Effect of glucose on renal excretion of electrolytes in the rat.

Abstract

Glucose ingestion or infusion increases calcium and magnesium excretion in the human. To assess the role of renal tubular glucose reabsorption and of the parathyroid glands in this phenomenon, we performed standard two-phase clearance experiments in fed, volume-expanded male Sprague-Dawley rats. When compared with a group of animals receiving only 0.9% NaCl (group I), animals infused with glucose (group II) excreted significantly more calcium at any given level of sodium excretion (delta FECa, 1.95 +/- 0.24 vs. 0.69 +/- 0.18, P < 0.001). Normoglycemic hyperinsulinemia (group III) did not reproduce this increase in calcium excretion. In the group given phloridzin during sustained hyperglycemia (group IV), calcium excretion was well below that of control animals at any given level of sodium excretion. The glycosuric-hyperglycemia group (group V) used to assess the effect of glycosuria seen in group IV responded with a striking calciuria (delta FECa, 3.31 +/- 0.43, P < 0.001, compared with group IV). TPTX animals responded to glucose in the same way as intact animals (delta FECa, 4.8 +/- 0.5 vs. 2.18 +/- 0.3 in TPTX saline controls, P < 0.001). Magnesium excretion in all groups followed the same pattern as calcium. We conclude that renal tubular glucose reabsorption is essential for glucose to augment calcium and magnesium excretion. The presence of the parathyroid glands was not required for this phenomenon to occur.