Esser N, Legrand-Poels S, Piette J, Paquot N, Scheen A J
Rev Med Liege. 2014;69 Spec No:57-61.
It is recognized that abdominal obesity is accompanied by a chronic low-grade inflammation that is involved in the pathogenesis of insulin resistance and type 2 diabetes. Metabolic syndrome and type 2 diabetes are associated with an abnormal production of pro-inflammatory cytokines, an increased level of acute-phase proteins and an activation of inflammatory signalling pathways. These pro-inflammatory cytokines, mainly produced by adipose tissue macrophages, are involved in development of obesity-associated insulin resistance and in the progression from obesity to type 2 diabetes. Particularly, the interleukin-1 beta may play a key role through the activation of the NLRP3 inflammasome. Adipose tissue topography, more than the total amount of fat, may play an important pathogenic role. Indeed, the presence of metabolic abnormalities in obesity is associated with a deleterious immunological and inflammatory profile of visceral adipose tissue and with an increased activation of the NLRP3 inflammasome in macrophages infiltrating visceral adipose tissue. Targeting inflammation, especially NLRP3 inflammasome, may offer potential novel therapeutic perspectives in the prevention and treatment of type 2 diabetes.
人们认识到，腹部肥胖伴随着一种慢性低度炎症，这种炎症参与胰岛素抵抗和2型糖尿病的发病机制。代谢综合征和2型糖尿病与促炎细胞因子的异常产生、急性期蛋白水平的升高以及炎症信号通路的激活有关。这些促炎细胞因子主要由脂肪组织巨噬细胞产生，参与肥胖相关胰岛素抵抗的发展以及从肥胖到2型糖尿病的进展。特别是，白细胞介素-1β可能通过激活NLRP3炎性小体发挥关键作用。脂肪组织的分布，而非脂肪总量，可能起重要的致病作用。事实上，肥胖中代谢异常的存在与内脏脂肪组织有害的免疫和炎症特征相关，并且与浸润内脏脂肪组织的巨噬细胞中NLRP3炎性小体的激活增加有关。针对炎症，尤其是NLRP3炎性小体，可能为2型糖尿病的预防和治疗提供潜在的新治疗前景。
