The specificity of the active sugar transport in kidney cortex cells

Abstract

The transport of some monosaccharides into renal tubular cells was investigated using slices of rabbit kidney cortex: 1. An active, Na+-dependent and phlorrhizin-sensitive cellular accumulation of β-methyl-d-glucoside, d-glucosamine and d-galactosamine was demonstrated. d-Mannitol, d-glucose, N-acetyl-d-glucosamine, 3-deoxy-d-glucose, d-allose, d-ribose and 2,6-dideoxy-d-altrose were not actively accumulated against their concentration gradients. 2-Deoxy-d-allose, 2-deoxy-d-ribose and possibly 2-deoxy-d-xylose were transported against a small concentration gradient by a Na+-independent mechanism. A comparison of the transport properties of 26 monosaccharides indicates the following structural requirements for active transport: a hemiacetal group, C-3-OH (in a configuration identical with that of d-glucose) and C-6-OH. The Na+ requirement for active transport is related to the presence of a hydrophilic (-OH or -NH2) group on C-2. 2. The apparent kinetic parameters, Km and vmax, are given for the active transport of a α-methyl-d-glucoside, d-galactose, 2-deoxy-d-glucose and 2-deoxy-d-galactose into renal tubular cells. The values of the apparent transport Km for these sugars varied only slightly between 0.79 ± 0.07 for d-galactose to 3.0 ± 0.11 for 2-deoxy-d-galactose; rather wide variations of vmax were found (12 μmoles per g cell water per h for 2-deoxy-d-glucose to 62 ± 4.7 for α-methyl-d-glucoside). 3. The competition for transport between a variety of monosaccharides was investigated: the found Ki was within the range of independently determined Km for the inhibition of galactose of 2-deoxy-d-galactose and 2-deoxy-d-glucose transport. However, the Ki for the inhibition of d-galactose transport by 2-deoxy-d-galactose was one order of magnitude higher than the Km of the latter sugar. Similarly, no agreement between the respective Ki and Km was found for the competitive inhibition between α-methyl-d-glucoside and galactose. d-Glucose, which competitively inhibited the transport of 2-deoxy-d-glucose, had practically no effect on the transport of 2-deoxy-d-galactose even at a molar ratio of 1:50. 4. These kinetic data indicate the existence of several pathways for the active sugar transport into renal tubular cells. 5. A correlation between the reabsorption of sugars in the kidney tubule (in vivo) and their active cellular accumulation (in vitro) is demonstrated.