The Macrophage Switch in Obesity Development.
The Macrophage Switch in Obesity Development.
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DOI：
10.3389/fimmu.2015.00637
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发表时间：
2015
影响因子：
7.3
通讯作者：
Moraes-Vieira PM
中科院分区：
文献类型：
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作者：
Castoldi A;Naffah de Souza C;Câmara NO;Moraes-Vieira PM
肥胖时(白色)脂肪组织(AT)中的免疫细胞浸润与胰岛素抵抗的发生有关。在AT中，白细胞主要是巨噬细胞。巨噬细胞可分为两大类：M1，经典激活的巨噬细胞；M2，交替激活的巨噬细胞，尽管最近的研究发现了广泛的巨噬细胞亚群。肥胖时，ATM1巨噬细胞数量增加，并与AT炎症和胰岛素抵抗相关。激活后，促炎症的M1巨噬细胞诱导有氧糖酵解。相比之下，在瘦人和小鼠中，M2巨噬细胞的数量占主导地位。M2巨噬细胞分泌抗炎细胞因子，利用氧化代谢维持AT动态平衡。在这里，我们综述了AT巨噬细胞的免疫和代谢功能及其在肥胖和代谢综合征中的不同方面。
Immune cell infiltration in (white) adipose tissue (AT) during obesity is associated with the development of insulin resistance. In AT, the main population of leukocytes are macrophages. Macrophages can be classified into two major populations: M1, classically activated macrophages, and M2, alternatively activated macrophages, although recent studies have identified a broad range of macrophage subsets. During obesity, AT M1 macrophage numbers increase and correlate with AT inflammation and insulin resistance. Upon activation, pro-inflammatory M1 macrophages induce aerobic glycolysis. By contrast, in lean humans and mice, the number of M2 macrophages predominates. M2 macrophages secrete anti-inflammatory cytokines and utilize oxidative metabolism to maintain AT homeostasis. Here, we review the immunologic and metabolic functions of AT macrophages and their different facets in obesity and the metabolic syndrome.