Diabetic Natriuresis is Due to the Loss of Insulin Dependent Proximal Tubular Sodium Reabsorption

Abstract

This study tested the role of hypo‐insulinemia in mediating the natriuresis in Type I diabetes. A 6‐day diabetic period was induced using either decreased insulin administration to induce hyperglycemia (D group), or clamped insulin administration (DG group) at the control‐period infusion rate and hyperglycemia was induced by infusing glucose continuously i.v. During diabetes, blood glucose increased from normal to 449±40 mg/dl in the D group, and 470±56 mg/dl in the DG group. Control urinary sodium excretion averaged 71±5 mEq/day and 69±7 in the D and DG groups respectively. Urinary sodium excretion increased during diabetes in the D group averaging 125±24 by day 5 while decreased to 54±9 by day 5 in the DG group. Fractional sodium reabsorption (FNaR) decreased by day 5 in the D group (99.8±0.02 vs. 98.2±0.08%, p<0.05) but tended to increase by day 5 in the DG group. Estimated proximal fractional sodium reabsorption (PFNaR) decreased from control during diabetes in the D group while PFNaR increased during the diabetic period in the DG group. This was corroborated by fractional lithium reabsorption, an indicator of PFNaR, which increased during the diabetic period in the DG group from 73±6% to 89±4 day 2 and 92±1 day 5, p<0.05) These data suggest that the decrease in plasma insulin in Type I diabetes plays a significant role in mediating the diabetic natriuresis by decreasing proximal tubular sodium reabsorption. (HL56259)