Abstract. Metabolic and renal clearance techniques were used to examine kidney function in conscious and anesthetised streptozotocin diabetic rats. All diabetics showed an enhanced calcium and magnesium excretion compared to controls. However, the renal handling of these ions in relation to other electrolytes varied with different experiments. In non-infused conscious rats, the excretion of all ions was higher in diabetics, but the increased output of Ca2+ and Mg2+ was far greater than that of other electrolytes. In infused anesthetised diabetics only the outputs of Ca2+ and Mg2+ were significantly raised. This resulted from a significant reduction in the tubular reabsorption of both ions (% Ca2+ reabsorption: Controls 97.0±0.5; Diabetics 86.1±2.1; p<0.001). Insulin treatment reversed these changes. Major differences therefore exist in the renal handling of Ca2+ and Mg2+ in control and diabetic kidneys. Such differences do not simply parallel changes in the handling of other ions, and thus represent specific Ca2+ and Mg2+ lesions. Anesthetised infused diabetic rats also showed a reduced glomerular filtration rate and urine output compared to controls. Such differences may relate to an altered fluid balance in the two groups, different responses to surgery and anesthesia, or the degree of hyperglycemia in diabetic animals.
Metabolic and isotopic dilution techniques were used to investigate fluid balance and fluid volumes in rats made diabetic with streptozotocin before and after infusion. Uninfused diabetic rats had significantly (P less than 0.01) lower total body water than controls (57.7 +/- 2.2 vs 65.7 +/- 1.4% (S.E.M.) fat free mass). This was due exclusively to a significantly (P less than 0.001) reduced intracellular fluid volume (38.2 +/- 1.5 vs 45.4 +/- 1.4% fat free mass). Metabolic studies over the preceding 2 weeks showed that the fluid deficit in the diabetic group had resulted from a failure of the rats to increase their fluid intake to the same extent as their combined fluid losses. A 4-h saline infusion halved the fluid deficit in diabetic animals. The retained fluid was used to restore intracellular fluid volume which became comparable in diabetic and control rats (47.2 +/- 2.0 vs 46.4 +/- 1.0% fat free mass). The retention of infusate by diabetic animals to counteract their intracellular dehydration may partly explain the reduced urine output reported elsewhere in infused anaesthetized diabetic rats.
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