Endocrine Metabolism V: Reproductive System
F I G U R E 3 4 - 6
Placental synthesis of estrogens. The placenta lacks the key enzyme necessary for formation of estrogens from
cholesterol (CYP 17) and relies on androgenic precursors from the maternal and fetal compartments. The major
androgen used comes from the fetal zone of the fetal adrenal; this is DHEAS, which is also taken up and metabolized by
fetal liver into 16«-hydroxy-DHEAS. The placenta converts DHEAS into estrone (Ej) and estradiol (E
) and processes
16a-hydroxy-DHEAS into estriol (E
). Estrogens enter the maternal circulation and appear in maternal urine as
conjugated estrogens.
resistance that benefits the fetus because it increases the
availability of maternal glucose for fetal consumption. In
the mother, hPL also exerts a prolactin-like effect and, with
estrogen and progesterone, promotes ductal and alveolar
growth in the mammary gland during the third trimester
of pregnancy. However, prolactin is believed to be more
important than hPL in this effect.
Decidual Prolactin
The maternal placenta (decidua basalis) is believed to
produce a hormone that is biologically and antigenically
similar to pituitary prolactin. If released into the amni-
otic fluid during the third trimester of pregnancy, it may
maintain amniotic fluid volume and osmolality.
The maternal placenta also produces relaxin, a hormone
produced by the ovaries. Relaxin causes relaxation of the
cervix during parturition.
Precisely what initiates parturition in humans is not
known. Unlike the situation in sheep, there is no induction
of placental CYP 17 by fetal cortisol to bring about a re-
duction in progesterone production and, hence, parturi-
tion. During late gestation, rising levels of estrogen are
thought to increase the synthesis of oxytocin in hypothala-
mic magnocellular neurons to induce oxytocin receptors in
the myometrium and to increase myométrial contractility
by lowering the membrane potential. During this period,
relaxin from the decidua softens the cervix for impending
delivery. At term an unidentified triggering factor in fetal
urine stimulates uterine production of PGE| and PGF2„,
which lead to myométrial contraction, mainly in the fun-
dus, and encourages movement of the infant through the
cervical canal. Dilation of the cervix by the infant stimu-
lates the release of oxytocin by neuroendocrine reflex, fur-
ther stimulating uterine contractions, which in turn causes
more cervical stretching and a positive feedback to oxy-
tocin release, until delivery is complete.
During midpregnancy and late pregnancy, growth and dif-
ferentiation of mammary glands are promoted by the com-
bined effects of estrogen, progesterone, and prolactin (or
hPL). In the presence of prolactin or hPL, estrogen stimu-
lates branching of the mammary ducts and increases their
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