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胰岛素增强缺血心肌葡萄糖转运子1基因表达的实验研究
引用本文:殷仁富,陈金明,吴宗贵,仇韶华,武瑞美,孔宪涛,KONG Xian-Tao.胰岛素增强缺血心肌葡萄糖转运子1基因表达的实验研究[J].中国病理生理杂志,2001,17(6):531-533.
作者姓名:殷仁富  陈金明  吴宗贵  仇韶华  武瑞美  孔宪涛  KONG Xian-Tao
作者单位:1. 第二军医大学长征医院, 心内科,上海200003;
2. 实验诊断科全军免疫中心,上海200003
摘    要:目的:探讨胰岛素刺激低血流缺血心肌增加葡萄糖摄取的机制。方法:采用Northern法分析缺血心肌葡萄糖转运子-1(GLUT1)mRNA和免疫法分析心肌葡萄糖转运子1(GLUT1)多肽水平。结果:胰岛素使局部低血流缺血心肌GLUT1 mRNA和GLUT1多肽表达明显增加。同时伴随缺血心肌葡萄糖摄取明显增多。结论:胰岛素能增强缺血心肌GLUT1 mRNA和GLUT1多肽表达,使GLUT1数增加,进而促进心肌葡萄糖摄取增多,胰岛素增强低血流缺血刺激的心肌GLUT1表达。

关 键 词:心肌  局部缺血  葡萄糖  代谢  
文章编号:1000-4718(2001)06-0531-03
收稿时间:2000-10-28
修稿时间:2000年10月28

Insulin enhances glucose transporter 1 gene expression of low-flow ischemic myocardium
YIN Ren-Fu,CHEN Jin-ming,WU Zong-gui,QIU Shao-hua,WANG Yong-mei,WU Rui-mei,KONG Xian-Tao.Insulin enhances glucose transporter 1 gene expression of low-flow ischemic myocardium[J].Chinese Journal of Pathophysiology,2001,17(6):531-533.
Authors:YIN Ren-Fu  CHEN Jin-ming  WU Zong-gui  QIU Shao-hua  WANG Yong-mei  WU Rui-mei  KONG Xian-Tao
Institution:1. Department of Cardiology,Immunology Center of PLA, Changzheng Hospital, Second Military Medical University,Shanghai 200003, China;
2. Department of Laboratory Diagnosis, Immunology Center of PLA, Changzheng Hospital, Second Military Medical University,Shanghai 200003, China
Abstract:AIM: To investigate the mechanism underlying insulin-stimulated increase in glucose uptake during low-flow myocardial ischemia. METHODS: The expression of myocardial GLUT1 polypeptide was determined by semiquantitative immunoblotting. The expression of GLUT1 mRNA was determined by semiquantitative Northern blotting. RESULTS: After infusing insulin during low- flow myocardial ischemia for 8 h,the expression of both GLUT1 mRNA and GLUT1 polypeptide was significantly higher in experimental myocardium than that in normal myocardium. The glucose uptake was upregulated at the same time in the exprimental myocardium. CONCLUSION: Insulin enhances the expression of GLUT1 mRNA and GLUT1 polypeptide in ischemic myocardial regions. GLUT1 expression may be an important mechanism by which myocardial cells enhance glucose uptake and metabolism during low-flow myocardial ischemia.
Keywords:Myocardium  Ischemia  Glucose  Metabolism
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