Inflammation, obésité et diabète de type 2 Rôle de l'inflammasome NL RP3 et du microbiote intestinal

Type 2 diabetes is characterized by chronic hyperglycaemia in a context of insulin resistance and β-cell dysfunction. A chronic low-grade inflammation is observed in obesity and has been associated with the development of metabolic disorders. The molecular mechanisms underlying this inflammation are not fully understood. Production of interleukin-1β by macrophages infiltrating insulin-sensitive tissues and pancreatic islets plays a major role in the pathogenesis of type 2 diabetes. This pro-inflammatory cytokine is produced through the activation of the NLRP3 inflammasome in response to danger signals that accumulate during obesity, including saturated fatty acids. The composition of the intestinal microbiota differs in obese subjects compared with lean individuals, particularly in response to high saturated fat diet. These modifications could trigger a chronic low-grade inflammation and promote the emergence of type 2 diabetes. The microbiota could therefore constitutes a therapeutic target in the prevention and management of metabolic abnormalities associated with obesity.