Tillotson L G, Yamada K, Isselbacher K J
Fed Proc. 1984 May 15;43(8):2262-4.
Chicken embryo fibroblasts (CEF) when exposed to glucose-deficient culture medium developed 4- to 10-fold enhanced hexose transport activity within a few hours. Plasma membrane fractions prepared from starved and fed CEF revealed that starved cell membranes had a threefold greater glucose transport activity and [3H]cytochalasin B binding. The close correlation between transport activities of whole CEF and plasma membrane fractions indicates that hexose transport regulation during starvation results primarily in an increase in the number of functioning hexose transporters. The effect of protein synthesis inhibition on the overall process was studied with emetine, an inhibitor of translational elongation. Glucose-fed CEF treated with low concentrations of emetine (0.1 microM) showed a loss of transport greater than 65% within 4 h, but with higher concentrations of emetine (10 microM) there was no significant effect. Emetine treatment (0.1-10 microM) of CEF undergoing starvation virtually blocked any enhancement in transport whereas treatment of starved CEF led to only a slight loss of transport. Starved CEF refed with glucose had a decline of transport that was potentiated by low concentrations of emetine (0.1 microM); however, under these conditions high concentrations of emetine (10 microM) largely prevented loss of transport. Thus hexose transport regulation of CEF seems to reflect a balance between transporter synthesis and turnover. Transporter synthesis appears more sensitive to inhibition by emetine than turnover, whereas with hexose starvation there appears to be a decline in the activity of the transporter turnover process.
鸡胚成纤维细胞(CEF)暴露于缺乏葡萄糖的培养基中时,在数小时内己糖转运活性增强了4至10倍。从饥饿和喂食的CEF制备的质膜部分显示,饥饿细胞膜的葡萄糖转运活性和[3H]细胞松弛素B结合量增加了三倍。整个CEF和质膜部分的转运活性之间的密切相关性表明,饥饿期间己糖转运调节主要导致功能性己糖转运蛋白数量增加。用翻译延伸抑制剂放线菌酮研究了蛋白质合成抑制对整个过程的影响。用低浓度放线菌酮(0.1 microM)处理的葡萄糖喂养的CEF在4小时内转运损失大于65%,但用高浓度放线菌酮(10 microM)处理则无显著影响。用放线菌酮(0.1 - 10 microM)处理正在饥饿的CEF实际上阻止了转运的任何增强,而处理饥饿的CEF仅导致轻微的转运损失。用葡萄糖重新喂养饥饿的CEF会导致转运下降,低浓度放线菌酮(0.1 microM)会加剧这种下降;然而,在这些条件下,高浓度放线菌酮(10 microM)在很大程度上阻止了转运损失。因此,CEF的己糖转运调节似乎反映了转运蛋白合成与周转之间的平衡。转运蛋白合成似乎比周转对放线菌酮抑制更敏感,而在己糖饥饿时,转运蛋白周转过程的活性似乎下降。