摘要
胰岛素抵抗在2型糖尿病、代谢综合征等肥胖相关性疾病中起到十分重要的作用。胰岛素抵抗是一个低度炎症状态,大量由免疫细胞和脂肪细胞分泌的炎性介质参与了胰岛素抵抗的发生、发展,其中包括肿瘤坏死因子α、白细胞介素6和一些脂肪因子。而且,抑制物激酶(IKK)/NF—κB通路、c-jun氨基末端激酶通路以及细胞因子信号抑制物3通路也参与了此过程。它们相互作用共同促进了胰岛素抵抗发生、发展,并为胰岛素相关性疾病的防治提供又一个新的靶点。
Insulin resistance(IR) plays a key role in the pathophysiology of obesity-related diseases such as type 2 diabetes and metabolic syndrome. It has been demonstrated that IR is associated with a state of chronic low-grade inflammation, and several mediators of inflammation released from various cell types, including immune cells and adipocytes, have been identified as being involved in the development of IR. Among those are several pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α) , interleukin-6 (IL-6) , and various adipo-cytokines. Furthermore,several transcription factors and kinases such as inhibitor of kappa B kinase-β ( IKKβ ) /nuclear factor-KB ( NF-κB ) , c-Jun N-terminal kinase ( JNK) , and suppressor of cytokine signalling-3 ( SOCS-3 ) participate in this process. As a complex network of inflammatory cytokines, adipo-cytokines, and transcription factors are involved in the development of IR, new therapeutic approaches in IR-re- lated diseases will be based on a better understanding of their complex interactions.
出处
《医学综述》
2009年第4期508-511,共4页
Medical Recapitulate
关键词
炎症
炎性因子
胰岛素抵抗
代谢综合征
Inflammation
Inflammatory cytokine
Insulin resistance
Metabolic syndrome