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SEFRI
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22.00519
Titre du projet
Early Interception of Inflammatory-mediated Type 2 Diabetes
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Résumé des résultats (Abstract)
(Anglais)
The overall concept of INTERCEPT-T2D is to establish whether an inflammatory-mediated profile contributes to the onset of Type 2 Diabetes (T2D) complications, thus enabling the identification of patients most at risk of complications and the design of personalized prevention measures. T2D is a heterogeneous disease, which is an obstacle to the delivery of an optimal tailored treatment. Consequently, patients’ individual trajectories of progressive hyperglycemia and risk of chronic complications are so far difficult to predict. In this context, onset of diabetic complications represents the most important transitional phase of T2D development toward premature disability and mortality. Chronic systemic inflammation has been suggested to be a major contributor to the onset and progression of T2D complications. INTERCEPTT2D will bring a new and clinically relevant dimension in T2D care considering at diagnosis inflammatory parameters that are of importance for the transition to T2D-related complications. The combination of state-of-the-art genomics and cell-biology technologies with targeted clinical interventions should lead to potent patients’ stratification. It should allow the identification and prognosis of a novel class or subclass of patients characterized by an “Inflammatory-mediated T2D” endotype. The project has access to the best-documented longitudinal human European cohorts of patients with T2D, with reliable clinical and biological data allowing to trace the transition and evolution towards organ complications. This, added to the exploitation of an extensive health data warehouse, will enable us to establish the inflammatory trajectory of citizens with T2D from diagnosis to the development of complications. To explore the ability to prevent the transition phase of T2D towards organ complications, INTERCEPT-T2D will conduct a phase II clinical trial with an anti-inflammatory therapy targeting NLRP3 Inflammasome activity in patients with T2D.
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