16-Dehydropregnenolone 3-Sulfate, Its Source and Metabolism in the Feto-Placental Unit

抄録

We have investigated the serum concentration of 16-dehydropregnenolone (3β-hydroxy-5, 16-pregnadien-20-one) 3-sulfate (16-DHPS) in the umbilical artery (U.A.), umbilical vein (U.V.) and maternal vein (M.V.) to discover the origin of 16-DHPS. Although there was no significant difference between the levels of 16-DHPS in U.A. (18±15ng/ml, mean±S.D., n=28) and U.V. (10±9ng/ml, n=28), these values were significantly higher (U.A., p<0.001; U.V., p<0.001) than that in M.V. (2±3ng/ml, n=28). These levels in the U.A. and U.V. did not fall in inafnts (30±18ng/ml, n=7) during the early neonatal period (2-7 d after birth). A significant correlation between the serum levels of 16-DHPS and 16-hydroxypregnenolone (3β, 16α-dihydroxy-5-pregnen-20-one) 3-sulfate (16-OH-PregS), which may be the precursor steroid for 16-DHPS, was observed in the U.A. (r=0.630, n=28, p<0.001), but not in the U.V. Moreover, this significant correlation persisted during the early neonatal period (p<0.05, r=0.842, n=7), although the neonate had been separated from the maternal milieu. These results suggest that 16-DHPS originates in the fetus.To confirm the metabolic pathway of 16-DHPS (i.e. pregnenolone (3β-hydroxy-5-pregnen-20-one) 3-sulfate (PregS)→16-OH-PregS→16-DHPS), we investigated the correlation between the serum concentrations of the precursor steroid and the product in both the U.A. and U.V. A significant correlation was obtained between the serum concentrations of PregS and 16-OH-PregS both in the U.A. (p<0.001, r=0.563, n=28) and U.V. (p<0.05, r=0.476, n=27). As described above, the serum levels of 16-DHPS and 16-OH-PregS only correlated significantly in the U.A. These findings support the existence of the pathway, PregS→16-OH-PregS→16-DHPS, in the fetus.