Department of Internal Medicine, Seoul St. Mary's Hospital, The Catholic University of Korea College of Medicine, Seoul, Korea.
Diabetes Metab J. 2013 Dec;37(6):475-83. doi: 10.4093/dmj.2013.37.6.475. Epub 2013 Dec 12.
We aimed to quantify stress-induced hyperglycemia and differentiate the glucose response between normal animals and those with diabetes. We also examined the pattern in glucose fluctuation induced by stress according to type of diabetes.
To load psychological stress on animal models, we used a predator stress model by exposing rats to a cat for 60 minutes and measured glucose level from the beginning to the end of the test to monitor glucose fluctuation. We induced type 1 diabetes model (T1D) for ten Sprague-Dawley rats using streptozotocin and used five Otsuka Long-Evans Tokushima Fatty rats as obese type 2 diabetes model (OT2D) and 10 Goto-Kakizaki rats as nonobese type 2 diabetes model (NOT2D). We performed the stress loading test in both the normal and diabetic states and compared patterns of glucose fluctuation among the three models. We classified the pattern of glucose fluctuation into A, B, and C types according to speed of change in glucose level.
Increase in glucose, total amount of hyperglycemic exposure, time of stress-induced hyperglycemia, and speed of glucose increase were significantly increased in all models compared to the normal state. While the early increase in glucose after exposure to stress was higher in T1D and NOT2D, it was slower in OT2D. The rate of speed of the decrease in glucose level was highest in NOT2D and lowest in OT2D.
The diabetic state was more vulnerable to stress compared to the normal state in all models, and the pattern of glucose fluctuation differed among the three types of diabetes. The study provides basic evidence for stress-induced hyperglycemia patterns and characteristics used for the management of diabetes patients.
我们旨在量化应激引起的高血糖,并区分正常动物和糖尿病动物的血糖反应。我们还根据糖尿病类型检查了应激引起的血糖波动模式。
为了给动物模型加载心理应激,我们使用了捕食者应激模型,即将大鼠暴露于猫中 60 分钟,并在测试开始到结束时测量血糖水平,以监测血糖波动。我们使用链脲佐菌素诱导 10 只 Sprague-Dawley 大鼠的 1 型糖尿病模型(T1D),并使用 5 只 Otsuka Long-Evans Tokushima Fatty 大鼠作为肥胖 2 型糖尿病模型(OT2D)和 10 只 Goto-Kakizaki 大鼠作为非肥胖 2 型糖尿病模型(NOT2D)。我们在正常和糖尿病状态下进行应激加载测试,并比较三种模型之间的血糖波动模式。我们根据血糖水平变化的速度将血糖波动模式分为 A、B 和 C 三种类型。
与正常状态相比,所有模型的血糖升高、高血糖暴露总量、应激性高血糖时间和血糖升高速度均显著增加。虽然 T1D 和 NOT2D 应激后血糖早期升高较高,但 OT2D 较慢。NOT2D 血糖水平下降速度最快,OT2D 最慢。
与正常状态相比,所有模型中的糖尿病状态对应激更为敏感,三种类型的糖尿病之间血糖波动模式存在差异。该研究为应激诱导的高血糖模式和特征提供了基础证据,用于糖尿病患者的管理。