期刊文献+

重症感染患者的糖代谢障碍及胰岛素抵抗的部位和机理 被引量:4

Glucose metabolic dysfunction in patients with sepsis and the mechanism of insulin resistance
原文传递
导出
摘要 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 0 5 )。RT PCR结果显示与对照组相比感染患者骨骼肌中GLUT4 mRNA表达显著下降 (P <0 0 5 ) ,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。 Objective [WT5”BZ] To investigate the mechanism of glucose metabolic dysfunction and insulin resistance induced by sepsis.[WT5”HZ] Methods [WT5”BZ] Patients with sepsis (10 cases) and control groups (8 cases) received glucose and insulin continuously, then had energy metabolism measured by indirect calorimetory. Insulin receptor and GLUT 4 mRNA expression in skeletal muscle were assessed in the meantime.[WT5”HZ] Results [WT5”BZ] All septic patients showed severe insulin resistance, and not only their glucose oxidation rate were significantly lower than that of control groups ( P <0 05),but also the capability of skeletal muscle glucose uptake decreased dramatically. The result of RT PCR showed that the expression of GLUT 4 in muscle of septic patients reduced significantly compared with controls( P <0 05).[WT5”HZ] Conclusions [WT5”BZ] The dysfunction of insulin mediated glucose uptake was the main character of insulin resistance during sepsis. The defective site was at postreceptor, and the decrease of content and action of GLUT 4 may play an important role in its induction. [WT5”HZ]
出处 《中华普通外科杂志》 CSCD 北大核心 2001年第1期41-43,共3页 Chinese Journal of General Surgery
关键词 感染 胰岛素 Infection Insulin
  • 引文网络
  • 相关文献

参考文献1

  • 1Zhong W W,Arch Surg,1993年,128卷,158页

同被引文献33

引证文献4

相关主题

;
使用帮助 返回顶部