We have investigated the effects of increasing gestational age, matern
al undernutrition or restricted placental growth on prolactin receptor
(PRLR) gene expression in perirenal adipose tissue collected from foe
tal sheep during late gestation (term = 147 d +/- 3 d of gestation). F
oetal nutrient supply was reduced by either restriction of placental g
rowth following removal of endometrial caruncles before mating or by r
educing maternal feed intake by 50% from 115 d of gestation. Total RNA
was extracted from adipose tissue taken from foetal sheep between 90
and 145 d of gestation, and only at 141-145 d in placentally restricte
d, nutrient restricted and control foetuses, Messenger RNAs encoding t
he long (PRLR1) and short (PRLR2) forms of the PRLR and glyceraldehyde
-phosphate-dehydrogenase (GAPDH) were detected and quantified in a rib
onuclease protection assay using an antisense RNA probe complementary
to ovine PRLR2 and GAPDH. There was a 7.5-fold increase in the amount
of perirenal adipose tissue between 90 and 125 d of gestation, compare
d with a 1.3-fold increase between 125 and 145 d of gestation. The abu
ndance of mRNA encoding PRLR1 and PRLR2 in perirenal adipose tissue in
creased 10- and sixfold, respectively, between 90 and 125 d of gestati
on, and then declined by 145 d of gestation. Both placental restrictio
n and maternal undernutrition significantly reduced foetal adipose tis
sue deposition. The abundance of PRLR1 but not PRLR2 mRNA was reduced
in adipose tissue from the placentally restricted group, where as GAPD
H mRNA was three times higher than in controls. In contrast, maternal
undernutrition from 115 d of gestation did not affect PRLR1, PRLR2 or
GAPDH mRNA expression in foetal adipose tissue. It is concluded that d
uring the period of rapid deposition of perirenal adipose tissue, ther
e is a concomitant increase in PRLR gene expression. This indicates th
at prolactin may play an important role in the growth and maturation o
f foetal adipose tissue which occurs before birth.