重症感染患者的糖代谢障碍及胰岛素抵抗的部位和机理

目的　探讨感染应激诱导的胰岛素抵抗的部位及其机理。方法　患者分为感染组10例及对照组8例，两组患者同时持续输注10%葡萄糖液及胰岛素，结合间接能量测定仪(CCM)，观察机体对葡萄糖的氧化利用情况。用逆转录聚合酶链反应（RT-PCR）方法，检测肌肉组织中胰岛素受体(INSR)、葡萄糖载体4(GLUT4)的基因表达。　结果　感染组患者出现明显的胰岛素抵抗（IR），不仅葡萄糖氧化率显著低于对照组，其肌肉组织对葡萄糖的摄取能力也明显降低(P＜0.05)。RT-PCR结果显示与对照组相比感染患者骨骼肌中GLUT4mRNA表达显著下降(P＜0.05)，而INSRmRNA表达却无明显差异。　结论　感染应激时IR的产生主要是由于胰岛素介导的葡萄糖摄取(IMGU)障碍。其受损部位在受体后。GLUT4含量及活性下降是其主要诱导原因。

Glucose metabolic dysfunction in patients with sepsis and the mechanism of insul in resistance

Objective　To investigate the mechanism of gluc ose metabolic dysfunction and insulin resistance induced by sepsis.　Methods　Patients with sepsis (10 cases) and c ontrol groups (8 cases) received glucose and insulin continuously, then had ener gy metabolism measured by indirect calorimetory. Insulin receptor and GLUT 4 mRNA expression in skeletal muscle were assessed in the meantime.　Results　All septic patients showed severe ins ulin resistance, and not only their glucose oxidation rate were significantly lo wer than that of control groups (P<0.05),but also the capability of skelet al muscle glucose uptake decreased dramatically. The result of RT-PCR showed th at the expression of GLUT4 in muscle of septic patients reduced significa ntly compared with controls(P<0.05).　Conclusio ns 　The dysfunction of insulin mediated glucose uptake was the main character of insulin resistance during sepsis. The defective site was at p ostreceptor, and the decrease of content and action of GLUT4 may play an important role in its induction.