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白细胞介素-6 在视神经脊髓炎谱系疾病患者胰岛素敏感性调节中的可能作用。

The possible role of Interleukin-6 as a regulator of insulin sensitivity in patients with neuromyelitis optica spectrum disorder.

机构信息

Multiple Sclerosis Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran.

出版信息

BMC Neurol. 2021 Apr 20;21(1):167. doi: 10.1186/s12883-021-02198-5.

Abstract

BACKGROUND

Neuromyelitis optica spectrum disorder (NMOSD) is associated with inflammatory mediators that may also trigger downstream signaling pathways leading to reduce insulin sensitivity.

METHODS

We aimed to determine the risk association of hyperinsulinemia in NMOSD patients with seropositive AQP4-IgG and the serum levels of interleukin (IL)-6 and IL-17A compared with the control group. Serum levels of metabolic (Insulin, Fasting Blood Sugar (FBS), lipid profile) and inflammatory (IL-6 and IL-17) markers were assessed in 56 NMOSD patients and 100 controls.

RESULTS

Hyperinsulinemia was more prevalent in NMOSD patients independent of age, sex and body mass index (BMI) (48.2% vs. 26%, p = 0.005) compared to control group. After adjusting age, sex and BMI, there was significant association between lower insulin sensitivity (IS) and NMOSD risk (95% CI: Beta = 0.73, 0.62 to 0.86, p = 0.0001). Circulating levels of IL-6 and IL-17 were higher in NMOSD patients, and only IL-6 had an effect modifier for the association between lower insulin sensitivity and NMOSD risk.

CONCLUSIONS

Our data suggests that inflammatory pathogenesis of NMOSD leads to hyperinsulinemia and increases the risk of insulin resistance.

摘要

背景

视神经脊髓炎谱系疾病(NMOSD)与炎症介质有关,这些炎症介质也可能触发下游信号通路,导致胰岛素敏感性降低。

方法

我们旨在确定 NMOSD 患者中与抗水通道蛋白 4 免疫球蛋白 G(AQP4-IgG)阳性相关的高胰岛素血症风险,以及与对照组相比,血清白细胞介素(IL)-6 和 IL-17A 的水平。评估了 56 名 NMOSD 患者和 100 名对照组的代谢(胰岛素、空腹血糖(FBS)、血脂谱)和炎症(IL-6 和 IL-17)标志物的血清水平。

结果

与对照组相比,NMOSD 患者不论年龄、性别和体重指数(BMI)如何,高胰岛素血症更为普遍(48.2%比 26%,p=0.005)。在调整年龄、性别和 BMI 后,较低的胰岛素敏感性(IS)与 NMOSD 风险之间存在显著关联(95%置信区间:Beta=0.73,0.62 至 0.86,p=0.0001)。NMOSD 患者的循环 IL-6 和 IL-17 水平较高,而只有 IL-6 对较低的胰岛素敏感性与 NMOSD 风险之间的关联具有效应修饰作用。

结论

我们的数据表明,NMOSD 的炎症发病机制导致高胰岛素血症,并增加胰岛素抵抗的风险。

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