Adipose tissue resident macrophages have important roles in the maintenance of tissue homeostasis and regulate insulin sensitivity for example by secreting pro-inflammatory or anti-inflammatory cytokines. Here, we show that M2-like macrophages in adipose tissue regulate systemic glucose homeostasis by inhibiting adipocyte progenitor proliferation via the CD206/TGFβ signaling pathway. We show that adipose tissue CD206⁺ cells are primarily M2-like macrophages, and ablation of CD206⁺ M2-like macrophages improves systemic insulin sensitivity, which was associated with an increased number of smaller adipocytes. Mice genetically engineered to have reduced numbers of CD206⁺ M2-like macrophages show a down-regulation of TGFβ signaling in adipose tissue, together with up-regulated proliferation and differentiation of adipocyte progenitors. Our findings indicate that CD206⁺ M2-like macrophages in adipose tissues create a microenvironment that inhibits growth and differentiation of adipocyte progenitors and, thereby, control adiposity and systemic insulin sensitivity.Adipose tissue contains macrophages that can influence both local and systemic metabolism via the secretion of cytokines. Here, Nawaz et al. report that M2-like macrophages, present in adipose tissue, create a microenvironment that inhibits proliferation of adipocyte progenitors due to the secretion of TGF-β1.

中文翻译：

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CD206 + M2样巨噬细胞通过抑制脂肪细胞祖细胞的增殖来调节全身性葡萄糖代谢。

驻留在脂肪组织中的脂肪巨噬细胞在维持组织稳态中起重要作用，并通过例如分泌促炎或抗炎细胞因子来调节胰岛素敏感性。在这里，我们表明，脂肪组织中的M2样巨噬细胞通过通过CD206 /TGFβ信号通路抑制脂肪细胞祖细胞的增殖来调节全身性葡萄糖稳态。我们显示，脂肪组织CD206 ⁺细胞主要是M2样巨噬细胞，而CD206 ⁺ M2样巨噬细胞的消融可改善全身胰岛素敏感性，这与较小的脂肪细胞数量增加有关。基因工程小鼠减少了CD206 ^+的数量M2样巨噬细胞显示脂肪组织中TGFβ信号的下调，以及脂肪细胞祖细胞的增殖和分化上调。我们的研究结果表明，脂肪组织中CD206 ⁺ M2样巨噬细胞可形成微环境，抑制脂肪细胞祖细胞的生长和分化，从而控制肥胖和全身性胰岛素敏感性。细胞因子。在这里，Nawaz等。报告指出，存在于脂肪组织中的M2样巨噬细胞会形成微环境，该环境会由于TGF-β1的分泌而抑制脂肪细胞祖细胞的增殖。