Department of Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.
Department of Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093, USA.
Immunity. 2014 Jul 17;41(1):36-48. doi: 10.1016/j.immuni.2014.05.010.
Chronic, low-grade adipose tissue inflammation is a key etiological mechanism linking the increasing incidence of type 2 diabetes (T2D) and obesity. It is well recognized that the immune system and metabolism are highly integrated, and macrophages, in particular, have been identified as critical effector cells in the initiation of inflammation and insulin resistance. Recent advances have been made in the understanding of macrophage recruitment and retention to adipose tissue and the participation of other immune cell populations in the regulation of this inflammatory process. Here we discuss the pathophysiological link between macrophages, obesity, and insulin resistance, highlighting the dynamic immune cell regulation of adipose tissue inflammation. We also describe the mechanisms by which inflammation causes insulin resistance and the new therapeutic targets that have emerged.
慢性、低度脂肪组织炎症是将 2 型糖尿病(T2D)和肥胖发病率不断增加联系起来的关键病因机制。人们普遍认识到免疫系统和新陈代谢高度整合,巨噬细胞已被确定为炎症和胰岛素抵抗发生的关键效应细胞。人们对巨噬细胞募集和保留到脂肪组织以及其他免疫细胞群体在调节这一炎症过程中的参与有了更多的了解。在这里,我们讨论了巨噬细胞、肥胖和胰岛素抵抗之间的病理生理联系,强调了脂肪组织炎症的动态免疫细胞调节。我们还描述了炎症引起胰岛素抵抗的机制以及新出现的治疗靶点。