Metabolic regulation by adipose tissue macrophage and interleulin-10

在本研究中，我们研究了脂肪组织M1/M2巨噬细胞与胰岛素敏感性的关系，重点研究了M2巨噬细胞和白介素10(IL-10)的作用。血管紧张素ⅡI型受体阻滞剂替米沙坦通过其PPARγ刺激活性诱导脂肪组织巨噬细胞M2极性，而脂肪组织缺氧则诱导M1极性。加入白喉毒素可使M2巨噬细胞数量减少的M2巨噬细胞消融小鼠，脂肪细胞体积变小，胰岛素敏感性提高。下丘脑IL-10信号的激活增加了骨骼肌线粒体相关基因的表达，改善了菊粉的敏感性。

In this study, we investigated the relationship between adipose tissue M1/M2 macrophages and insulin sensitivity, focusing on the roles of M2 macrophage and interleukin10 （IL-10). Telmisartan, an angiotensin II type I receptor blocker, induced M2 polarity of adipose tissue macrophages with its PPARγ-stimulating activity, while adipose tissue hypoxia induced the M1 polarity. M2 macrophage ablation mice, in which the number of M2 macrophage could be decreased by adding diphtheria toxin, showed smaller adipocyte size and improved insulin sensitivity. The activation of IL-10 signaling in hypothalamus increased the expression of mitochondria-related genes in skeletal muscle and improved inulin sensitivity.