The mechanism of phloridzin glucosuria

Abstract

Phloridzin at a conc. of 0.001 M inhibits glucose utilization and lactic acid formation by minced kidney cortex. This inhibition is dependent upon the presence of both O2 and inorganic phosphate. Oxidation of pyruvic and citric acids, but not of succinate, is inhibited by concs. of phloridzin as low as 0.0002 M. The phosphorylation of crea-tine is inhibited by M/4000 phloridzin. The inhibition is abolished by M/100 succinate, but not by M/800 succinate which stimulates the phosphorylation in the absence of phloridzin. Phloridzin given in vivo depresses creatine phosphorylation in minced kidney. The results are explained by the assumption that phloridzin acts primarily on dehydro-genase systems that are coupled with phosphorylation. The bearing of these results on the question of the mechanism of phloridzin glucosuria is discussed.