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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(IR)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GLUT4 mRNA和GLUT4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 changes of glucose transport ability and its relationship with posttraumatic insulin resistance (IR) in posttraumatic skeletal muscle. Methods The traumatic model was established by partial resection of the intestine in rats. The changes of blood glucose and serum insulin were observed. Evaluation of Peripheral Tissue Glucose Clearance by High Insulin - Glycemic Monitoring System. Changes of Glucose Transport Capacity in Skeletal Muscles Detected by [~ 3H] Labeled Glucose Tracing Method. Finally, the mRNA and protein expression of glucose transporter-4 (GLUT-4) in rat skeletal muscle were measured respectively. Results After partial resection of the small intestine, blood glucose levels were significantly increased, while serum insulin concentration decreased first and then increased. Peripheral tissue in trauma rats showed a 47% reduction of glucose clearance (P <0.01). The ability of skeletal muscle to transport glucose in trauma group was significantly lower than that in control group (P <0.01). There was no significant difference in the expression of GLUT4 mRNA and GLUT4 protein between the two groups (P> 0.05), but the content of GLUT-4 protein in the skeletal muscle cell membrane of the trauma group was significantly less than that of the control group (P < 0.05). Conclusion There was insulin resistance in the early stage after operation in rats, but the amount of insulin secretion did not decrease. One of the mechanisms that lead to post-traumatic insulin resistance is the decrease of GLUT-4 distribution and the decrease of glucose transport ability in the early posttraumatic rat skeletal muscle cells.