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作 者:胡小健[1] 任笛 彭锋[1] 周汉清[1] 张志鸿[1] 程威英[2] 冯菡芳[2]
机构地区:[1]复旦大学生理学和生物物理学系立人实验室,上海200433 [2]上海第二医科大学附属新华医院,上海200093
出 处:《生物物理学报》2000年第2期231-236,共6页Acta Biophysica Sinica
基 金:国家自然科学基金资助项目!(39730150;39570203)
摘 要:红细胞膜葡萄糖运输的温度依赖性研究结果表明 ,Ⅱ型糖尿病患者的葡萄糖输入的活化能比正常增大约30 % ,这和患者葡萄糖输入速率减小的结果相一致。但葡萄糖跨膜输出的活化能没有显著变化。对在红细胞葡萄糖转运蛋白(GLUT1)内侧特异结合的细胞松弛素B(CB)的抑制效应研究结果表明 ,糖尿病人的CB抑制常数无明显变化。结合以前我们用根皮素抑制剂的实验 ,表明Ⅱ型糖尿病患者红细胞膜上GLUT1很可能发生了结构的变化 ,发生变异的位点在在此膜蛋白的膜外侧区域。The temperature dependence of the glucose transport across the erythrocyte membranes showed that the Arrehnius activation energy for zero-trans influx increased by about 30% in type Ⅱdiabetic patients compared with the healthy controls. This consisted with the result of the decrease in the glucose influx rate. Meanwhile, there was no difference between the activation energy for glucose efflux in the erythrocyte membranes of the patients and controls. The measurement of the inhibitory effect of Cytochalasin B on the glucose transport showed that the inhibitory constants of both glucose influx and efflux were the same in patients as in healthy controls. The result, in combination with our previous study on the decrease in the inhibitory effect of Phloretin,confirmed the presumption about the structural change of type Ⅰglucose transporter (GLUT1) in the patients erythrocyte membranes. The defect in the protein would mostly located at the outer domain of GLUT1.
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