title: Increased placental nutrient transporter expression at midgestation after maternal growth hormone treatment in pigs: a placental mechanism for increased fetal growth.
abstract: Growth hormone (GH) is important in maternal adaptation to pregnancy, and maternal circulating GH concentrations are reduced in human growth-restricted pregnancies. In the pig, maternal GH treatment throughout early to mid pregnancy increases fetal growth, despite constraining effects of adolescent and primiparous pregnancy, high litter size, and restricted maternal nutrition. Because GH cannot cross the placenta and does not increase placental weight, we hypothesized that its effects on fetal growth might be via improved placental structure or function. We therefore investigated effects of maternal GH treatment in pigs on structural correlates of placental function and placental expression of nutrient transporters important to fetal growth. Multiparous (sows) and primiparous pregnant pigs (gilts) were treated with GH (~15 μg kg(-1) day(-1)) or vehicle from Days 25-50 of gestation (n = 7-8 per group, term ~115 days). Placentas were collected at Day 50 of gestation, and we measured structural correlates of function and expression of SLC2A1 (previously known as GLUT1) and SLC38A2 (previously known as SNAT2) nutrient transporters. Maternal GH treatment did not alter placental size or structure, increased protein expression of SLC2A1 in trophoblast (+35%; P = 0.037) and on its basal membrane (+44%; P = 0.011), and increased SLC38A2 protein expression in the basal (+44%; P = 0.001) but not the apical cytoplasm of trophoblast. Our findings suggest that maternal GH treatment increases fetal growth, in part, by enhancing placental nutrient transporter protein expression and hence fetal nutrient supply as well as trophoblast proliferation and differentiation and may have the potential to ameliorate intrauterine growth restriction.
authors.affiliation: Robinson Institute, University of Adelaide, Adelaide, South Australia, Australia.
authors.forename: Elena
authors.initials: E
authors.lastname: Tung
authors.forename: Claire T
authors.initials: CT
authors.lastname: Roberts
authors.forename: Gary K
authors.initials: GK
authors.lastname: Heinemann
authors.forename: Miles J
authors.initials: MJ
authors.lastname: De Blasio
authors.forename: Karen L
authors.initials: KL
authors.lastname: Kind
authors.forename: William H E J
authors.initials: WH
authors.lastname: van Wettere
authors.forename: Julie A
authors.initials: JA
authors.lastname: Owens
authors.forename: Kathryn L
authors.initials: KL
authors.lastname: Gatford
mesh_terms: D026924:Amino Acid Transport System A / Q000032:analysis* / Q000502:physiology; D000818:Animals; D005260:Female; D047109:Fetal Development / Q000187:drug effects* / Q000502:physiology; D020567:Fetal Weight / Q000187:drug effects; D005865:Gestational Age; D051272:Glucose Transporter Type 1 / Q000032:analysis* / Q000502:physiology; D013006:Growth Hormone / Q000008:administration & dosage*; D007150:Immunohistochemistry; D009929:Organ Size; D010920:Placenta / Q000737:chemistry / Q000187:drug effects / Q000502:physiology*; D011247:Pregnancy; D017526:Receptor, IGF Type 1 / Q000032:analysis; D034421:Sus scrofa; D014327:Trophoblasts / Q000737:chemistry
chemical_list: D026924:Amino Acid Transport System A; D051272:Glucose Transporter Type 1; D013006:Growth Hormone; D017526:Receptor, IGF Type 1