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ENDOCRINE CONTROL OF RBC AND ADIPOSE SUGAR TRANSPORT

红细胞和脂肪糖运输的内分泌控制

基本信息

批准号：
3154432
负责人：
ANTHONY CARRUTHERS
金额：
$ 13.9万
依托单位：
UNIV OF MASSACHUSETTS MED SCH WORCESTER
依托单位国家：
美国
项目类别：
财政年份：
1985
资助国家：
美国
起止时间：
1985-09-25 至 1988-08-31
项目状态：
已结题

项目摘要

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.

现在看来，脂肪己糖转移至少有两种形式监管 - 有据可查的胰岛素诱导的载体招募从细胞质到质膜和招募独立的机制。在这里，我们表明大鼠脂肪和红细胞糖转运可能都对这种监管有着共同的敏感性独立于“招聘”的机制。糖转运动力学正常大鼠的脂肪和红细胞是对称的。跟踪大鼠然而，垂体切除术中，脂肪和红细胞糖的运输都变得不对称——退出率高于进入率。在这些之下在某些情况下，胰岛素会加速脂肪糖的摄取，但不会加速脂肪糖的排出。这脂肪和红细胞己糖转移反应之间存在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此类运输监管。结果是在大鼠血清和红细胞胞浆中发现“活性成分” 控制红细胞糖表达的垂体切除大鼠运输对称性、红细胞己糖运输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一点内分泌学方法确定： 1. 红细胞增多的起源己糖转移蛋白数量。 2. 红细胞转运的分子基础对称表达式。 3. 脂肪己糖转移的易感性这些运输调节因素。 4. 这些因素的影响胰岛素诱导的脂肪载体募集。