[A study on the mechanism of bile acid transport in the human placenta (the passive transport system of taurocholate across microvillous membrane)].
The uptake of taurocholate into microvillous membrane vesicles prepared from human normal full term placenta was studied using a rapid filtration technique. The taurocholate uptake into microvillous membrane vesicles was sensitive to extravesicular osmolarity, and preincubation with the taurocholate increased the uptake of taurocholate into the vesicles. These findings indicate that the uptake of taurocholate by microvillous membrane vesicles represents transport into vesicles. The uptake of taurocholate into vesicles was not dependent on sodium electrochemical gradient (extravesicular greater than intravesicular). But, this uptake was markedly increased when the intravesicular space was rendered electrically more positive by the use of lowly permeant anions or K+ diffusion potentials via valinomycin. These findings indicated that taurocholate was transported into microvillous membrane vesicles as anion. Cholic acid inhibited the uptake of taurocholate into vesicles, but taurine didn't inhibit this uptake. The initial rate of taurocholate transport exhibited saturation kinetics with respect to the taurocholate concentration; an apparent Km of 67 microM and Vmax of 0.30n mol/mg protein/20 sec were calculated. These results indicated that placental taurocholate transport was not active but passive (facilitated diffusion), and taurocholate was transported from fetus to mother via placenta because the blood concentration was higher in fetus than mother.
D001647:Bile Acids and Salts / Q000378:metabolism*; D001692:Biological Transport; D002824:Chorionic Villi / Q000378:metabolism*; D005260:Female; D006801:Humans; D008431:Maternal-Fetal Exchange; D008564:Membrane Potentials; D009994:Osmolar Concentration; D011247:Pregnancy; D013656:Taurocholic Acid / Q000378:metabolism*; D013696:Temperature
D001647:Bile Acids and Salts; D013656:Taurocholic Acid