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Gewählte Publikation:
SHR Neuro Krebs Kardio Lipid Stoffw Microb
Scholler, M; Wadsack, C; Lang, I; Etschmaier, K; Schweinzer, C; Marsche, G; Dieber-Rotheneder, M; Desoye, G; Panzenboeck, U.
Phospholipid transfer protein in the placental endothelium is affected by gestational diabetes mellitus.
J Clin Endocrinol Metab. 2012; 97(2): 437-445.
Doi: 10.1210/jc.2011-1942
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- Führende Autor*innen der Med Uni Graz
- Scholler Monika
- Wadsack Christian
- Co-Autor*innen der Med Uni Graz
- Desoye Gernot
- Dieber-Rotheneder Martina
- Etschmaier Karoline
- Lang-Olip Ingrid
- Marsche Gunther
- Panzenboeck Ute
- Schweinzer Cornelia Katrin
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- Abstract:
- Context: 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. Design: 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. Conclusion: 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. (J Clin Endocrinol Metab 97:437-445, 2012)
- Find related publications in this database (using NLM MeSH Indexing)
- Adult -
- Cells, Cultured -
- Cholesterol, HDL - blood Cholesterol, HDL - metabolism
- Diabetes, Gestational - genetics Diabetes, Gestational - metabolism Diabetes, Gestational - pathology
- Endothelium, Vascular - metabolism Endothelium, Vascular - pathology
- Female -
- Fetal Blood - metabolism
- Fetus - metabolism
- Gene Expression Regulation -
- Hep G2 Cells -
- Humans -
- Models, Biological -
- Phospholipid Transfer Proteins - genetics Phospholipid Transfer Proteins - metabolism
- Placenta - metabolism Placenta - pathology
- Pregnancy -
- Umbilical Cord - metabolism