Fetal growth is increased when pregnant gilts are treated with recombinant
porcine somatotropin. The mechanism for increased fetal growth was examined
by measuring the expression of IGF-I and -II and IGF-binding protein-2 (IG
FBP-2) mRNA in liver and reproductive tissues of somatotropin- and saline-t
reated pregnant gilts.
Twenty-four pregnant gilts received daily injections of either saline (cont
rol; n=12) or 5 mg recombinant porcine somatotropin (n=12) from day 30 to d
ay 43 of gestation. Gilts were slaughtered on day 44 of gestation and liver
, ovary, placenta, placental uterus (uterus with adjacent placental tissue)
and non-placental uterus (region of the necrotic tip) were collected. The
mRNAs for somatotropin receptor, IGFs-I and -II, IGFBP-2 and pregnancy-asso
ciated glycoprotein (a marker of trophoblast tissue) were analyzed by North
ern blotting or ribonuclease protection assay.
Gilts treated with somatotropin had heavier fetuses and placentas. The conc
entration of mRNA for the components of the IGF system was tissue-dependent
. The uterine IGF-I mRNA concentration was greater in non-placental than in
placental uterus. The greatest IGF-II mRNA concentration was observed in p
lacenta, and adjacent uterine tissue expressed IGFBP-2 mRNA intensely. In n
on-placental uterus, IGFBP-2 mRNA was nearly undetectable. Somatotropin-dep
endent regulation of IGF-I was only observed in liver, where the greatest s
omatotropin receptor mRNA concentration was found. In the pregnant uterus,
somatotropin failed to change the concentration of IGF or IGFBP-2 mRNA. Pre
gnancy-associated glycoprotein mRNA concentration was decreased by somatotr
opin.
In summary, increased fetal growth in somatotropin-treated pregnant pigs wa
s not associated with changes in IGF or IGFBP-2 mRNA concentration in repro
ductive tissues. Other mechanisms, therefore, lead to enhanced fetal growth
in somatotropin-treated pregnant pigs.