RT Journal Article
SR Electronic
T1 Increased Renal Metabolism in Diabetes: Mechanism and Functional Implications
JF Diabetes
JO Diabetes
FD American Diabetes Association
SP 629
OP 633
DO 10.2337/diab.43.5.629
VO 43
IS 5
A1 Körner, Anna
A1 Eklöf, Ann-Christine
A1 Celsi, Gianni
A1 Aperia, Anita
YR 1994
UL http://diabetes.diabetesjournals.org/content/43/5/629.abstract
AB The coupling between the Na+/glucose cotransporter and Na+-K+-ATPase (NKA) described for epithelial cells (1) prompted us to study in rats with streptozocin-induced diabetes the effect of increased tubular glucose load on tubular Na+ reabsorption, NKA-dependent O2 consumption (QO2), and NKA activity. Filtered glucose is mainly reabsorbed in the proximal tubuli via the phlorizin-sensitive Na+/glucose cotransporter. In this study, the diabetic rats had a significantly higher renal blood flow (RBF), glomerular filtration rate (GFR), and Na+ reabsorption than the control rats. Total renal QO2 as well as QO2 in cortical tissue, which consists mainly of proximal tubular cells, was significantly higher in diabetic than in control rats. The increase in tissue QO2 was entirely caused by increased NKA-dependent QO2. NKA activity, measured as rate of ATP hydrolysis, was increased in cortical tubular but not glomerular tissue from diabetic rats. Phlorizin treatment abolished the increase in NKA activity, Na+ reabsorption, and QO2, as well as the increase in RBF and GFR in diabetic rats. We conclude that diabetes is associated with increased renal O2 metabolism secondary to the increase in coupled Na+ reabsorption via the Na+/glucose cotransporter and NKA. The increased oxygen consumption might contribute to the hyperperfusion and hyperfiltration in the diabetic kidney.