Glucose-mediated inhibition of phosphate reabsorption in rat kidney

Clearance, tracer intra-arterial injection, and tracer intratubular microinjection techniques were used on two strains of Wistar rats. In Saclay rats, clearance studies during hyperphosphatemia showed that glucose significantly decreased reabsorption of phosphate; during normal phosphatemia, glucose induced a 25% inhibition both in nondiuretic and in volume-expanded animals; thyroparathyroidectomy did not modify this inhibition. When mannitol was substituted for glucose, no change in phosphate reabsorption was noted. Tracer injection into the renal arteries of [3H]inulin, [14C]glucose, and [32P]-phosphate with or without additional unlabeled glucose or mannitol showed that the presence of glucose significantly increased 14C and 32P urinary recoveries but not mannitol. Intratubular paired microinjections into early proximal tubules of the same tracers with and without glucose showed that addition of sugar also increased the 14C and 32P urinary recoveries. In Munich rats, the effects were much less marked than in Saclay rats. It is concluded that the inhibitory effect of glucose 1) partly results from intrarenal factors, 2) is linked to glucose reabsorption per se but not to a nonspecific osmotic intraluminal effect, 3) is localized on the tubular luminal side, and 4) is subject to strain differences.