Glucose-dependent respiration in suspensions of rabbit cortical tubules

Summary 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·min (P<0.01). The transported but nonmetabolized analogue of glucose, -methyl-d-glucoside (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 liminalk glucose-sodium cotransport, also significantly reduced QO₂ by 10±1%. Phlorizin inhibition of QO₂ was also evident in the presence of MG but was abolished when glucose was removed from the bathing medium. Finally, measurement of NADH fluorescence showed that addition of glucose (5mm) 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.