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肥胖相关炎症和胰岛素抵抗中 T 淋巴细胞 IL-6 信号传导的时间和组织特异性要求。

Temporal and tissue-specific requirements for T-lymphocyte IL-6 signalling in obesity-associated inflammation and insulin resistance.

机构信息

Max Planck Institute for Metabolism Research, Department of Neuronal Control of Metabolism, 50931 Cologne, Germany.

Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), University Hospital, 50924 Cologne, Germany.

出版信息

Nat Commun. 2017 May 3;8:14803. doi: 10.1038/ncomms14803.

DOI:10.1038/ncomms14803
PMID:28466852
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5418621/
Abstract

Low-grade inflammation links obesity to insulin resistance through the activation of tissue-infiltrating immune cells. Interleukin-6 (IL-6) is a crucial regulator of T cells and is increased in obesity. Here we report that classical IL-6 signalling in T cells promotes inflammation and insulin resistance during the first 8 weeks on a high-fat diet (HFD), but becomes dispensable at later stages (after 16 weeks). Mice with T cell-specific deficiency of IL-6 receptor-α (IL-6Rα) exposed to a HFD display improved glucose tolerance, insulin sensitivity and inflammation in liver and EWAT after 8 weeks. However, after 16 weeks, insulin resistance in IL-6Rα epididymal white adipose tissue (EWAT) is comparable to that of controls, whereas the inflammatory profile is significantly worse. This coincided with a shift from classical T cell IL-6 signalling at 8 weeks, to enhanced IL-6 trans-signalling at 16 weeks. Collectively, our studies reveal that IL-6 action in T cells through classical IL-6 signalling promotes inflammation and insulin resistance early during obesity development, which can be compensated for by enhanced IL-6 trans-signalling at later stages.

摘要

低度炎症通过浸润组织的免疫细胞激活将肥胖与胰岛素抵抗联系起来。白细胞介素-6（IL-6）是 T 细胞的关键调节剂，在肥胖中增加。在这里，我们报告说，T 细胞中的经典 IL-6 信号在高脂肪饮食（HFD）的前 8 周内促进炎症和胰岛素抵抗，但在后期（16 周后）变得可有可无。在高脂肪饮食暴露下，具有 T 细胞特异性缺乏 IL-6 受体-α（IL-6Rα）的小鼠在 8 周后表现出改善的葡萄糖耐量、胰岛素敏感性和肝脏及 EWAT 中的炎症。然而，在 16 周后，IL-6Rα 附睾白色脂肪组织（EWAT）中的胰岛素抵抗与对照组相当，而炎症特征明显恶化。这与 8 周时经典 T 细胞 IL-6 信号的转变，以及 16 周时增强的 IL-6 转信号相一致。总之，我们的研究揭示了 T 细胞中通过经典 IL-6 信号的 IL-6 作用在肥胖发展的早期促进炎症和胰岛素抵抗，而在后期通过增强的 IL-6 转信号可以得到补偿。

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