Insulin stimulates the Na+,K(+)-ATPase and the Na+/K+/Cl- cotransporter of human fibroblasts.
Insulin stimulates the Na+,K(+)-ATPase and the Na+/K+/Cl- cotransporter of human fibroblasts.
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胰岛素刺激人成纤维细胞的 Na ,K( )-ATP 酶和 Na /K /Cl- 协同转运蛋白。
DOI：
10.1016/0005-2736(96)00004-1
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
Longo,N
中科院分区：
文献类型：
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作者：
Longo,N
胰岛素对K+(Rb+)转运的调节在培养的人成纤维细胞中使用非放射性方法进行了研究，该方法可以同时测定细胞内其他一价阳离子的浓度。胰岛素通过Na+、K+- atp酶和Na+/K+/Cl -共转运蛋白刺激人成纤维细胞中的Rb+内流。胰岛素刺激非常迅速，在10分钟内达到最大效果。胰岛素通过Na+、K+- atp酶和Na+/K+/Cl -共转运体对Rb+摄取的刺激是剂量依赖性的，在激素的2-3 nM时有一半的最大刺激。胰岛素增加了两种转运蛋白的vmax，但对Km的影响很小。在其他细胞中，胰岛素通过Na+/H+交换器增加Na+的可用性，从而刺激Na+，K+泵。在人成纤维细胞中，胰岛素对Na+，K+- atp酶的刺激发生在Na+/H+交换剂的抑制剂乙基异丙基酰胺存在的情况下，而细胞内[Na+]没有持续的变化。相比之下，胰岛素对Na+，K+- atp酶的作用被蛋白激酶抑制剂staurosporine和genistein破坏。这些结果表明，在人成纤维细胞中，胰岛素刺激Na+，K+- atp酶和Na+/K+/Cl -共转运体，Na+，K+- atp酶的刺激发生在细胞内[Na+]没有变化的情况下，蛋白激酶活性对胰岛素的作用至关重要。
Insulin regulation of K+(Rb+) transport was investigated in cultured human fibroblasts using a non-radioactive method which allows the simultaneous determination of the intracellular concentration of other monovalent cations. Insulin stimulated Rb+influx through the Na+,K+-ATPase and the Na+/K+/Cl−cotransporter in human fibroblasts. Insulin stimulation was very rapid and maximal effect was observed within 10 min. Insulin stimulation of Rb+uptake via the Na+,K+-ATPase and the Na+/K+/Cl−cotransporter was dose-dependent, with half-maximal stimulation at 2–3 nM of hormone. Insulin increased the Vmaxof both transporters involved, affecting only minimally their Km. In other cells, insulin stimulates the Na+,K+-pump by increasing Na+availability through the Na+/H+exchanger. In human fibroblasts, insulin stimulation of Na+,K+-ATPase occurred in the presence of ethyl-isopropyl amiloride, an inhibitor of the Na+/H+exchanger, and without sustained changes in intracellular [Na+]. By contrast, insulin action on Na+,K+-ATPase was impaired by the protein kinase inhibitors staurosporine and genistein. These results indicate that, in human fibroblasts, insulin stimulates both the Na+,K+-ATPase and the Na+/K+/Cl−cotransporter, that stimulation of the Na+,K+-ATPase occurs in the absence of changes in intracellular [Na+], and that protein kinase activity is essential for this insulin action.