The effects of glucose and insulin on renal electrolyte transport.
The effects of glucose and insulin on renal electrolyte transport.
复制标题
葡萄糖和胰岛素对肾电解质转运的影响。
DOI：
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发表时间：
1976
影响因子：
15.9
通讯作者：
Z. Agus
中科院分区：
文献类型：
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作者：
R. DeFronzo;M. Goldberg;Z. Agus
采用回忆微穿刺技术研究了高血糖和高胰岛素血症对狗肾处理钠、钙和磷酸盐的影响。阈下持续高血糖导致近端小管钠、液体、钙和磷酸盐重吸收的等电位抑制8-14%。然而，钠和磷酸盐的部分排泄量下降（P < 0.01），表明这些离子的增加递送在穿刺部位远端的肾元部分被重新吸收，此外，钠和磷酸盐的净运输增强，导致显著的抗尿钠和抗磷尿。在维持血糖水平的同时，高胰岛素血症的稳定平台的建立模拟了高血糖对近端小管运输和钠和钙的部分排泄的影响。管状液与血浆胰岛素比率下降，与高血糖研究相似。这些结果表明，高血糖对肾处理钠和钙的影响可能是通过血浆胰岛素浓度的变化介导的。然而，与高血糖相反，高胰岛素血症导致管状液与血浆磷酸盐比率显著下降，近端管状磷酸盐重吸收增强（P < 0.02）。这与近端小管钠运输的显著抑制同时发生。这些数据表明，胰岛素对近端小管磷酸盐重吸收有直接影响，而当继发高血糖的高胰岛素血症发生时，小管中未重吸收的葡萄糖数量增加，从而掩盖了胰岛素的这种影响。在胰岛素输注期间，磷酸盐的部分排泄量显著下降，但与高血糖研究不同，磷酸盐排泄量的下降完全可以由近端重吸收增强来解释。
The effects of hyperglycemia and hyperinsulinemia on renal handling of sodium, calcium, and phosphate were studied in dogs employing the recollection micropuncture technique. Subthreshold sustained hyperglycemia resulted in an isonatric inhibition of proximal tubular sodium, fluid, calcium, and phosphate reabsorption by 8-14%. Fractional excretion of sodium and phosphate, however, fell (P is less than 0.01) indicating that the increased delivery of these ions was reabsorbed in portions of the nephron distal to the site of puncture and in addition net sodium and phosphate transport was enhanced resulting in a significant antinatriuresis and antiphosphaturia. The creation of a steady state plateau of hyperinsulinemia while maintaining the blood glucose concentration of euglycemic levels mimicked the effects of hyperglycemia on proximal tubular transport and fractional excretion of sodium and calcium. Tubular fluid to plasma insulin ratio fell, similar to the hyperglycemic studies. These results suggest that the effects of hyperglycemia on renal handling of sodium and calcium may be mediated through changes in plasma insulin concentration. In contrast to hyperglycemia, however, hyperinsulinemia cuased a significant fall in tubular fluid to plasma phosphate ratio with enhanced proximal tubular phosphate reabsorption (P is less than 0.02). This occurred concomitantly with a significant inhibition of proximal tubular sodium transport. These data indicate that insulin has a direct effect on proximal tubular phosphate reabsorption, and this effect of insulin is masked by the presence of increased amounts of unreabsorbed glucose in the tubule that ensues when hyperinsulinemia occurs secondary to hyperglycemia. Fractional excretion of phosphate fell significantly during insulin infusion but unlike the hyperglycemic studies, the fall in phosphate excretion could be entirely accounted for by enhanced proximal reabsorption.