Abstract
Taurine is a β-amino compound with a large number of known and putative functions. The specific mechanism by which dietary taurine is absorbed by the intestine is not known. The intestinal BBM associated taurine transport mechanism was therefore examined using rat jejunal vesicles prepared by Mg++ precipitation. Osmotic sensitivity analysis showed that less than 5% of 3H -taurine uptake (pmoles/mg vesicle protein) resulted from binding. The initial rate (10s) of 10 μM uptake was stimulated 3.5 fold by an inwardly directed Na+-gradient when compared with a K+-gradient. The Cl− salt of Na+ supported uptake to a significantly greater degree than did more (SCN−) or less (SO4=) permeant salts. Na+-stimulated uptake at 1 min. achieved a value 2.5 times greater than equilibrium (“overshoot”). When Na+-stimulated 10s uptake was examined over a range of concentrations (10-1000 μM), the relationship was curvilinear. Half-maximal uptake occurred at 25±9 μM taurine (Km). Vmax was 24±2 pmoles/mg protein. An inside negative, valinomycin induced, K+-diffusion potential stimulated 10s uptake when compared to voltage clamped conditions (4.9 vs 2.6 pmoles/mg protein; p<.05). Incubation with a structural analog, hypotaurine, reduced 10s taurine uptake by 89%.
These data support the existence of a rat jejunal BBM associated taurine transport mechanism which is Na+-gradient stimulated and modified by external Cl−, saturable, electrogenic, and inhibited by a structural analog. These features are similar to those described for the renal BBM taurine transporter.
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Barnard, J., Thaxter, S. & Ghishan, F. TAURINE TRANSPORT BY RAT JEJUNAL BRUSH BORDER MEMBRANE (BBM) VASICLES. Pediatr Res 21 (Suppl 4), 263 (1987). https://doi.org/10.1203/00006450-198704010-00578
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DOI: https://doi.org/10.1203/00006450-198704010-00578