Esser N, Paquot N
Service de Diabétologie, Nutrition et Maladies métaboliques, CHU Liège, Belgique.
Laboratoire d'Immunométabolisme et Nutrition, GIGA-I3, ULiège, Belgique.
Rev Med Liege. 2022 May;77(5-6):310-315.
Type 2 diabetes is characterized by chronic hyperglycaemia in a context of insulin resistance and ?-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-1? 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.
2型糖尿病的特征是在胰岛素抵抗和β细胞功能障碍的情况下出现慢性高血糖。肥胖中观察到慢性低度炎症，并且与代谢紊乱的发生有关。这种炎症的潜在分子机制尚未完全了解。浸润胰岛素敏感组织和胰岛的巨噬细胞产生白细胞介素-1β在2型糖尿病的发病机制中起主要作用。这种促炎细胞因子是通过NLRP3炎性小体的激活产生的，以响应肥胖期间积累的危险信号，包括饱和脂肪酸。与瘦人相比，肥胖受试者的肠道微生物群组成不同，特别是对高饱和脂肪饮食的反应。这些改变可能引发慢性低度炎症并促进2型糖尿病的出现。因此，微生物群可能构成预防和管理与肥胖相关的代谢异常的治疗靶点。
