ENDOCRINE CONTROL OF RBC AND ADIPOSE SUGAR TRANSPORT

现在看来，脂肪己糖转移至少有两种形式 监管-有充分记录的胰岛素诱导的携带者招募 从胞浆到质膜，以及一种不依赖募集的机制。 在这里，我们证明了大鼠脂肪和红细胞糖的转运都可能 共有一个共同的易受监管的敏感性 “招聘”--独立的机制。植物体内糖运输的动力学研究 正常大鼠脂肪和红细胞是对称的。跟随率 然而，切除脑下垂体，脂肪和红细胞糖的运输都变得 不对称--退出速度大于进入速度。在这些下面 在此条件下，胰岛素可加速脂肪糖的摄取，但不会退出。这个 脂肪和RBC己糖转移反应之间惊人的相似之处 脑垂体切除术使我们能够利用RBC作为模型系统 研究这种类型的运输管制。其结果就是 大鼠血清和红细胞胞浆中“活性成分”的发现 控制红细胞糖表达的去脑垂体大鼠 转运对称性、RBC己糖转运蛋白的数量和 转运蛋白的平均分子质量。我们的目标是利用这一点 内分泌学方法确定：1.红细胞增加的来源 己糖转移蛋白的数量。2.红细胞转运的分子基础 对称表达式。3.脂肪己糖转移易感性 这些运输调节因素。4.这些因素对经济增长的影响 胰岛素诱导的脂肪携带者募集。

It now seems that adipose hexose transfer is subject to at least two forms of regulation - the well-documented, insulin-induced carrier recruitment from cytosol to plasma membrane and a recruitment-independent mechanism. Here we show that both rat adipose and erythrocyte sugar transport may share a common susceptibility to regulation by this 'recruitment'-independent mechanism. The kinetics of sugar transport in normal rat adipose and erythrocytes are symmetric. Following rat hypophysectomy, however, both adipose and RBC sugar transport become asymmetric - exit rates being greater than those for entry. Under these conditions, insulin accelerates adipose sugar uptake but not exit. The striking parallels between adipose and RBC hexose transfer responses to hypophysectomy have enabled us to exploit the RBC as a model system for the study of this type of transport regulation. The result has been the discovery of 'active principles' in both rat serum and RBC cytosol from hypophysectomized rats that control the expression of red cell sugar transport symmetry, the number of RBC hexose transport proteins and the average molecular weight of the transporter. Our goal is to exploit this endocrinological approach to determine: 1. The origin of increased RBC hexose transfer protein numbers. 2. The molecular basis of RBC transport symmetry expression. 3. The susceptibility of adipose hexose transfer to these transport modulating factors. 4. The effects of these factors on insulin-induced adipose carrier recruitment.