Submitted to: Journal of Animal Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/1/2002
Publication Date: 3/1/2003
Citation: STERLE, J.A., CANTLEY, T.C., MATTERI, R.L., CARROLL, J.A., LUCY, M.C., LAMBERSON, W.R. EFFECT OF RECOMBINANT PORCINE SOMATOTROPIN ON FETAL AND PLACENTAL GROWTH IN GILTS WITH REDUCED UTERINE CAPACITY. JOURNAL OF ANIMAL SCIENCE. 2003. v. 81. p. 765-771.
Interpretive Summary: The study was conducted to gain further knowledge regarding the effect of uterine crowding in a litter-bearing animal, as well as the effect of exogenous growth hormone treatment on uterine-placental interactions and overall fetal growth. Gilts were injected daily with saline or exogenous growth hormone during either the early or late stages of pregnancy. Data were collected on serum hormone concentrations and placenta characteristic for the gilt, and fetal growth was recorded. Both early and late gestational treatment with growth hormone increased serum concentrations of insulin-like growth hormone in the gilts. Exogenous growth hormone treatment also increased the contact area between the uterus and the placenta. However, this increase in contact area between the uterus and the placenta did not increase the body weight of the fetuses. In fact, those gilts treated with exogenous growth hormone during the early stages of pregnancy had fetuses with lower body weights. This research suggests that under crowded uterine conditions, early fetal growth is independent of serum concentrations of insulin-like growth factor in the gilt, and independent of the contact area between the uterus and the placenta. Results from this study will mainly be of interest to scientists due to the basic information gained regarding the effects of exogenous growth hormone on fetal growth.
Technical Abstract: Crowded uterine conditions were induced by unilateral hysterectomy- ovariectomy (UHO) in 42 gilts to determine the effect of recombinant porcine somatotropin on fetal and placental growth. Gilts were randomly assigned across three replicates to one of three treatments: Control (C), daily injections of 1 mL saline d 0 to 64 of gestation; Early (E), 5 mg of rpST/d from d 0 to 30, followed by 1 mL saline from d 31 to 64; and Late (L), 1 mL saline/d from d 0 to 29, followed by 5 mg of rpST/d from d 30 to 64 of gestation. Blood was collected from each gilt via jugular venipuncture at d 0 and every 15 d thereafter. Gilts were hysterectomized on d 65 of gestation. Length of placental attachment and fetal crown-rump length were measured. Placentas and fetuses were weighed. Placental length, wet weight, and dry weight were recorded. Treatment with rpST (either E or L) increased (P<.0001) maternal plasma IGF-I concentrations relative to controls. Treatment with rpST did not affect placenta wet weight or placenta DNA content. However, E and L treatments increased the percentage of placental protein (P=.01) and placental dry matter (P=.10) and increased contact area of uterine-placental interface (P=.01). Despite changes in placental composition and morphology, weights of fetuses collected from L-treated gilts were similar to controls whereas weights of fetuses collected from E-treated gilts tended to be less than controls (P<.06). Administration of rpST increased maternal IGF-I concentrations and placental surface area but failed to increase fetal growth in the UHO model. Therefore, mechanisms that are independent of maternal IGF-I or placental contact area may control early fetal growth under crowded uterine conditions.