Insulin level regulators may affect cognitive ability caused by motion sickness: an experimental study

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.