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E. MUÑOZ Y M.ª E. LÓPEZ-OLIVA AN. R. ACAD. NAC. FARM.

clínico de mutantes que eliminan la contribución de parte del potencial hormonal
del sistema GH/PRL así como de un mutante antagonista de GH, que suprime la
redundancia a nivel receptor y origina un profundo retardo del crecimiento intrau-
terino, sugiere que sería la acción concatenada de estas hormonas, actuando sobre
los receptores somatógeno y lactógeno fetales, los que mediante la estimulación de
la producción de IGF-I determinaría el crecimiento fetal. Ello implica, que la
sensibilidad tisular a la GH podría iniciarse a partir del segundo tercio de la
gestación, momento en que el eje somatotrópico sería activo sobre el crecimiento
fetal.

Palabras clave: Regulación.—GH/Prolactina.—Crecimiento prenatal.

SUMMARY

GH/Prolactine system and prenatal growth

For many years it was believed that the growth hormone (GH) axis does not
play a role in growth before birth or during the first year after birth. More recently,
studies of genetic disorders of growth and the elucidation of the tissue-specific
profile of expression of the prolactin (PRLR) and growth hormone (GHR) recep-
tors during embryonic and fetal development in a range of species has provided a
new impetus for the delineation of the specific roles of the hormone ligands (GH/
Prolactin system) for these receptors in development. There are both maternal and
fetal contributions to the GH/Prolactin system during fetal life: has been well
established that placental hormones (GH and placental lactogen (LP)) are secreted
into the maternal circulation and that the fetal pituitary gland in many species
secretes PRL and GH in fetal circulation, but the physiological roles and/or target
sites of action for these hormones in fetal life have remained unclear. Actual stu-
dies show that lactogen and somatogen receptors stimulation for GH/Prolactin
system hormones are implicated in a range of developmental processes. These
include the successful implantation of the fertilized ovum in a receptive uterus, the
differentiation and development of embryonic organs and tissues and the succes-
sful transition of the fetus to extrauterine life, with actions on both embryo/fetus
and mother contributing to successful fetal development and requiring IGF-I factor
and its receptor for normal growth. Studies of genetic disorders of growth have led
to propose two possible models for the relationships between IGF-I production and
other components of the maternal-fetal GH axis: independence of the IGF-I axis
from somatotropic influences during the second trimester of gestation, or alterna-
tively, redundancy of somatotropic hormones and their receptors. From reports of
individuals with naturally occurring mutations that eliminate contributors to the
GH axis, redundancy does indeed appears to be a feature of the maternal-fetal GH
axis. An antagonist mutant GH can eliminate redundancy at the receptor level by
binding to, and preventing activation of, both the GH and the PRL receptors lea-
ding to profound intrauterine growth retardation. Thus, fetal pituitary GH may
activate either GH or PRL receptors, and fetal pituitary PRL or placental LP may

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