Rattigan S, Appleby G J, Clark M G
Department of Biochemistry, University of Tasmania, Hobart, Australia.
Biochim Biophys Acta. 1991 Sep 3;1094(2):217-23. doi: 10.1016/0167-4889(91)90012-m.
The uptake of 2-deoxyglucose by perfused rat hearts was compared to the distribution of the insulin-regulatable glucose transporter (GLUT4) in membrane preparations from the same hearts. The hearts were treated with the alpha-adrenergic combination of epinephrine + propranolol, the beta-adrenergic agonist isoproterenol, high (8 mM) Ca2+ concentrations, insulin and the alpha adrenergic combination or insulin alone. Epinephrine (1 microM) + propranolol (10 microM), isoproterenol (10 microM), high Ca2+, insulin (1 microM) + epinephrine (1 microM) + propranolol (10 microM) and insulin (1 microM) each led to an increase in 2-deoxyglucose uptake and a shift in the recovery of the GLUT4 from a high-speed pellet membrane fraction (putatively intracellular) to a low-speed pellet membrane fraction (putatively sarcolemmal). There were significant correlations (r = -0.673, P less than 0.001) between the stimulation of 2-deoxyglucose uptake and the loss of GLUT4 from the intracellular membrane fraction, or the increase in the sarcolemmal fraction. The data provide evidence that the GLUT4 is translocated by agents that stimulate glucose transport in heart, and therefore this mechanism is not restricted to insulin.
将灌注大鼠心脏对2-脱氧葡萄糖的摄取与来自相同心脏的膜制剂中胰岛素可调节的葡萄糖转运蛋白(GLUT4)的分布进行比较。心脏分别用肾上腺素+普萘洛尔的α-肾上腺素能组合、β-肾上腺素能激动剂异丙肾上腺素、高浓度(8 mM)Ca2+、胰岛素以及α-肾上腺素能组合或单独使用胰岛素进行处理。肾上腺素(1 μM)+普萘洛尔(10 μM)、异丙肾上腺素(10 μM)、高Ca2+、胰岛素(1 μM)+肾上腺素(1 μM)+普萘洛尔(10 μM)和胰岛素(1 μM)均导致2-脱氧葡萄糖摄取增加,并且GLUT4的回收从高速沉淀膜部分(推测为细胞内)转移到低速沉淀膜部分(推测为肌膜)。2-脱氧葡萄糖摄取的刺激与细胞内膜部分GLUT4的丢失或肌膜部分的增加之间存在显著相关性(r = -0.673,P < 0.001)。这些数据提供了证据,表明GLUT4可被刺激心脏葡萄糖转运的物质转运,因此这种机制并不局限于胰岛素。