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首页> 外文期刊>Cellular Physiology and Biochemistry >Allograft Inflammatory Factor-1 Mediates Macrophage-Induced Impairment of Insulin Signaling in Adipocytes
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Allograft Inflammatory Factor-1 Mediates Macrophage-Induced Impairment of Insulin Signaling in Adipocytes

机译：同种异体移植炎症因子1介导巨噬细胞诱导的脂肪细胞中胰岛素信号传导的损害。

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Background/Aims Allograft inflammatory factor-1 (AIF-1) is an inflammatory cytokine produced mainly by macrophages within human white adipose tissue. Its expression is increased in obese subjects and positively correlated with insulin resistance. The purpose of this study is to characterize the regulatory role of AIF-1 in insulin signaling of adipocyte. Methods AIF-1 was over-expressed via transfection of AIF-1 cDNA into murine RAW 264.7 macrophages, and the constitutive expression of AIF-1 was decreased via transfection of targeting siRNA. Murine 3T3L1 adipocytes were treated with macrophage-conditioned medium or AIF-1 protein. Intracellular lipid accumulation was assayed by oil red O stain. Reactive oxygen species production was determinated by a flow cytometer and adipokine secretion was measured with ELISA. Glucose uptake was detected using the glucose oxidase method and insulin-signal-transduction related molecules were analyzed by Western blot. Results Short term (48 h) AIF-1 treatment slightly promoted intracellular lipid storage in differentiating 3T3L1 cells. The protein stimulated reactive oxygen species production, provoked TNFα, IL6, resistin, but suppressed adiponectin release and insulin-stimulated glucose uptake both under normal basal and insulin resistance conditions. Furthermore, AIF-1 induced NF-κB activation, inhibited PPARγ expression, GLUT4 translocation to plasma membrane and Akt phosphorylation. Conclusion Macrophage-derived AIF-1 up-regulated reactive oxygen species production, adipokine TNFα, IL6, resistin release, and inhibited adiponectin secretion. Moreover, it suppressed insulin-stimulated glucose uptake by down-regulating insulin signaling. Thus, AIF-1 could be related to obesity-related diseases.
机译：背景/目的同种异体移植炎症因子-1（AIF-1）是一种炎症细胞因子，主要由人类白色脂肪组织中的巨噬细胞产生。它的表达在肥胖的受试者中增加并且与胰岛素抵抗呈正相关。这项研究的目的是表征AIF-1在脂肪细胞胰岛素信号传导中的调节作用。方法通过将AIF-1 cDNA转染到鼠RAW 264.7巨噬细胞中来过表达AIF-1，并通过靶向siRNA转染来降低AIF-1的组成型表达。小鼠3T3L1脂肪细胞用巨噬细胞条件培养基或AIF-1蛋白处理。通过油红O染色测定细胞内脂质蓄积。用流式细胞仪确定活性氧的产生，并用ELISA测定脂肪因子的分泌。使用葡萄糖氧化酶法检测葡萄糖摄取，并通过蛋白质印迹法分析胰岛素信号转导相关分子。结果短期（48小时）AIF-1处理在分化3T3L1细胞中略微促进了细胞内脂质的储存。在正常的基础和胰岛素抵抗条件下，该蛋白刺激了活性氧的产生，激发了TNFα，IL6，抵抗素，但抑制了脂联素的释放和胰岛素刺激的葡萄糖摄取。此外，AIF-1诱导NF-κB活化，抑制PPARγ表达，GLUT4易位至质膜和Akt磷酸化。结论巨噬细胞源性AIF-1上调了活性氧的产生，脂肪因子TNFα，IL6，抵抗素的释放并抑制了脂联素的分泌。此外，它通过下调胰岛素信号传导来抑制胰岛素刺激的葡萄糖摄取。因此，AIF-1可能与肥胖相关疾病有关。

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