Insulin-like growth factor (IGF)-I, IGF-II, IGF-binding protein-2 and pregnancy-associated glycoprotein mRNA in pigs with somatotropin-enhanced fetal growth.
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 (IGFBP-2) mRNA in liver and reproductive tissues of somatotropin- and saline-treated pregnant gilts. Twenty-four pregnant gilts received daily injections of either saline (control; n=12) or 5 mg recombinant porcine somatotropin (n=12) from day 30 to day 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-associated glycoprotein (a marker of trophoblast tissue) were analyzed by Northern blotting or ribonuclease protection assay. Gilts treated with somatotropin had heavier fetuses and placentas. The concentration 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 placenta, and adjacent uterine tissue expressed IGFBP-2 mRNA intensely. In non-placental uterus, IGFBP-2 mRNA was nearly undetectable. Somatotropin-dependent regulation of IGF-I was only observed in liver, where the greatest somatotropin receptor mRNA concentration was found. In the pregnant uterus, somatotropin failed to change the concentration of IGF or IGFBP-2 mRNA. Pregnancy-associated glycoprotein mRNA concentration was decreased by somatotropin. In summary, increased fetal growth in somatotropin-treated pregnant pigs was not associated with changes in IGF or IGFBP-2 mRNA concentration in reproductive tissues. Other mechanisms, therefore, lead to enhanced fetal growth in somatotropin-treated pregnant pigs.
Sterle
J A
JA
Department of Animal Sciences, 164 ASRC, University of Missouri, Columbia, Missouri 65211, USA.
Boyd
C
C
Peacock
J T
JT
Koenigsfeld
A T
AT
Lamberson
W R
WR
Gerrard
D E
DE
Lucy
M C
MC
D000818:Animals; D016282:Aspartic Acid Endopeptidases / Q000235:genetics*; D001345:Autoradiography; D015152:Blotting, Northern; D005314:Embryonic and Fetal Development / Q000187:drug effects*; D004717:Endometrium / Q000737:chemistry; D005260:Female; D015870:Gene Expression; D013006:Growth Hormone / Q000494:pharmacology*; D018971:Insulin-Like Growth Factor Binding Protein 2 / Q000235:genetics*; D007334:Insulin-Like Growth Factor I / Q000235:genetics; D007335:Insulin-Like Growth Factor II / Q000235:genetics; D008099:Liver / Q000737:chemistry; D010920:Placenta / Q000737:chemistry; D011247:Pregnancy; D012333:RNA, Messenger / Q000032:analysis; D011986:Receptors, Somatotropin / Q000235:genetics; D013002:Somatomedins / Q000235:genetics*; D013552:Swine; D014599:Uterus / Q000737:chemistry
D018971:Insulin-Like Growth Factor Binding Protein 2; D012333:RNA, Messenger; D011986:Receptors, Somatotropin; D013002:Somatomedins; D007334:Insulin-Like Growth Factor I; D007335:Insulin-Like Growth Factor II; D013006:Growth Hormone; D016282:Aspartic Acid Endopeptidases; C095584:pregnancy-associated glycoprotein 2