Haworth R A, Hunter D R, Berkoff H A
Arch Biochem Biophys. 1985 May 15;239(1):191-9. doi: 10.1016/0003-9861(85)90826-4.
When cells (2.4 mg/ml) in the presence of glucose were exposed to 0.15 microM p-trifluoromethoxyphenylhydrazone (FCCP), the time until 50% of the rod-shaped cells had undergone contracture was more than twice as long for cells without isoproterenol as for cells with isoproterenol. The cause of this large effect was revealed in experiments without glucose where 3-O-methylglucose entry, ATP levels, and cellular configuration were measured simultaneously. It was found that the onset of contracture was almost coincident with the decline in total measured ATP, suggesting that, in any cell, contracture was accompanied by a sudden and total ATP loss. In control cells, FCCP stimulated 3-O-methylglucose entry at or before the time this ATP catastrophe occurred. In cells exposed to isoproterenol, however, the stimulation of 3-O-methylglucose entry by FCCP did not occur until after the ATP catastrophe, and the extent of stimulation was reduced. This suggests that, when glucose was present, the FCCP-induced glucose influx was sufficient to significantly delay the onset of contracture in control cells but not in cells treated with isoproterenol. This conclusion was borne out by the observation that the effect of isoproterenol on contracture could be overcome with insulin.
当存在葡萄糖时，将细胞（2.4毫克/毫升）暴露于0.15微摩尔对三氟甲氧基苯腙（FCCP），对于未用异丙肾上腺素处理的细胞，直至50%的杆状细胞发生挛缩的时间是用异丙肾上腺素处理的细胞的两倍多。在无葡萄糖的实验中揭示了这种显著效应的原因，在该实验中同时测量了3 - O - 甲基葡萄糖的摄取、ATP水平和细胞形态。发现挛缩的开始几乎与总测量ATP的下降同时发生，这表明在任何细胞中，挛缩都伴随着ATP的突然完全丧失。在对照细胞中，FCCP在这种ATP灾难发生时或之前刺激3 - O - 甲基葡萄糖的摄取。然而，在暴露于异丙肾上腺素的细胞中，FCCP对3 - O - 甲基葡萄糖摄取的刺激直到ATP灾难发生后才出现，并且刺激程度降低。这表明，当存在葡萄糖时，FCCP诱导的葡萄糖内流足以显著延迟对照细胞中挛缩的开始，但在用异丙肾上腺素处理的细胞中则不然。这一结论得到了以下观察结果的证实：胰岛素可以克服异丙肾上腺素对挛缩的影响。
