大鼠创伤后胰岛素抵抗与葡萄糖转运关系的研究

Relationship between posttraumatic insulin resistance and glucose transportation in rats

目的探讨创伤后骨骼肌对葡萄糖转运能力的改变及其与创伤后胰岛素抵抗（m）之间的关系。方法通过对大鼠实施小肠部分切除手术建立创伤模型，观察大鼠血糖和血清胰岛素浓度的变化规律。运用高胰岛素-正常血糖钳夹技术评估外周组织葡萄糖廓清率。[^3H]标记葡萄糖示踪法检测创伤后骨骼肌葡萄糖转运能力的变化。最后分别测定大鼠骨骼肌组织中葡萄糖转运蛋白-4（GLUT-4）的mRNA和蛋白表达。结果大鼠小肠部分切除术后血糖浓度明显升高，血清胰岛素浓度则先短暂降低然后升高。创伤组大鼠外周组织对葡萄糖的廓清率下降了47％（P〈0．01）。创伤组大鼠骨骼肌对葡萄糖的转运能力明显低于对照组（P〈0．01）。两组大鼠骨骼肌中GLUT4mRNA和GLUT-4蛋白总量的表达差异无统计学意义（P〉0．05），但是创伤组大鼠骨骼肌细胞膜上的GLUT-4蛋白含量明显少于对照组（P〈0．05）。结论大鼠手术后早期即存在胰岛素抵抗现象，但胰岛素分泌量并未减少。创伤后早期骨骼肌细胞膜上GLUT-4分布减少以及对葡萄糖转运能力降低可能是导致创伤后胰岛素抵抗的机制之一。

Objective To investigate the relationship between posttraumatic insulin resistance and the change of glucose transportation by skeleton muscle after surgical trauma in rats. Methods Small intestine bowel resection was performed to establish the surgical traumatic model in rats. Blood samples were obtained for determination of the level of blood glucose and serum insulin. The hyperinsulinemic-eug- lycemic clamp techrtique was also used after surgical trauma to investigate the glucose disposal rate by the periphery tissue. The [ ^3H ] labeled glucose uptake experiment was carried out to evaluate the glucose transportation function in both groups. Finally, the expression and the distribution of glucose transporter 4 （GLUT-4） in skeletal muscle were detected. Results The level of blood glucose was elevated significant- ly after small bowel resection in rats. The level of serum insulin was decreased during the first 30 min after operation but elevated in the following time. The glucose disposal rate or clearance rate by periphery tissue was decreased by 47% after small bowel resection. The rate of 2-Deoxy-D-[ 1-^3H] glucose transported by skeletal muscle in the operation group was significantly lower than in the control group. Both the expression of GLUT-4 mRNA and the total content of GLUT-4 protein in two groups had no significant difference. But the expression of GLUT-4 in the plasma membrane was decreased in the operation group as compared with the control group. Conclusion The posttraamatic insulin resistance occurred soon after surgical＇trauma in rats. The surgical trauma induced marked alterations in glucose metabolism during the immediate postoperative period. The later appearance of elevated serum insulin argued against the opinion that secretion of insulin was reduced after trauma. The operation led to the decrease in glucose uptake which associated with a defect in insulin-stimulated glucose transport and GLUT-4 translocation.