SEX-DIFFERENCES IN UMBILICAL-CORD SERUM LEVELS OF INHIBIN, TESTOSTERONE, ESTRADIOL, DEHYDROEPIANDROSTERONE-SULFATE, AND SEX HORMONE-BINDINGGLOBULIN IN HUMAN TERM NEONATES
D. Simmons et al., SEX-DIFFERENCES IN UMBILICAL-CORD SERUM LEVELS OF INHIBIN, TESTOSTERONE, ESTRADIOL, DEHYDROEPIANDROSTERONE-SULFATE, AND SEX HORMONE-BINDINGGLOBULIN IN HUMAN TERM NEONATES, Biology of the neonate, 65(5), 1994, pp. 287-294
The contribution of the fetus to inhibin production in human pregnancy
is unclear. Previous studies have reported inhibin concentrations in
cord blood but on limited sample numbers. The present study is a more
extensive examination of sex differences in immunoreactive inhibin and
steroidal hormones in term umbilical cord blood. Venous serum concent
rations of inhibin were found to be significantly higher in males (mea
n +/- SD 2,168 +/- 914 pg/ml, n = 62) than in females (1,761 +/- 951 p
g/ml, n = 63) (p < 0.01). Male concentrations of total testosterone (p
< 0.005), free testosterone (p < 0.005), and estradiol (p < 0.05) wer
e also significantly higher. The concentration of dehydroepiandrostero
ne sulphate (DHEAS) and the sex hormone-binding globulin (SHBG) capaci
ty were similar in males and females. Multivariate regression analysis
showed that the inhibin concentration in males correlated with the te
stosterone concentration and in females it correlated not only with te
stosterone concentration but also with gestational age at delivery and
SHBG capacity (all p < 0.001). Inhibin concentrations in cord arteria
l serum in a subgroup of 24 males and 31 females were higher than in t
he venous serum in both sexes but the differences were not statistical
ly significant. Concentrations of DHEAS determined in 22 female cord a
rterial blood samples(6.0 +/- 2.5 mu mol/l) were significantly higher
than the venous concentrations(5.2 +/- 1.8 mu mol/l) (p < 0.05). Inhib
in did not correlate with DHEAS either in their arterial serum concent
rations or in the arteriovenous concentration differences. The finding
s of this study are consistent with the placenta being the principal s
ource of inhibin circulating in the human fetus in late pregnancy. Fur
ther, they suggest that there are minor sex differences in placental m
etabolism of inhibin and the steroidal sex hormones.