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Effect of recombinant porcine somatotropin on fetal and placental growthin gilts with reduced uterine capacity^1,2,3,4

J. A. Sterle^*,5, T. C. Cantley^*, R. L. Matteri^,6, J. A. Carroll, M. C. Lucy^* and W. R. Lamberson^*,7

^* Department of Animal Sciences, University of Missouri, Columbia 65211 and and USDA, ARS, Animal Physiology Research Unit, Columbia, MO 65211

⁷ Correspondence:
159 Animal Science Research Center, University of Missouri, Columbia 65211 (fax: 573-882-2687; E-mail:
LambersonW{at}missouri.edu).

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; n = 14), daily injections of 1 mL saline from d 0 to 64 of gestation, Early (E; n = 12), 5 mg of rpST/d from d 0 to 30, followed by 1 mL saline from d 31 to 64, and Late (L; n = 16), 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 < 0.0001) maternal plasma IGF-I concentrations relative to controls. Treatment with rpST did not affect placental wet weight or placental DNA content. However, E and L treatments increased the percentage of placental protein (P = 0.01) and placental dry matter (P = 0.10) and increased contact area of uterine-placental interface (P = 0.01). Despite changes in placental composition and morphology, weights of fetuses collected from L-treated gilts did not differ from controls, whereas weights of fetuses collected from E-treated gilts tended to be less than controls (P < 0.06). 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.

Key Words: Fetal Growth • Insulin-like Growth Factor • Pigs • Placenta • Pregnancy • Somatotropin

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