Regulation of insulin resistance by adipose tissue M1/M2 macrophages.

在肥胖的脂肪组织中，炎性M1巨噬细胞的数量显著增加，而炎性M2巨噬细胞的比例降低，导致胰岛素敏感性降低和肥胖并发症的发展（Diabetes 58：2574-2582，2009）。我发现替米沙坦（一种血管紧张素II I型受体阻滞剂）通过调节M1/M2巨噬细胞比率，通过其PPARγ活性改善胰岛素抵抗（Endocrinology，152：1789-1799，2011）。我还发现，肥胖引起的脂肪组织缺氧参与了巨噬细胞的M1极化。

In obese adipose tissues, the number of inflammatory M1 macrophage is dramatically increased and the ratio of antiinflammatory M2 macrophage is reduced, resulting the decrease of insulin sensitivity and development of obesity complications(Diabetes 58 : 2574-2582, 2009). I found that telmisartan, an angiotensin II type I receptor blocker, improved insulin resistance with its PPARγactivity, by modulating M1/M2 macrophage ratio(Endocrinology, 152 : 1789-1799, 2011). I also found that obesity-induced hypoxia in adipose tissue is involved in M1 polarization of macrophages.