title: Increased placental nutrient transport in a novel mouse model of maternal obesity with fetal overgrowth.
abstract: OBJECTIVE
  To identify possible mechanisms linking obesity in pregnancy to increased fetal adiposity and growth, a unique mouse model of maternal obesity associated with fetal overgrowth was developed, and the hypothesis that maternal obesity causes up-regulation of placental nutrient transporter expression and activity was tested.
  
  
  METHODS
  C57BL/6J female mice were fed a control (C) or a high-fat/high-sugar (HF/HS) pelleted diet supplemented by ad libitum access to sucrose (20%) solution, mated, and studied at embryonic day 18.5.
  
  
  RESULTS
  HF/HS diet increased maternal fat mass by 2.2-fold (P < 0.01) and resulted in glucose intolerance with normal fasting glucose. Maternal circulating insulin, leptin, and cholesterol were increased (P < 0.05) whereas total and high-molecular-weight adiponectin was decreased (P < 0.05). HF/HS diet increased fetal weight (+18%, P = 0.0005). In trophoblast plasma membranes (TPM) isolated from placentas of HF/HS-fed animals, protein expression of glucose transporter (GLUT) 1 and 3, sodium-coupled neutral amino acid transporter (SNAT) 2, and large neutral amino acid transporter 1 (LAT1) was increased. TPM System A and L amino acid transporter activity was increased in the HF/HS group.
  
  
  CONCLUSIONS
  Up-regulation of specific placental nutrient transporter isoforms may constitute a mechanism underlying fetal overgrowth in maternal obesity.
authors.affiliation: Center for Pregnancy and Newborn Research, Department of OB/GYN, University of Texas Health Science Center, San Antonio, Texas, USA.|Division of Basic Reproductive Sciences, Department of OB/GYN, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA.
authors.forename: Fredrick J
authors.initials: FJ
authors.lastname: Rosario
authors.affiliation: Division of Bio-System Pharmacology, Department of Pharmacology, Graduate School of Medicine, Osaka University, Osaka, Japan.
authors.forename: Yoshikatsu
authors.initials: Y
authors.lastname: Kanai
authors.affiliation: Section of Neonatology, Department of Pediatrics, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA.
authors.forename: Theresa L
authors.initials: TL
authors.lastname: Powell
authors.affiliation: Center for Pregnancy and Newborn Research, Department of OB/GYN, University of Texas Health Science Center, San Antonio, Texas, USA.|Section of Neonatology, Department of Pediatrics, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA.
authors.forename: Thomas
authors.initials: T
authors.lastname: Jansson
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D005260:Female; D020567:Fetal Weight / Q000235:genetics*; D007328:Insulin / Q000097:blood*; D020738:Leptin / Q000378:metabolism*; D051379:Mice; D008810:Mice, Inbred C57BL; D009035:Mothers; D009765:Obesity / Q000150:complications* / Q000503:physiopathology; D011247:Pregnancy; D015854:Up-Regulation; D015430:Weight Gain / Q000502:physiology*
chemical_list: D007328:Insulin; D020738:Leptin