EFFECTS OF GLUCOSE AND INSULIN ON RENAL ELECTROLYTE TRANSPORT

The effects of hyperglycemia and hyperinsulinemia on renal handling of Na, Ca and phosphate were studied in dogs employing the recollection micropuncture technique. Subthreshold sustained hyperglycemia resulted in an isonatric inhibition of proximal tubular Na, fluid, Ca and phosphate readsorption by 8-14%. Fractional excretion of Na and phosphate, however, fell (P < 0.01) indicating that the increased delivery of these ions was readsorbed in portions of the nephron distal to the site of puncture and in addition net Na and phosphate transport was enhanced resulting in a signficant antinatriuresis and antiphosphaturia. The creation of a steady state plateau of hyperinsulinemia while maintaining the blood glucose concentration at euglycemic levels mimicked the effects of hyperglycemia on proximal tubular transport and fractional excretional excretion of Na and Ca. Tubular fluid to plasma inulin ratio fell, similar to the hyperglycemic studies. The effects of hyperglycemia on renal handling of Na and Ca may be mediated through changes in plasma insulin concentration. In contrast to hyperglycemia, however, hyperinsulinemia caused a signficant fall in tubular fluid to plasma phosphate ratio with enhanced proximal tubular phosphate reabsorption (P < 0.02). This occurred concomitantly with a significant inhibition of proximal tubular Na transport. 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.