Metabolic regulation by adipose tissue macrophage and interleulin-10

本研究探讨了脂肪组织M1/M2巨噬细胞与胰岛素敏感性的关系，重点探讨了M2巨噬细胞和白细胞介素10（IL-10）的作用。替米沙坦是一种血管紧张素II I型受体阻滞剂，通过其PPARγ刺激活性诱导脂肪组织巨噬细胞的M2极性，而脂肪组织缺氧诱导M1极性。M2巨噬细胞消融小鼠，其中M2巨噬细胞的数量可以通过添加白喉毒素来减少，显示出较小的脂肪细胞尺寸和改善的胰岛素敏感性。下丘脑中IL-10信号的激活增加了骨骼肌中与菊糖相关的基因的表达，并提高了菊糖的敏感性。

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.