title: Phospholipid transfer protein in the placental endothelium is affected by gestational diabetes mellitus.
abstract: BACKGROUND
  Gestational diabetes mellitus (GDM) causes alterations in fetal high-density lipoproteins (HDL). Because phospholipid transfer protein (PLTP) is important for HDL (re)assembly and is expressed in the human placenta, we hypothesized that circulating fetal and/or placental PLTP expression and activity are altered in GDM.
  
  
  METHODS
  PLTP levels and activity were determined in maternal and fetal sera from GDM and controls. Placental PLTP was immunolocalized, and its expression was measured in placental tissue. PLTP regulation by glucose/insulin was studied in human endothelial cells isolated from placental vessels (HPEC).
  
  
  RESULTS
  Placental Pltp expression was up-regulated in GDM (1.8-fold, P < 0.05). PLTP protein (5-fold, P < 0.01) and activity (1.4- to 2.5-fold) were higher in fetal than in maternal serum. The placental endothelium was identified as a major PLTP location. Insulin treatment of HPEC significantly increased secreted PLTP levels and activity. In GDM, fetal cholesterol, HDL-triglycerides and phospholipids were elevated compared with controls. Fetal PLTP activity was higher than maternal but unaltered in GDM.
  
  
  CONCLUSIONS
  HPEC contribute to the release of active PLTP into the fetal circulation. Pltp expression is increased in GDM with hyperglycemia and/or hyperinsulinemia contributing. High PLTP activity in fetal serum may enhance conversion of HDL into cholesterol-accepting particles, thereby increasing maternal-fetal cholesterol transfer.
authors.affiliation: Institute of Pathophysiology and Immunology, Medical University of Graz, A-8036 Graz, Austria.
authors.forename: Monika
authors.initials: M
authors.lastname: Scholler
authors.forename: Christian
authors.initials: C
authors.lastname: Wadsack
authors.forename: Ingrid
authors.initials: I
authors.lastname: Lang
authors.forename: Karoline
authors.initials: K
authors.lastname: Etschmaier
authors.forename: Cornelia
authors.initials: C
authors.lastname: Schweinzer
authors.forename: Gunther
authors.initials: G
authors.lastname: Marsche
authors.forename: Martina
authors.initials: M
authors.lastname: Dieber-Rotheneder
authors.forename: Gernot
authors.initials: G
authors.lastname: Desoye
authors.forename: Ute
authors.initials: U
authors.lastname: Panzenboeck
mesh_terms: D000328:Adult; D002478:Cells, Cultured; D008076:Cholesterol, HDL / Q000097:blood / Q000378:metabolism; D016640:Diabetes, Gestational / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D004730:Endothelium, Vascular / Q000378:metabolism* / Q000473:pathology; D005260:Female; D005312:Fetal Blood / Q000378:metabolism; D005333:Fetus / Q000378:metabolism; D005786:Gene Expression Regulation; D056945:Hep G2 Cells; D006801:Humans; D008954:Models, Biological; D049294:Phospholipid Transfer Proteins / Q000235:genetics / Q000378:metabolism*; D010920:Placenta / Q000378:metabolism* / Q000473:pathology; D011247:Pregnancy; D014470:Umbilical Cord / Q000378:metabolism
chemical_list: D008076:Cholesterol, HDL; D049294:Phospholipid Transfer Proteins