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  • Title: Hepatic taurine transport: a Na+-dependent carrier on the basolateral plasma membrane.
    Author: Bucuvalas JC, Goodrich AL, Suchy FJ.
    Journal: Am J Physiol; 1987 Sep; 253(3 Pt 1):G351-8. PubMed ID: 3631271.
    Abstract:
    Highly purified rat basolateral liver plasma membrane vesicles were used to examine the mechanism and the driving forces for hepatic uptake of the beta-amino acid, taurine. An inwardly directed 100 mM NaCl gradient stimulated the initial rate of taurine uptake and energized a transient twofold accumulation of taurine above equilibrium ("overshoot"). In contrast, uptake was slower and no overshoot was detected in the presence of a KCl gradient. A negative intravesicular electrical potential generated by the presence of permeant anions or an outwardly directed K+ gradient with valinomycin increased Na+-stimulated taurine uptake. External Cl- stimulated Na+-dependent taurine uptake independent of effects on the transmembrane electrical potential difference. Na+-dependent taurine uptake showed a sigmoidal dependence on extravesicular Na+ concentration, suggesting multiple Na+ ions are involved in the translocation of each taurine molecule. Na+-dependent taurine uptake demonstrated Michaelis-Menten kinetics with a maximum velocity of 0.537 nmol.mg protein-1.min-1 and an apparent Km of 174 microM. [3H]taurine uptake was inhibited by the presence of excess unlabeled taurine, beta-alanine, or hypotaurine but not by L-glutamine or L-alanine. In summary, using basolateral liver plasma membrane vesicles, we have shown that hepatic uptake of taurine occurs by a carrier-mediated, secondary active transport process specific for beta-amino acids. Uptake is electrogenic, stimulated by external Cl-, and requires multiple Na+ ions for the translocation of each taurine molecule.
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