摘要
目的 :探讨心肌缺氧时 AMP激活的蛋白激酶 (AMPK)激活对葡萄糖转运子 4(GL U T4)移位和葡萄糖摄取的作用。方法 :大鼠心室肌经 5 0 0 μm ol/ L 腺嘌呤 - 9- β- D-阿糖呋喃腺苷 (ara A)处理后 ,分别与胰岛素、氰化钾、5 -氨基咪唑 - 4-氨基甲酰 - 1- β- D核糖呋喃腺苷 (AICAR)孵育 ,用放射性核素分析技术测定其葡萄糖摄取量和 AMPK活力 ,应用 Western印迹法分析心肌细胞 GL UT4含量。 结果 :AMPK特异性激活剂 AICAR和氰化钾可使心肌葡萄糖摄取增加 (1倍和 1.5倍 ) ,但均受ara A抑制。AICAR增加心肌 AMPK活力和葡萄糖摄取 ,而 ara A则有抑制作用。心肌细胞质膜 GL U T4分布明显增加而细胞器膜 GL U T4分布相应减少。 结论 :氰化钾所致的心肌缺氧与 AICAR一样可通过 AMPK激活途径 ,促进 GL U T4移位和葡萄糖摄取 ,它有别于胰岛素所通过的 PI3K激活途径。
Objective: To investigate the effects of AMP activated protein kinase (AMPK) activation on translocation of glucose transporter 4(GLUT4) and glucose uptake in hypoxic rat myocardium. Methods: Left ventricular papillary muscle was treated with 500 μmol/L araA, and glucose concentration was determined after incubated with insulin, potassium cyanide and 5 aminoimidazole 4 carboxyamide 1 β D ribofuranoside (AICAR). Myocardial GLUT4 content and AMPK activity were studied. Results: AICAR and potassium cyanide increased myocardial glucose uptake by 1 and 1.5 times respectively. The effects of both AICAR and potassium cyanide were inhibited by araA. AICAR increased myocardial AMPK activity whereas araA inhibited it. After incubating with AICAR and potassium cyanide, GLUT4 content increased in myocardial sarcolemma significantly and decreased in intracellular membrane at the same time. Conclusion: The activated AMPK pathway, through which myocardial hypoxia is induced by potassium cyanide and AICAR, facilitates translocation of GLUT4 and glucose uptake, which is different from insulin activated PI3K pathway. [
出处
《第二军医大学学报》
CAS
CSCD
北大核心
2000年第11期1065-1067,共3页
Academic Journal of Second Military Medical University
关键词
心肌缺氧
葡萄糖摄取
葡萄糖转运子4
蛋白激酶
myocardiumhypoxia
glucose uptake
glucose transporter 4
insulin
protein kinase,AMP activated
