Kimmich G, Randles J
Am J Physiol. 1980 May;238(5):C177-83. doi: 10.1152/ajpcell.1980.238.5.C177.
Exogenous ATP (1 mM) exerts a dramatic biphasic effect on the accumulation of 100 micro M 3-O-methylglucose by isolated intestinal epithelial cells. The initial effect ensues approximately 15 s after exposure and inhibits 80% of the undirectional sugar influx. Cellular phosphatases totally degrade the added ATP within a period of 20 min leading to a reactivation of transport capability. The cells exposed to ATP ultimately establish a concentration gradient of sugar about twice that observed for control cells. Pyrophosphate (10 mM) delays the degradation of added ATP and prolongs the interval of transport inhibition. The late effect of gradient enhancement is still observed. No other nucleoside triphosphate induces the early inhibition of transport, but ADP is approximately two-thirds as effective as ATP. AMP and other molecules containing the adenine ring system can cause the late effect of gradient enhancement without causing an early transport inhibition. Because rotenone-treated ATP-depleted cells also show an ATP-induced inhibition of sugar influx, it seems likely that the early effect represents a direct modification of carrier capability rather than an effect mediated via an alteration of cellular energetics.
外源性ATP（1毫摩尔）对离体肠上皮细胞积累100微摩尔3 - O - 甲基葡萄糖具有显著的双相效应。最初的效应在暴露后约15秒出现，抑制了80%的单向糖流入。细胞磷酸酶在20分钟内完全降解添加的ATP，导致转运能力重新激活。暴露于ATP的细胞最终建立的糖浓度梯度约为对照细胞的两倍。焦磷酸（10毫摩尔）延迟了添加ATP的降解，并延长了转运抑制的时间间隔。仍可观察到梯度增强的后期效应。没有其他核苷三磷酸能诱导早期的转运抑制，但ADP的效力约为ATP的三分之二。AMP和其他含有腺嘌呤环系统的分子可引起梯度增强的后期效应，而不会引起早期的转运抑制。由于用鱼藤酮处理的ATP耗尽细胞也表现出ATP诱导的糖流入抑制，早期效应似乎可能代表载体能力的直接改变，而不是通过细胞能量学改变介导的效应。
