Morphological and therapeutic interventions have uncovered an inflammatory process in patients with type 2 diabetes. This inflammation is due to a pathological activation of the innate immune system by metabolic stress and is largely governed by IL-1 signaling. Initially, the inflammatory response is probably deployed to promote adaptation and regeneration. Indeed, we identified a role for IL-1β and insulin in the regulation of both metabolism and immunity in response to feeding. Yet, as it becomes chronic, activation of auto-inflammatory processes may then become deleterious. It follows that modulation of inflammatory mediators may present as a possible causal therapy. This is supported by clinical studies showing that IL-1 antagonism decreases glycated hemoglobin. Furthermore, IL-1 antagonism prevents heart failure and cardiovascular diseases and may improve, NASH, retinopathy, nephropathy.
Online event (Zoom)
Meeting ID 929 0249 0627 - Code 223854