Abstract
AbstractSerum taurine concentration in the human fetus (umbilical blood) and neonate was measured from the 24th to 40th week of pregnancy. The concentration was considerably higher than in maternal serum with a peak at the 24th week of pregnancy and then a gradual decrease until it approached the adult level on the 9th day after birth.To clarify the underlying mechanism of the human findings, the distribution of 14C‐taurine was investigated after intravenous injection to maternal rats on the 20th day of pregnancy. The taurine administered to the maternal side became concentrated in the placenta and reached the fetus. It was confirmed that taurine accumulated in the human placenta was present in a higher concentration than any other free animo acid.Placental transport of taurine was studied in isolated brush border microvillous plasma membrane vesicles by a rapid filtration technique. The membrane vesicles exhibited uptake of H3‐labeled traurine into an osmotically reactive intravesicular space. Taurine uptake by vesicles was stimulated specifically by an inward sodium gradient, and replacement of NaCl in the transport medium by KCl, LiCl or choline chloride had no effect on the transport activity of the vesicles. Taurine transport was inhibited competivively by the presence of β‐alanine and GABA. The initial rate of transport followed saturation kinetics with respect to taurine concentration: an apparent Km of 0.22 mM and Vmax of 67 pmol/mg protein were calculated in 20 seconds. These results indicate that transport of taurine across the placental brush border membrane is sodium‐dependent and carrier‐mediated.The taurine transport system in human fetal small intestine, especially in the jejunum, is a passive transport system quite unlike that of other amino acids.Reabsorption of taurine through the proximal convoluted tubule is by active transport which depends on sodium. This transport system is developed from the 24th to the 32nd gestational week.
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