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葡萄糖饥饿对大鼠脑原代培养神经元细胞中葡萄糖转运的影响。

Effect of glucose starvation on glucose transport in neuronal cells in primary culture from rat brain.

作者信息

Hara M, Matsuda Y, Okumura N, Hirai K, Nakagawa H

机构信息

Institute for Protein Research, Osaka University, Japan.

出版信息

J Neurochem. 1989 Mar;52(3):909-12. doi: 10.1111/j.1471-4159.1989.tb02541.x.

Abstract

The regulation of glucose transport into cultured brain cells during glucose starvation was studied. On glucose deprivation for 40 h, 2-deoxy-D-glucose (2-DG) uptake was stimulated twofold in neuronal cells but was not changed significantly in astrocytes. On refeeding, the increased activity of neuronal cells rapidly returned to the basal level, an observation indicating that the effect of glucose starvation was reversible. The increase was due solely to change in the Vmax, a finding suggesting that the number of glucose transporters on the plasma membrane is increased in starved cells. Cycloheximide inhibited this increase. In the presence of cycloheximide, the activity of 2-DG uptake of starved cells remained constant for 12 h and then slowly decreased, whereas that of fed cells decreased rapidly. These findings suggest that glucose starvation regulates glucose transport by changing the rate of net synthesis of the transporter in neuronal cells in culture.

摘要

研究了葡萄糖饥饿期间培养的脑细胞中葡萄糖转运的调节情况。在葡萄糖剥夺40小时后,神经元细胞中2-脱氧-D-葡萄糖(2-DG)的摄取增加了两倍,但星形胶质细胞中的摄取没有显著变化。重新喂食后,神经元细胞增加的活性迅速恢复到基础水平,这一观察结果表明葡萄糖饥饿的影响是可逆的。这种增加仅归因于Vmax的变化,这一发现表明饥饿细胞中质膜上葡萄糖转运蛋白的数量增加。放线菌酮抑制了这种增加。在放线菌酮存在的情况下,饥饿细胞的2-DG摄取活性在12小时内保持恒定,然后缓慢下降,而喂食细胞的活性则迅速下降。这些发现表明,葡萄糖饥饿通过改变培养的神经元细胞中转运蛋白的净合成速率来调节葡萄糖转运。

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