Sato Koji, Nishijima Takeshi, Yokokawa Takumi, Fujita Satoshi
Faculty of Sport and Health Science, Ritsumeikan University, Shiga, Japan.
Graduate School of Human Development and Environment, Kobe University, Kobe, Japan.
PLoS One. 2017 Jun 1;12(6):e0178505. doi: 10.1371/journal.pone.0178505. eCollection 2017.
Previous studies have demonstrated that an acute bout of aerobic exercise induces a subsequent delayed onset of hypoglycemia among patients with type 1 diabetes. However, the mechanisms of exercise-induced hypoglycemia in type 1 diabetes are still unclear. Streptozotocin (STZ) was injected to 6-week-old male Wistar rats, and three days after STZ injection, animals were randomly assigned into 2 groups: STZ with insulin only (STZ) and STZ with insulin and exercise (STZ+EX). Normal Wistar rats with exercise were used as control (CON+EX). Insulin was intraperitoneally injected (0.5 U/kg) to both STZ groups (-0.5 h), and a bout of aerobic exercise (15 m/min for 30 min) was conducted at euglycemic conditions (0 h). Blood was collected at 0, 1, 3, and 5 h after exercise from the carotid artery. While the blood glucose level was stable during the post-exercise period (0-5 h) in the STZ and CON+EX groups, it decreased significantly only in the STZ+EX group at 3 h. Plasma glucagon, adrenalin, and noradrenalin levels significantly increased at 1 h in the STZ group, whereas significant hormonal responses were observed at 5 h in the STZ+EX group. In skeletal muscle glucose metabolism-related pathway, the level of glucose transporter-4 (GLUT-4) translocation was significantly higher at 1 h in the CON and STZ groups. However, in the STZ+EX group, these activations were maintained by 5 h, indicating a sustained glucose metabolism in the STZ+EX group. A single bout of aerobic exercise induced a delayed onset of hypoglycemia in STZ-treated rats. A prolonged enhancement of GLUT-4 translocation and delayed counter-regulatory hormone responses may have contributed to the induction of hypoglycemia.
先前的研究表明，一次急性有氧运动可导致1型糖尿病患者随后出现延迟性低血糖。然而，1型糖尿病运动诱发低血糖的机制仍不清楚。将链脲佐菌素（STZ）注射到6周龄雄性Wistar大鼠体内，在注射STZ三天后，将动物随机分为两组：仅注射胰岛素的STZ组（STZ）和注射胰岛素并运动的STZ组（STZ+EX）。将进行运动的正常Wistar大鼠作为对照（CON+EX）。对两个STZ组均在-0.5小时腹腔注射胰岛素（0.5 U/kg），并在血糖正常的条件下（0小时）进行一次有氧运动（15米/分钟，持续30分钟）。运动后0、1、3和5小时从颈动脉采集血液。虽然STZ组和CON+EX组在运动后期间（0-5小时）血糖水平稳定，但仅STZ+EX组在3小时时血糖显著下降。STZ组血浆胰高血糖素、肾上腺素和去甲肾上腺素水平在1小时时显著升高，而STZ+EX组在5小时时观察到显著的激素反应。在骨骼肌葡萄糖代谢相关途径中，CON组和STZ组葡萄糖转运蛋白4（GLUT-4）转位水平在1小时时显著更高。然而，在STZ+EX组中，这些激活持续到5小时，表明STZ+EX组葡萄糖代谢持续存在。一次有氧运动在STZ处理的大鼠中诱发了延迟性低血糖。GLUT-4转位的长期增强和延迟的反调节激素反应可能促成了低血糖的发生。
