Beck J C, Sacktor B
J Biol Chem. 1978 Oct 25;253(20):7158-62.
When D-glucose was added to a suspension of renal brush border membrane vesicles equilibrated in a Na+-containing medium, there was a rapid transient increase in the fluorescence of the probe, 3,3'-dipropyl thiodicarbocyanine iodide (DiS-C3-(5)). This sugar-induced response was stereospecific for the D isomer, dependent on Na+, inhibited by phlorizin, and blocked by ionophores, valinomycin plus nigericin, which dissipate ionic gradients. The enhancement in fluorescence suggests the entrance into the vesicle of Na+, cotransported with the sugar. This would lead to the interior of the membrane vesicle becoming more positive, resulting in depolarization of the membrane potential. That the sugar induced the transport of Na+ was confirmed by direct measurement of 22Na+ uptake. Thus, the Na+-sugar co-transport system provides a mechanism for D-glucose to stimulate the flux of Na+ as well as for the Na+ electrochemical gradient to enhance the transport of D-glucose.
当将D-葡萄糖添加到在含钠介质中平衡的肾刷状缘膜囊泡悬浮液中时,探针3,3'-二丙基硫代二羰花青碘化物(DiS-C3-(5))的荧光会迅速出现短暂增强。这种糖诱导的反应对D-异构体具有立体特异性,依赖于钠离子,被根皮苷抑制,并被能消除离子梯度的离子载体缬氨霉素和尼日利亚菌素阻断。荧光增强表明钠离子与糖共转运进入囊泡。这将导致膜囊泡内部变得更正,从而使膜电位去极化。通过直接测量22Na+摄取证实了糖诱导了钠离子的转运。因此,钠-糖共转运系统为D-葡萄糖刺激钠离子通量以及钠离子电化学梯度增强D-葡萄糖转运提供了一种机制。