title: Placental glucose transporter 3 (GLUT3) is up-regulated in human pregnancies complicated by late-onset intrauterine growth restriction.
abstract: BACKGROUND
  Transport of glucose from maternal blood across the placental trophoblastic tissue barrier is critical to sustain fetal growth. The mechanism by which GLUTs are regulated in trophoblasts in response to ischemic hypoxia encountered with intrauterine growth restriction (IUGR) has not been suitably investigated.
  
  
  OBJECTIVE
  To investigate placental expression of GLUT1, GLUT3 and GLUT4 and possible mechanisms of GLUT regulation in idiopathic IUGR.
  
  
  METHODS
  We analyzed clinical, biochemical and histological data from placentas collected from women affected by idiopathic full-term IUGR (n = 10) and gestational age-matched healthy controls (n = 10).
  
  
  RESULTS
  We found increased GLUT3 protein expression in the trophoblast (cytotrophoblast greater than syncytiotrophoblast) on the maternal aspect of the placenta in IUGR compared to normal placenta, but no differences in GLUT1 or GLUT4 were found. No differential methylation of the GLUT3 promoter between normal and IUGR placentas was observed. Increased GLUT3 expression was associated with an increased nuclear concentration of HIF-1α, suggesting hypoxia may play a role in the up-regulation of GLUT3.
  
  
  CONCLUSIONS
  Further studies are needed to elucidate whether increased GLUT3 expression in IUGR is a marker for defective villous maturation or an adaptive response of the trophoblast in response to chronic hypoxia.
  
  
  CONCLUSIONS
  Patients with IUGR have increased trophoblast expression of GLUT3, as found under the low-oxygen conditions of the first trimester.
authors.affiliation: Department of Obstetrics and Gynecology, Division of Perinatology, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA. Electronic address: cjanzen@mednet.ucla.edu.
authors.forename: C
authors.initials: C
authors.lastname: Janzen
authors.forename: M Y Y
authors.initials: MY
authors.lastname: Lei
authors.forename: J
authors.initials: J
authors.lastname: Cho
authors.forename: P
authors.initials: P
authors.lastname: Sullivan
authors.forename: B-C
authors.initials: BC
authors.lastname: Shin
authors.forename: S U
authors.initials: SU
authors.lastname: Devaskar
mesh_terms: D000328:Adult; D015687:Cell Hypoxia; D002467:Cell Nucleus / Q000378:metabolism / Q000473:pathology; D005260:Female; D005317:Fetal Growth Retardation / Q000378:metabolism* / Q000473:pathology; D051272:Glucose Transporter Type 1 / Q000235:genetics / Q000378:metabolism; D051274:Glucose Transporter Type 3 / Q000096:biosynthesis* / Q000235:genetics / Q000378:metabolism; D051275:Glucose Transporter Type 4 / Q000235:genetics / Q000378:metabolism; D006801:Humans; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000378:metabolism; D010920:Placenta / Q000098:blood supply / Q000378:metabolism* / Q000473:pathology; D010929:Placentation; D011225:Pre-Eclampsia / Q000378:metabolism / Q000473:pathology; D011247:Pregnancy; D021381:Protein Transport; D012333:RNA, Messenger / Q000378:metabolism; D047929:Term Birth; D014327:Trophoblasts / Q000378:metabolism / Q000473:pathology; D015854:Up-Regulation; D055815:Young Adult
chemical_list: D051272:Glucose Transporter Type 1; D051274:Glucose Transporter Type 3; D051275:Glucose Transporter Type 4; C497442:HIF1A protein, human; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D012333:RNA, Messenger; C495677:SLC2A1 protein, human; C495687:SLC2A3 protein, human; C495692:SLC2A4 protein, human
keywords: GLUT; Glucose; Intrauterine growth restriction; Placenta; Transport