Renal tubular reabsorption of 1,5-anhydro-D-glucitol and D-mannose in vivo in the rat.

1,5-Anhydro-D-glucitol (AG) is efficiently reabsorbed in renal tubuli by a mechanism that is saturated at high AG concentrations. To gain insight into the stereospecific requirements of the mechanism, we employed an in vivo loading test technique in which rats were injected with anhydrosugars and aldohexoses in doses that led to excretion of the sugar injected, thus saturating tubular reabsorption. Administration of AG elicited an increase in the excretion of D-mannose (P less than 0.0005), while D-mannose caused AG to appear in urine. Administration of 1,5-anhydro-D-mannitol led to increased excretion of D-mannose (P less than 0.0005) and the appearance of AG in urine. The effects of 1,5-anhydro-D-mannitol on the excretion of D-mannose and AG, and the effect of D-mannose on AG were dependent on the dose. Myoinositiol, mannitol and C-3-C-6 epimers of AG did not interfere with the reabsorption. The mechanism was highly phlorizin-sensitive. Repeated administration of 1,5-anhydro-D-mannitol rapidly depleted the rat organism from mobilizable AG. The AG space calculated (53% of body weight) suggested the presence of considerable cellular stores of AG. D-Mannose and AG are regular components of the plasma monosaccharide profile. The data suggest that the two sugars are reabsorbed in renal tubuli by a common mechanism, which is distinct from the main D-glucose reabsorption system. The presence of a glucose-type C-3-C-6 and pyranose structure is required for a sugar to be transported by the system.(ABSTRACT TRUNCATED AT 250 WORDS)