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蛋白质合成抑制剂对葡萄糖转运至L6肌细胞的激活作用。

Activation by protein synthesis inhibitors of glucose transport into L6 muscle cells.

作者信息

Hayes N, Biswas C, Strout H V, Berger J

机构信息

Department of Membrane Biochemistry and Biophysics, Merck Research Laboratories, Rahway, NJ 07065.

出版信息

Biochem Biophys Res Commun. 1993 Feb 15;190(3):881-7. doi: 10.1006/bbrc.1993.1131.

Abstract

The effects of protein synthesis inhibitors on glucose transport into L6 myotubes was examined. Similar to the acute effects of insulin, short-term treatment with anisomycin or cycloheximide increased transport 2-fold. Kinetic studies demonstrated that this activation was due to a doubling in the Vmax values. The effects of anisomycin or cycloheximide were not additive to that of insulin. Both protein synthesis inhibitors caused only small increases in GLUT4 expression and negligible effects on GLUT1 expression. Anisomycin, as well as insulin, induced the translocation of both transporters from intracellular vesicles to the plasma membrane through not in quantities sufficient to entirely account for the activation of transport. The results indicate that protein synthesis inhibitors stimulate hexose transport in L6 myotubes by increasing the number of transporters in the plasma membrane and augmenting the intrinsic catalytic activity of the transporters.

摘要

研究了蛋白质合成抑制剂对葡萄糖转运进入L6肌管的影响。与胰岛素的急性作用相似,茴香霉素或环己酰亚胺短期处理使转运增加了2倍。动力学研究表明,这种激活是由于Vmax值加倍。茴香霉素或环己酰亚胺的作用与胰岛素的作用不是相加的。两种蛋白质合成抑制剂仅使GLUT4表达略有增加,对GLUT1表达的影响可忽略不计。茴香霉素以及胰岛素诱导两种转运体从细胞内囊泡转运至质膜,但数量不足以完全解释转运的激活。结果表明,蛋白质合成抑制剂通过增加质膜中转运体的数量并增强转运体的内在催化活性来刺激L6肌管中的己糖转运。

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