Hexose transport stimulation and membrane redistribution of glucose transporter isoforms in response to cholera toxin, dibutyryl cyclic AMP, and insulin in 3T3-L1 adipocytes.
Hexose transport stimulation and membrane redistribution of glucose transporter isoforms in response to cholera toxin, dibutyryl cyclic AMP, and insulin in 3T3-L1 adipocytes.
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DOI：
10.1016/s0021-9258(19)38365-6
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发表时间：
1990-07
期刊：
影响因子：
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通讯作者：
B. Clancy;M. Czech
中科院分区：
文献类型：
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作者：
B. Clancy;M. Czech
3 T3-L1脂肪细胞暴露于100 ng/ml的霍乱毒素或1 mM的二丁酰环AMP引起脱氧葡萄糖转运的显着刺激。暴露12-24小时后观察到最大增加10- 15倍，而100 nM胰岛素在30 min内引起类似幅度的增加。短期暴露（4 h）细胞霍乱毒素或二丁酰环AMP导致脱氧葡萄糖转运增加3- 4倍，这与HepG 2/红细胞（GLUT 1）的显著再分布有关。和肌肉/脂肪细胞（GLUT 4）葡萄糖转运蛋白从低密度微粒体到质膜部分。两种转运蛋白的总细胞量保持恒定。与此相反，细胞暴露于霍乱毒素或二丁酰环AMP 12小时表现出升高GLUT 1（但不是GLUT 4）蛋白的总细胞含量约1.5和2.5倍以上的控制，分别。虽然霍乱毒素（12小时）与胰岛素（30分钟）引起类似的脱氧葡萄糖转运的10倍增强细胞的这种治疗，观察到一个显着的差异，相对于在质膜组分中的葡萄糖转运蛋白的含量。虽然胰岛素引起质膜组分中GLUT 4蛋白水平增加2.6倍，但霍乱毒素仅使该转运蛋白的量增加30%。胰岛素或霍乱毒素增加GLUT 1蛋白在质膜部分的水平相等（1.6倍）。因此，与霍乱毒素相比，质膜部分中更多数量的葡萄糖转运蛋白与胰岛素的转运刺激相关。我们的结论是：1）在向3 T3-L1脂肪细胞添加霍乱毒素或二丁酰环AMP后的早期（4小时），葡萄糖转运蛋白向质膜的再分布似乎有助于提高脱氧葡萄糖摄取速率，和2）长时间处理（12-18小时）后刺激己糖摄取霍乱毒素对细胞的毒性可能涉及一种或两种葡萄糖转运蛋白同种型内在活性的额外增加。
Exposure of 3T3-L1 adipocytes to 100 ng/ml of cholera toxin or 1 mM dibutyryl cyclic AMP caused a marked stimulation of deoxyglucose transport. A maximal increase of 10- to 15-fold was observed after 12-24 h of exposure, while 100 nM insulin elicited an increase of similar magnitude within 30 min. A short term exposure (4 h) of cells to cholera toxin or dibutyryl cyclic AMP resulted in a 3- to 4-fold increase in deoxyglucose transport which was associated with significant redistribution of both the HepG2/erythrocyte (GLUT1) and muscle/adipocyte (GLUT4) glucose transporters from low density microsomes to the plasma membrane fraction. Total cellular amounts of both transporter proteins remained constant. In contrast, cells exposed to cholera toxin or dibutyryl cyclic AMP for 12 h exhibited elevations in total cellular contents of GLUT1 (but not GLUT4) protein to about 1.5- and 2.5-fold above controls, respectively. Although such treatments of cells with cholera toxin (12 h) versus insulin (30 min) caused similar 10-fold enhancements of deoxyglucose transport, a striking discrepancy was observed with respect to the content of glucose transporter proteins in the plasma membrane fraction. While insulin elicited a 2.6-fold increase in the levels of GLUT4 protein in the plasma membrane fraction, cholera toxin increased the amount of this transporter by only 30%. Insulin or cholera toxin increased the levels of GLUT1 protein in the plasma membrane fraction equally (1.6-fold). Thus, a greater number of glucose transporters in the plasma membrane fraction is associated with transport stimulation by insulin compared to cholera toxin. We conclude that: 1) at early times (4 h) after the addition of cholera toxin or dibutyryl cyclic AMP to 3T3-L1 adipocytes, redistribution of glucose transporters to the plasma membrane appears to contribute to elevated deoxyglucose uptake rates, and 2) the stimulation of hexose uptake after prolonged treatment (12-18 h) of cells with cholera toxin may involve an additional increase in the intrinsic activity of one or both glucose transporter isoforms.