大鼠重度创伤后感染与胰岛素抵抗的相关机制研究  被引量:4

Mechanisms of insulin resistance and post-traumatic infection in rats

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作  者:王芳[1] 王言理[1] 朱小浩[1] 许锁[1] 彭庆荣[1] WANG Fang;WANG Yan-li;ZHU Xiao-hao;XU Suo;PENG Qing-rong(Lianyung ang First People′s Hospital,Lianyungang,Jiangsu 222000,China)

机构地区:[1]连云港市第一人民医院急诊科,江苏连云港222000

出  处:《中华医院感染学杂志》2020年第12期1810-1815,共6页Chinese Journal of Nosocomiology

基  金:连云港市卫生计生科技基金资助项目(201712)。

摘  要:目的探索大鼠重度创伤感染后出现的急性胰岛素抵抗和高血糖的特点及相关机制,为临床危重患者诊疗提供参考。方法以30只SD大鼠为基础组,另选取90只SD大鼠接受盲肠穿孔术制作感染模型,通过测定造模大鼠创伤感染后12 h内各个时间点血糖、胰高血糖素、皮质醇及胰岛素浓度,计算创伤感染组胰岛素抵抗指数(HOMA-IR);分别在创伤感染后3~10 h内通过胰岛素敏感性实验(IST)测定胰岛素敏感性和腹腔注射葡萄糖耐量实验(IPGTT)。用Western-blot测定创伤组在创伤感染后大鼠pAkt、pGSK3β和peNOS在各时间点的表达量与活性变化。结果创伤感染大鼠在伤后12 h内出现血糖双峰现象。与基础组比较,创伤组大鼠血清胰高血糖素、皮质激素、胰岛素在创伤后12 h内均有升高现象(P<0.05)。HOMA-IR值显示创伤感染后出现胰岛素抵抗;腹腔糖耐量和胰岛素敏感性实验提示在创伤后3 h胰岛素敏感性最低(P<0.05)。Western-blot结果显示感染组大鼠pAkt、pGSK3β和peNOS蛋白水平升高,且1 h后达到峰值(P<0.05)随后下降趋以稳定。结论大鼠在重度创伤感染12 h内会出现两个高血糖峰值及创伤感染后3 h胰岛素抵抗最为强烈,其与调控胰岛素信号转导通路pAkt-peNOS有关。OBJECTIVE To explore the characteristics of acute insulin resistance and hyperglycemia in rats with severe post-traumatic infection and analyze the related mechanisms so as to provide guidance for clinical diagnosis and treatment of critically ill patients.METHODS Totally 30 Sprague-Dawley(SD)rats were assigned as the baseline group,and 90 SD rats were chosen to establish the infection model by carrying out the cecal puncture.The levels of blood glucose,serum insulin,serum glucagon and serum cortisol were detected within 12 hours after establishment of the infection model,the insulin resistance index(HOMA-IR)of the traumatic infection group was calculated,the intraperitoneal glucose tolerance test(IPGTT)and insulin sensitivity test(IST)were performed to detect the sensitivity of insulin within 3-10 hours after the traumatic infection,and the expression and activity of pAkt,pGSK3βand peNOS of the rats with post-traumatic infection were determined by using Western-blot.RESULTS Two peaks of intermittent hyperglycemia were observed within 12 hours after the traumatic infection.As compared with the baseline group,the levels of serum cortisol,serum insulin,and serum glucagon of the trauma group were significantly elevated within 12 hours after the trauma(P<0.05).HOMA-IR indicated that there was insulin resistance after traumatic infection;IPGTT and IST showed that the sensitivity of insulin was significantly lowest after the trauma for 3 hours(P<0.05).Western-blot indicated that the levels of pAkt,pGSK3βand peNOS of the infection group were significantly elevated and reached to the peak 1 hour later(P<0.05)and then declined to be stable.CONCLUSION The rats have two peaks of intermittent hyperglycemia within 12 hours after severe traumatic infection and have the most powerful insulin resistance after the traumatic infection for 3 hours,which is associated with the regulation of insulin signaling pathway pAkt-peNOS.

关 键 词:创伤感染 高血糖 胰岛素抵抗 信号转导 

分 类 号:R641[医药卫生—外科学]

 

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