The IL-6 Paradox: Context Dependent Interplay of SOCS3 and AMPK.
The IL-6 Paradox: Context Dependent Interplay of SOCS3 and AMPK.
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DOI：
10.4172/2155-6156.s13-003
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发表时间：
2013-05-24
期刊：
影响因子：
--
通讯作者：
Lees SJ
中科院分区：
文献类型：
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作者：
Sarvas JL;Khaper N;Lees SJ
胰岛素抵抗是2型糖尿病进展的主要步骤，并且与细胞因子循环水平增加有关，导致慢性低度炎症。具体来说，在慢性疾病状态下，IL-6的增加被认为在调节外周组织的胰岛素抵抗方面发挥关键作用，并已被用作胰岛素抵抗的标志物。还存在响应于运动的IL-6的内源性上调，这与改善的胰岛素敏感性有关。这就引出了一个问题：“IL-6升高如何导致胰岛素抵抗的发展，同时又导致胰岛素敏感性增加？”解决IL-6在调节胰岛素抵抗/敏感性中的双重作用对于开发潜在的治疗干预至关重要。本文综述了IL-6升高对胰岛素信号传导的看似矛盾的作用，包括AMPK的激活和瘦素和SOCS 3的参与。
Insulin resistance is the principle step towards the progression of type 2 diabetes, and has been linked to increased circulating levels of cytokines, leading to chronic low-grade inflammation. Specifically, in chronic disease states increased IL-6 is thought to play a critical role in the regulation of insulin resistance in the peripheral tissues, and has been used as a marker of insulin resistance. There is also an endogenous up-regulation of IL-6 in response to exercise, which has been linked to improved insulin sensitivity. This leads to the question “how can elevated IL-6 lead to the development of insulin resistance, and yet also lead to increased insulin sensitivity?” Resolving the dual role of IL-6 in regulating insulin resistance/sensitivity is critical to the development of potential therapeutic interventions. This review summarizes the literature on the seemingly paradoxical role of elevated IL-6 on insulin signalling, including the activation of AMPK and the involvement of leptin and SOCS3.