摘要
目的 观察胰岛素是否增强低血流缺血对心肌葡萄糖转运子 4(GLUT4)基因表达的刺激作用。方法 采用Northern法分析心肌GLUT4mRNA和免疫法分析心肌GLUT4多肽。比较单纯给予胰岛素、单纯心肌缺血和心肌缺血时给予胰岛素心肌GLUT4mRNA和GLUT4多肽的表达情况 ,并与正常心肌比较。结果 正常心肌GLUT4mRNA和GLUT4多肽心外层分别为 :1.3± 0 .16 ;0 .72± 0 .0 1(relativedens,units) ,心内层分别为 :1.4± 0 .15 ;0 .73± 0 .0 1。单纯给予胰岛素心肌GLUT4mRNA表达比正常心肌增加 1.2倍 ,GLUT4多肽表达增加 1倍 (P <0 .0 5 ) ;单纯缺血心肌则分别增高 1.7和 1.8倍 (P <0 .0 1) ;而心肌缺血时给予胰岛素GLUT4mRNA表达增高 2 .5倍 ,GLUT4多肽表达则增加 2 .3倍 (P <0 .0 1)。心肌葡萄糖摄取量亦比正常心肌明显增高。结论 胰岛素与低血流缺血均能刺激心肌GLUT4mRNA和GLUT4多肽表达 ,而心肌缺血时给予胰岛素则增强缺血刺激的GLUT4mRNA和GLUT4的表达作用 ,其结果使GLUT4数明显增加 ,进而使心肌葡萄糖摄取量相应增加。胰岛素增强低血流缺血对心肌GLUT4表达的刺激作用 。
Objective To investigate if insulin was able to enhance the stimulated effect of low flow ischemia on canine myocardial GLUT4 gene expression. Methods The expression of myocardial GLUT4 polypeptide was determined by semiquantitative immunobloting. The expression of GLUT4 mRNA was determined by semiquantitative Northern blotting. The animals were divided into four groups(insulin alone, ischemia alone, ischemia treated by insulin and normal controls). Results The levels of GLUT4mRNA and GLUT4 polypepetide in normal subepicardium were 1.3±0.16; 0.72±0.01(relative density units) respectively. The levels of GLUT4 mRNA and GLUT4 polypeptide in normal subendocardium were 1.4±0.15; 0.73±0.01 respectively. Regional GLUT4 mRNA and GLUT4 polypeptide levels in hearts treated by insulin alone were 1～1.2 fold than that of the expression in normal hearts( P <0.05). Both 1.7 and 1.8 fold higher in ischemic hearts than in normal hearts( P <0.01) was also shown. After treated by insulin for 8 h, regional GLUT4 mRNA and GLUT4 polypeptide levels in ischemic hearts were increased even higher up to 2.5 and 2.3 fold that of expression in normal hearts( P <0.01). Conclusions Both insulin and low flow ischemia can stimulate the expression of canine myocardial GLUT4 mRNA and GLUT4 polypeptide. Enhanced GLUT4 expression is an important regulating mechanism to increase the myocardial glucose uptake during low flow ischemia.
出处
《高血压杂志》
CSCD
2001年第3期234-236,共3页
Chinese Journal of Hypertension
