Glucose-dependent respiration in suspensions of rabbit cortical tubules.
The effects of glucose on cellular respiration were examined in suspensions of rabbit cortical tubules. When glucose was removed from the bathing fluid, oxygen consumption (QO2) decreased from 18.6 +/- 0.8 to 15.7 +/- 0.5 nmol O2/mg protein X min (P less than 0.01). The transported but nonmetabolized analogue of glucose, alpha-methyl-D-glucoside (alpha MG), was found to support QO2 to the same extent as glucose. These observations were also evident in the presence of butyrate, a readily oxidized substrate of the renal cortex. Additional studies with nystatin and ouabain indicated that glucose-related changes in QO2 were the result of changes in Na, K-ATPase associated respiration. The effect of glucose was localized to the luminal membrane since phlorizin (10(-5) M), a specific inhibitor of luminal glucose-sodium cotransport, also significantly reduced QO2 by 10 +/- 1%. Phlorizin inhibition of QO2 was also evident in the presence of alpha MG but was abolished when glucose was removed from the bathing medium. Finally, measurement of NADH fluorescence showed that addition of glucose (5 mM) to a tubule suspension causes an oxidation of NAD. These data are all consistent with glucose acting to increase respiration by stimulating sodium entry at the luminal membrane (via glucose-sodium cotransport) followed by increased sodium pump activity and its associated increase in mitochondrial respiration.
D000818:Animals; D002087:Butyrates / Q000378:metabolism; D005260:Female; D005947:Glucose / Q000378:metabolism*; D007684:Kidney Tubules / Q000378:metabolism*; D008757:Methylglucosides / Q000494:pharmacology; D009761:Nystatin / Q000494:pharmacology; D010042:Ouabain / Q000494:pharmacology; D010101:Oxygen Consumption / Q000187:drug effects; D010695:Phlorhizin / Q000494:pharmacology; D011817:Rabbits
D002087:Butyrates; D008757:Methylglucosides; D009761:Nystatin; D010042:Ouabain; D010695:Phlorhizin; D005947:Glucose