Seifert S A, Hsiao S C, Murer H, Biber J, Kempson S A
Department of Physiology & Biophysics, Indiana University School of Medicine, Indianapolis 46223, USA.
Cell Biochem Funct. 1997 Mar;15(1):9-14. doi: 10.1002/(SICI)1099-0844(199703)15:1<9::AID-CBF703>3.0.CO;2-K.
Chronic renal adaptation to dietary deprivation of Pi is accompanied by increased Na+/Pi co-transport across the brush border membrane of the renal proximal tubule. The increased activity of this co-transport system depends on de novo protein synthesis and insulin. The present study used normal and diabetic rats to determine if the endosomal pool of Na+/Pi co-transporters was altered by Pi deprivation and the possible role of insulin. In response to 5 days of dietary Pi deprivation there was a significant increase in endosomal Na+/Pi co-transport in control rats but there was no change in diabetic rats. The increase in endosomal Pi uptake was restored in diabetic rats treated with exogenous insulin. Na(+)-independent Pi uptake and proline uptake remained unchanged in all groups. The changes in endosomal Na+/Pi co-transport correlated with the abundance of the specific Na+/Pi co-transporter protein, as determined by Western blots. The pattern of endosomal changes paralleled that observed in brush border membranes. One possibility consistent with these findings is that the endosomal fraction contains newly synthesized Na+/Pi co-transporters targeted for delivery to the apical brush border membrane. Increased synthesis and delivery is required to maintain the adaptation to chronic Pi deprivation.
慢性肾脏对饮食中磷缺乏的适应性变化伴随着肾近端小管刷状缘膜上钠/磷共转运的增加。这种共转运系统活性的增加依赖于从头合成蛋白质和胰岛素。本研究使用正常和糖尿病大鼠来确定钠/磷共转运体的内体池是否因磷缺乏而改变以及胰岛素可能发挥的作用。在5天的饮食磷缺乏后，对照大鼠的内体钠/磷共转运显著增加，而糖尿病大鼠则无变化。用外源性胰岛素治疗的糖尿病大鼠内体磷摄取的增加得以恢复。所有组中不依赖钠的磷摄取和脯氨酸摄取均保持不变。通过蛋白质免疫印迹法测定，内体钠/磷共转运的变化与特定钠/磷共转运体蛋白的丰度相关。内体变化模式与在刷状缘膜中观察到的一致。与这些发现一致的一种可能性是，内体部分包含新合成的、靶向顶端刷状缘膜的钠/磷共转运体。需要增加合成和转运来维持对慢性磷缺乏的适应性。
