DIFFERENTIAL-EFFECTS OF MATERNAL OVINE PLACENTAL-LACTOGEN AND GROWTH-HORMONE (GH) ADMINISTRATION ON GH RECEPTOR, INSULIN-LIKE GROWTH-FACTOR(IGF)-1 AND IGF BINDING PROTEIN-3 GENE-EXPRESSION IN THE PREGNANT ANDFETAL SHEEP
Mj. Currie et al., DIFFERENTIAL-EFFECTS OF MATERNAL OVINE PLACENTAL-LACTOGEN AND GROWTH-HORMONE (GH) ADMINISTRATION ON GH RECEPTOR, INSULIN-LIKE GROWTH-FACTOR(IGF)-1 AND IGF BINDING PROTEIN-3 GENE-EXPRESSION IN THE PREGNANT ANDFETAL SHEEP, Growth regulation, 6(3), 1996, pp. 123-129
The role of placental lactogen (PL) in the regulation of maternal meta
bolism and fetal growth is not understood, Both PL and growth hormone
(GH) have been suggested as possible regulators of mammogenesis, Our a
im was to compare the effects of recombinant ovine placental lactogen
(oPL) and bovine growth hormone (bGH) on maternal mammary gland develo
pment and fetal growth. Pregnant ewes were treated from day 101 to 107
of gestation with twice daily subcutaneous injections of recombinant
oPL (n=7), bGH (n=8) (0.15 mg/kg live weight/day) or saline (n=8). On
day 108 of gestation, fetal and maternal tissues were collected, The r
elative abundance of growth hormone receptor (GHR), insulin-like growt
h factor-1 (IGF-1) and insulin-like growth factor binding protein-3 (I
GFBP-3) mRNA was assessed in mammary gland, maternal liver and heart,
and in fetal and placental tissues. There was no detectable change in
mammary tissue GHR, IGF-1 or IGFBP-3 gene expression with either bGH o
r oPL treatment, Maternal administration of bGH, but not oPL, during p
regnancy caused an increase in maternal hepatic IGF-1 gene expression
(P<0.005). Treatment with oPL, but not bGH, resulted in a significant
increase (P<0.025) in the relative abundance of fetal hepatic IGFBP-3
mRNA, Maternal hepatic GHR gene expression was not affected by treatme
nt. This study suggests that while bGH treatment of pregnant ewes indu
ces characteristic somatogenic responses, oPL treatment does not have
comparable effects, However, oPL may indirectly influence the fetal so
matotropic axis by altering fetal hepatic IGFBP-3 production.