Increased placental nutrient transporter expression at mid-gestation after maternal growth hormone treatment in pigs: A placental mechanism for increased fetal growth — ASN Events
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  3. Increased placental nutrient transporter expression at mid-gestation after maternal growth hormone treatment in pigs: A placental mechanism for increased fetal growth

Increased placental nutrient transporter expression at mid-gestation after maternal growth hormone treatment in pigs: A placental mechanism for increased fetal growth (#171)

Elena Tung 1 2 , Claire T Roberts 1 2 , Gary K Heinemann 1 2 , Miles J De Blasio 1 2 3 , Karen L Kind 1 4 , William HEJ van Wettere 4 , Julie A Owens 1 2 , Kathryn L Gatford 1 2
  1. Robinson Institute, University of Adelaide, Adelaide, SA, Australia
  2. School of Paediatrics & Reproductive Health, University of Adelaide, Adelaide, SA, Australia
  3. Department of Physiology, Development and Neuroscience, University of Cambridge, Cambridge, United Kingdom
  4. School of Animal and Veterinary Sciences, University of Adelaide, Adelaide, SA, Australia

Background: Growth hormone (GH) is important in maternal adaptation to pregnancy. In the pig, maternal GH treatment throughout early-mid pregnancy increases fetal growth1, despite constraining effects of adolescent and primiparous pregnancy, high litter size and restricted maternal nutrition. GH cannot cross the placenta2, suggesting that placental responses may contribute to its fetal growth-promoting effects. The facilitated glucose transporter GLUT1 and the system A amino acid transporter SNAT2 are important regulators of fetal growth, and the aim of this study was to investigate whether maternal GH treatment increased their expression in the pig.

Methods: Fetuses and placentas were collected at d 50 of gestation (term ~115 d) from multiparous (sows) and primiparous pregnant pigs (gilts) treated with GH (~15 μg.kg-1.d-1) or vehicle from d 25-50 of gestation (n=7-8 per group) for assessment of weight and size, structural correlates of function and expression of GLUT1 and SNAT2 nutrient transporters.

Results: Maternal GH treatment increased fetal growth (10%, P=0.018), and did not alter placental size or structure. GLUT1 was localised to endothelial cells and trophoblast, especially in the basal membrane, whereas SNAT2 was expressed in trophoblast, predominantly basally, and endothelial cells and amnion of the mid-gestation porcine placenta. Maternal GH treatment increased protein expression of GLUT1 (+35%, P=0.037) in trophoblast and on its basal membrane (+44%, P=0.011), and increased SNAT2 protein expression in the basal (+44%, P=0.001), but not the apical, trophoblast cytoplasm.

Conclusions: Our findings suggest that maternal GH treatment increases fetal growth, in part, by enhancing placental nutrient transporter protein expression and hence fetal nutrient supply and may have potential to ameliorate intrauterine growth restriction.

  1. Gatford KL, De Blasio MJ, Roberts CT, Nottle MB, Kind KL, et al. (2009) Responses to maternal growth hormone or ractopamine during early-mid pregnancy are similar in primiparous and multiparous pregnant pigs. Journal of Endocrinology 203: 143-154.
  2. Fholenhag KI, Sandstrom IM, Malmlof K, Skottner AI, Nyberg FJ (1994) Human growth hormone does not cross the placenta of the pregnant rat. Growth Regulation 4: 181-187.