第二军医大学学报
第二軍醫大學學報
제이군의대학학보
ACADEMIC JOURNAL OF SECOND MILITARY MEDICAL UNIVERSITY
2001年
2期
115-117
,共3页
殷仁富%赵君%陈金明%吴宗贵%仇韶华%王咏梅%武瑞美
慇仁富%趙君%陳金明%吳宗貴%仇韶華%王詠梅%武瑞美
은인부%조군%진금명%오종귀%구소화%왕영매%무서미
心肌缺血%葡萄糖%胰岛素%葡萄糖转运子4
心肌缺血%葡萄糖%胰島素%葡萄糖轉運子4
심기결혈%포도당%이도소%포도당전운자4
目的:观察胰岛素与低血糖缺血 刺激心肌葡萄糖转运子4(GLUT4)基因表达是否呈相加作用。方法:采 用Northern blot法分析心肌GLUT4 mRNA,采用免疫印迹法分析心肌GLUT4基因表达。结果:输注胰岛素使局部低血流心肌GLUT4 mRNA和GLUT4基因表达增加2.3~2. 5倍,同时伴随心肌葡萄糖摄取明显增多达4倍。结论:胰岛素与低血 流缺血刺激心肌致GLUT4 mRNA和GLUT4表达呈相加作用,其结果使GLUT4数量明显增加,进而 使心肌葡萄糖摄取量增加。此机制在缺血心肌能量代谢过程中起着重要的代谢性调节作用。
目的:觀察胰島素與低血糖缺血 刺激心肌葡萄糖轉運子4(GLUT4)基因錶達是否呈相加作用。方法:採 用Northern blot法分析心肌GLUT4 mRNA,採用免疫印跡法分析心肌GLUT4基因錶達。結果:輸註胰島素使跼部低血流心肌GLUT4 mRNA和GLUT4基因錶達增加2.3~2. 5倍,同時伴隨心肌葡萄糖攝取明顯增多達4倍。結論:胰島素與低血 流缺血刺激心肌緻GLUT4 mRNA和GLUT4錶達呈相加作用,其結果使GLUT4數量明顯增加,進而 使心肌葡萄糖攝取量增加。此機製在缺血心肌能量代謝過程中起著重要的代謝性調節作用。
목적:관찰이도소여저혈당결혈 자격심기포도당전운자4(GLUT4)기인표체시부정상가작용。방법:채 용Northern blot법분석심기GLUT4 mRNA,채용면역인적법분석심기GLUT4기인표체。결과:수주이도소사국부저혈류심기GLUT4 mRNA화GLUT4기인표체증가2.3~2. 5배,동시반수심기포도당섭취명현증다체4배。결론:이도소여저혈 류결혈자격심기치GLUT4 mRNA화GLUT4표체정상가작용,기결과사GLUT4수량명현증가,진이 사심기포도당섭취량증가。차궤제재결혈심기능량대사과정중기착중요적대사성조절작용。
Objective: To investigate whether there is additi ve effects of hyperinsulinemia and ischemia on expression of canine myocardial G LUT4 gene in vivo. Methods: The expression of myocardial GLU T4 was determined by semiquantitative immunoblotting.The expression of GLUT4 mRN A was determined by semiquantitative Northern blotting. Results: Dramatic changes were seen in GLUT4 mRNA and GLUT4 expression in the ischemic hearts.After infusing insulin for 8 h,regional GLUT4 mRNA and GLUT4 levels in is chemic hearts were 2.5, 2.3-fold that of expression in normal hearts(P<0.01 ). Myocardial glucose uptake in ischemic hearts was increased by 4-fold when co mpared with normal hearts(P<0.01). Conclusion: There are not only additive effects of hyperinsulinemia and low-flow ischemia on canine myoc ardial GLUT4 mRNA and GLUT4 expression in vivo, but also increase of myocar dial glucose uptake. Enhanced GLUT4 expression may be an important protective m echanism by which myocardial cells enhance glucose uptake and metabolism during low-flow ischemia.