中文摘要：

肥胖是由多种炎性因子诱导产生的一种全身性的慢性低度炎症状态。在肥胖过程中,脂肪组织内稳态平衡被打破,巨噬细胞数量增加。极化的巨噬细胞在肥胖状态下的脂肪组织微环境中,与脂肪细胞相互作用引起脂肪组织的慢性炎症。脂肪组织区域免疫异常引起的慢性炎症是肥胖胰岛素抵抗的始动因素,巨噬细胞募集/极化及脂肪前体细胞巨噬样变是脂肪组织区域免疫异常的中心环节,通过炎症信号通路与胰岛素信号通路之间的交叉对话抑制胰岛素信号通路关键分子,引起胰岛素抵抗。这种免疫异常为肥胖、2型糖尿病等代谢性疾病及心血管疾病治疗提供了新的靶点,为肥胖及糖尿病的治疗提供思路。

英文摘要：

Obesity is a chronic,low-grade inflammatory body status induced by a variety of inflammatory cytokines. In the obese state,the homeostasis of adipose tissue is disbalanced,accompanied by the expanding population of adipose tissue macrophages（ ATM）. In the obese adipose tissue microenvironment,the polarized macrophages interact with the fat adipocytes,leading to the chronic inflammation,which becomes the initial factor for insulin resistance（ IR）. The ATM recruitment / polarization and the macrophage-like reprogramming of adipose precursor cells play a leading role. Based on the crosstalk between inflammatory signaling pathways and the insulin signaling pathway,the key signaling molecule is suppressed,which leads to IR. These immune abnormalities provide a new target for metabolic disease treatment.