Identification of a sorbitol permease in human erythrocytes.
Level 5 - mechanism / opinion, no new human data
In vitro laboratory study using human erythrocytes (bench research).
PubMed 8141248 · doi:10.1152/ajpcell.1994.266.2.C343
What was done
Researchers investigated sorbitol transport in human red blood cells by measuring D-[14C]sorbitol influx under varying substrate concentrations (0.05 to 100 mM), temperatures (10–50 °C), osmolar/volume conditions, sodium presence, and in the presence of various transport inhibitors and competing sugars (glucose, fructose, mannitol, myo-inositol, and gluconate).
What was found
Sorbitol influx at 37 °C was linear across 0.05–100 mM sorbitol. The activation energy was 10.0 kcal/mol with a Q10 of 1.8 between 10 °C and 50 °C. Classic glucose transport inhibitors had minimal or no effect: 1 mM phloridzin had no effect, whereas 10 µM cytochalasin B and 250 µM phloretin reduced influx by approximately 35%. In contrast, 0.5 mM p-chloromercuribenzoic acid increased influx twofold, an effect reversed by 2 mM dithiothreitol. Influx was sodium-independent, unaffected by cell volume changes, and not inhibited by a 4- to 5-fold molar excess of glucose, fructose, mannitol, myo-inositol, or gluconate.
Why it matters
These findings demonstrate that human erythrocytes express a specific, mediated sorbitol permease rather than relying on simple aqueous pore diffusion or standard GLUT-mediated pathways, clarifying potential mechanisms of cellular polyol handling relevant to diabetic osmotic stress.
Limits
The abstract does not disclose the number of biological donors or experimental replicates. As an in vitro study on isolated red blood cells, it does not assess physiological flux in vivo or evaluate whether transport characteristics are altered in patients with diabetes.
Cited by
- context Glucose-derived polyols such as sorbitol and mannitol cannot passively cross cell membranes.