ABSTRACT
Several studies on biotin intestinal transport in the hamster have shown a biotin-specific carrier, but there are conflicting reports on whether it is transported actively, or by facilitated diffusion and on its Na+ dependence. We have studied it for the first time using brush-border membrane vesicles (BBMV), with concentrations in a more physiological (nanomolar)range and found an overshoot component, evidencing a carrier-mediated active process, driving the vitamin against a concentration gradient. Uptake was substantially reduced when potassium substituted for sodium. When the vesicles were treated with trypsin, Na+-dependent uptake was markedly reduced and the overshoot phenomenon was abolished, providing additional evidence for the carrier-mediated trasnport. The amount of uptake in a K+ gradient was considered due to passive diffusion and was about 30 percent of that observed in a Na+ gradient. A similar amount was observed when trypsinized vesicle were incubated in this latter gradient. Our results indicate that in the hamster's brush border intestinal epithelium, Na+-dependent active transport is the most important component in the intestinal uptake of biotin at nanomolar concentrations