not coding for proteins. The functions of these RNAs is still largely unknown. Thanks to the support of the FFRD, we are studying the role of these molecules in the acquisition of the phenotype of ß-cells and we are assessing their contribution to the dysfunction and death of insulin-secreting cells during the development of diabetes.
Early and predictive blood biomarkers of diabetes: a new door opened towards prevention
The number of type 2 diabetes patients is still expanding; it has been associated with a combination of familial andgenetic predispositions, and environmental factors: fetal exposure, diet, lifestyle etc… Using comprehensive globalapproaches and thanks to the support of the FFRD, our project is identifying, with the analysis of blood metabolites andproteins, early (7 years before) and/or predictive circulating biomarkers of the development of the disease, in additionof studying their specificity regarding the fetal environment. These results should help to better target at-risk subjectsand open the door towards a better preventive approach and a more personalized medicine.
A gut microbiota dysbiosis reduces intestinal defense and trigger type 2 diabetes
Our recent work demonstrates in mice that a gut microbiota dysbiosis impairs the role of the intestinal lymphocyte to protect against the passage of intestinal bacteria towards tissues. This tissue microbiota triggers an inflammatory process which impairs insulin action and secretion leading to type 2 diabetes. Thanks to the subside from the FFRD we will determine whether this observation is true in humans by studying the immune system and microbiota from intestinal biopsies obtained during colonoscopy. The transfer of the human gut microbiota to germ free mice should help arguing for the role of gut microbiota dysbiosis on the pandemic development of type 2 diabetes.