长期COVID导致的胰岛素抵抗增加与抑郁症状有关,并在一定程度上由急性感染期间的炎症反应预测

H. Al-Hakeim, Haneen Tahseen Al-Rubaye, Abdulsahib S. Jubran, A. Almulla, S. Moustafa, Michael Maes
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引用次数: 9

摘要

背景。在COVID-19急性感染缓解几个月后,一些人表现出抑郁症状,这可以通过峰值体温(PBT)升高和血氧饱和度(SpO2)降低来预测。然而,没有数据表明长COVID是否与胰岛素抵抗(IR)升高相关,并与抑郁症状和免疫、氧化和亚硝化(IO&NS)过程相关。方法。我们使用稳态模型评估2 (HOMA2)计算器计算β细胞功能、胰岛素敏感性和抵抗(HOMA2- ir),并测量了86名长冠患者和39名对照组的贝克抑郁量表(BDI)和汉密尔顿抑郁评定量表(HAMD)。我们检测了急性感染期间HOMA2指数与PBT和SpO2之间的关系,以及急性感染后3-4个月的抑郁、io和ns生物标志物(c反应蛋白、NLRP3激活、髓过氧化物酶和晚期氧化蛋白产物)之间的关系。结果。长冠肺炎患者伴有HOMA2-IR升高、空腹血糖和胰岛素水平升高。我们发现33.7%的患者和0%的对照组的HOMA2-IR值>1.8,表明存在IR。急性感染期间PBT,而不是SpO2,显著预测IR,尽管效应大小较小。通过BDI和HAMD评估,IR的增加与抑郁症状显著相关,超过了IO&NS通路的影响。在长COVID期间,IR增加与激活的IO&NS通路之间没有显著关联。结论。在一部分患者中,长COVID与新发IR相关。IR升高可能通过增强整体神经毒性而促进长COVID所致抑郁症状的发作。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Increased insulin resistance due to long COVID is associated with depressive symptoms and partly predicted by the inflammatory response during acute infection
Background. Some months after the remission of acute COVID-19 infection, some people show depressive symptoms, which are predicted by increased peak body temperature (PBT) and lowered blood oxygen saturation (SpO2). Nevertheless, no data indicate whether Long COVID is associated with increased insulin resistance (IR) in association with depressive symptoms and immune, oxidative, and nitrosative (IO&NS) processes. Methods. We used the homeostasis Model Assessment 2 (HOMA2) calculator to compute beta-cell function, insulin sensitivity and resistance (HOMA2-IR) and measured the Beck Depression Inventory (BDI) and the Hamilton Depression Rating Scale (HAMD) in 86 Long COVID patients and 39 controls. We examined the associations between the HOMA2 indices and PBT and SpO2 during acute infection, and depression, IO&NS biomarkers (C-reactive protein, NLRP3 activation, myeloperoxidase, and advanced oxidation protein products) 3-4 months after the acute infection. Results. Long COVID is accompanied by increased HOMA2-IR, fasting blood glucose, and insulin levels. We found that 33.7% of the patients versus 0% of the controls had HOMA2-IR values >1.8, suggesting IR. PBT, but not SpO2, during acute infection significantly predicted IR, albeit with a small effect size. Increased IR was significantly associated with depressive symptoms as assessed with the BDI and HAMD above and beyond the effects of IO&NS pathways. There were no significant associations between increased IR and the activated IO&NS pathways during Long COVID. Conclusion. Long COVID is associated with new-onset IR in a subset of patients. Increased IR may contribute to the onset of depressive symptoms due to Long COVID by enhancing overall neurotoxicity.
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