Zhong Mengyu, Zhu Jian, Zhang Bohan, Shen Hui, Li Hongxia, Tang Yuxiao, Nie Shuang, Mo Fengfeng
Department of Naval Nutrition and Food Hygiene, Faculty of Navy Medicine, Naval Medical University, 800 Xiangyin Rd, Yangpu District, Shanghai, 200433, China.
School of Chemistry and Chemical Engineering, Shanghai University of Engineering Science, 333 Longteng Rd, Songjiang District, Shanghai, 201620, China.
Metab Brain Dis. 2025 May 16;40(5):203. doi: 10.1007/s11011-025-01630-w.
Abnormal acceleration induced motion sickness (MS) and elevated blood glucose levels, showing obviously cognitive impairments. The mechanism of cognitive impairment caused by MS is still unclear. Here, blood metabolite detection, insulin level regulators, stress hormones, cytokines and MS assessment were conducted for the population and MS model rats, correlation analysis of motion sickness index (MSI) and above factors were conducted by correlation analysis. We found glucose after acceleration was positively correlated with Graybiel's score. Insulin and leptin levels decreased, while ghrelin level increased after acceleration in both human and rat groups. We injected insulin level regulators into rats before being exposed to acceleration, the results showed that MSI of the insulin group (INS) was significantly lower than rotation group (ROT), streptozotocin group (STZ) and streptozotocin & insulin group (SINS). MSI in STZ was higher than ROT and INS. Rats injected with ghrelin showed higher MSI than the control group and ghrelin antagonist group. Acceleration stimulation induced phosphorylation of insulin receptor substrate 1 (IRS1) and expression of synaptic protein in hippocampus. We also found that the insulin microinjection into hippocampus prevented MS symptoms and cognitive ability as measured by the MSI, the Open Field Test, the T-maze, and the Morris water maze. Our study indicates that insulin and insulin level regulators can affect MS symptoms and cognitive ability.
异常加速度诱发晕动病（MS）并导致血糖水平升高，表现出明显的认知障碍。MS导致认知障碍的机制仍不清楚。在此，对人群和MS模型大鼠进行了血液代谢物检测、胰岛素水平调节剂、应激激素、细胞因子及MS评估，并通过相关性分析对晕动病指数（MSI）与上述因素进行了相关性分析。我们发现加速度后的血糖与格雷比尔评分呈正相关。在人和大鼠组中，加速度后胰岛素和瘦素水平降低，而胃饥饿素水平升高。在大鼠暴露于加速度之前注射胰岛素水平调节剂，结果显示胰岛素组（INS）的MSI显著低于旋转组（ROT）、链脲佐菌素组（STZ）和链脲佐菌素&胰岛素组（SINS）。STZ组的MSI高于ROT组和INS组。注射胃饥饿素的大鼠的MSI高于对照组和胃饥饿素拮抗剂组。加速度刺激诱导胰岛素受体底物1（IRS1）磷酸化及海马区突触蛋白表达。我们还发现，向海马区微量注射胰岛素可预防MS症状以及通过MSI、旷场试验、T迷宫和莫里斯水迷宫测量的认知能力。我们的研究表明，胰岛素和胰岛素水平调节剂可影响MS症状和认知能力。
