ENDOCRINE CONTROL OF RBC AND ADIPOSE SUGAR TRANSPORT

现在看来，脂肪己糖转移是受至少两种形式 监管-有据可查，胰岛素诱导的携带者招募 从胞质溶胶到质膜和一个募集独立的机制。 在这里，我们表明，大鼠脂肪和红细胞的糖转运可能 都有一个共同的敏感性， “招聘”-独立机制。 葡萄糖转运动力学研究 正常大鼠脂肪和红细胞是对称的。 后续大鼠 然而，垂体切除术后，脂肪和RBC糖转运变得 不对称-退出率大于进入率。 根据这些 在这种情况下，胰岛素加速脂肪糖的摄取，但不排出。 的 脂肪和红细胞己糖转移反应之间惊人的相似之处， 垂体切除术使我们能够利用红细胞作为模型系统， 研究这类交通法规。 其结果是 在大鼠血清和红细胞胞液中发现了“活性成分”， 控制红细胞糖表达的垂体切除大鼠 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量。 我们的目标是利用这个 内分泌学方法来确定：1。RBC增加的原因 己糖转运蛋白数量。 2.红细胞转运的分子基础 对称表达式 3.脂肪己糖转移对 这些运输调节因素。 4.这些因素对 胰岛素诱导的脂肪载体募集。

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.