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高脂肪饮食可刺激小鼠骨骼肌中 IL-1 型 I 受体介导的炎症信号转导。

High-fat diet stimulates IL-1 type I receptor-mediated inflammatory signaling in the skeletal muscle of mice.

机构信息

Department of Food and Nutrition, Brain Korea 21 Project, Yonsei University, Seoul 120-749, Korea.

出版信息

Mol Nutr Food Res. 2010 Jul;54(7):1014-20. doi: 10.1002/mnfr.200800512.

DOI:10.1002/mnfr.200800512
PMID:20166142
Abstract

Recently, substantial attention has been focused on the association between obesity and chronic inflammation. The aim of the present study was to investigate whether high-fat diet (HFD)-induced obesity induces the activation of the IL-1 type I receptor (IL-1RI)-mediated inflammatory signaling cascade in the skeletal muscle of mice. Male C57BL/6J mice were fed either an HFD or a normal diet (ND) for 12 wk. Compared with the results in mice receiving the ND, the HFD increased the expression of IL-1RI and downstream signaling proteins, such as myeloid differentiation primary response gene 88 (MyD88), IL-1R-associated kinase 4 and phospho-transforming growth factor-activated kinase 1 in the skeletal muscle. Additionally, activities of both inhibitor of kappaB kinase beta and inhibitor of kappaB degradation were significantly elevated in the skeletal muscle of mice fed with an HFD compared with mice receiving an ND. In contrast, the levels of other downstream transcription factors, such as activator protein-1 and INF regulatory factor 5, were not affected by the HFD. These results suggest that the IL-1RI-MyD88-nuclear factor kappaB signaling pathway might be involved in the induction of the inflammatory response in the skeletal muscle of mice fed with an HFD.

摘要

最近,人们对肥胖症与慢性炎症之间的关联给予了大量关注。本研究旨在探究高脂肪饮食(HFD)诱导的肥胖是否会激活小鼠骨骼肌中白细胞介素-1 型受体(IL-1RI)介导的炎症信号级联反应。雄性 C57BL/6J 小鼠分别喂食 HFD 或正常饮食(ND)12 周。与接受 ND 的小鼠相比,HFD 增加了骨骼肌中 IL-1RI 及其下游信号蛋白(如髓样分化初级反应基因 88(MyD88)、IL-1R 相关激酶 4 和磷酸化转化生长因子激活激酶 1)的表达。此外,与接受 ND 的小鼠相比,HFD 喂养的小鼠骨骼肌中κB 激酶β的抑制剂和κB 降解抑制剂的活性显著升高。相比之下,HFD 并不影响其他下游转录因子(如激活蛋白-1 和 INF 调节因子 5)的水平。这些结果表明,IL-1RI-MyD88-核因子 kappaB 信号通路可能参与了 HFD 喂养的小鼠骨骼肌中炎症反应的诱导。

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