CAJ | 학술논문

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。
목적：탐토이도소자격저혈류결혈심기증가포도당섭취적궤제。방법：채용Northern법분석결혈심기포도당전운자-1(GLUT1) mRNA화면역법분석심기포도당전운자1（GLUT1）다태수평。결과：이도소사국부저혈류결혈심기GLUT1 mRNA화GLUT1다태표체명현증가。동시반수결혈심기포도당섭취명현증다。결론：이도소능증강결혈심기GLUT1 mRNA화GLUT1다태표체，사GLUT1수증가，진이촉진심기포도당섭취증다，이도소증강저혈류결혈자격적심기GLUT1표체。
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.