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SHR Neuro Krebs Kardio Lipid

Gauster, M; Hiden, U; Vanpoppel, M; Frank, S; Wadsack, C; Hauguel-de Mouzon, S; Desoye, G.
Dysregulation of placental endothelial lipase in obese women with gestational diabetes mellitus.
Diabetes. 2011; 60(10): 2457-2464. [OPEN ACCESS]
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Autor/innen der Med Uni Graz:
Desoye Gernot
Frank Saša
Gauster Martin
Hiden Ursula
Wadsack Christian

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Number of Figures: 5
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OBJECTIVE-This study addressed the hypothesis that placental endothelial lipase (EL) expression is affected by pregnancies complicated by obesity and gestational diabetes mellitus (GDM). RESEARCH DESIGN AND METHODS-EL expression in placental tissues from pregnancies complicated by obesity, GDM, or obesity combined with GDM (obese-GDM) was analyzed by quantitative RT-PCR. Moreover, primary placental cells were isolated and treated with insulin, glucose, leptin, or tumor necrosis factor (TNF)-alpha, and EL expression was measured. Inhibitors of nuclear factor (NF)-kappa B or mitogen-activated protein kinase (MAPK) signaling were used to detect potential pathways of EL regulation in primary placental endothelial cells (ECs). RESULTS-In placentas from obese-GDM pregnancies, EL expression was upregulated by 1.9-fold (P < 0.05) compared with lean pregnancies, whereas obesity or GDM alone had no significant effect. Analyses of metabolic parameters in maternal venous and umbilical venous plasma revealed significantly increased insulin and leptin as well as slightly increased glucose and TNF-alpha values in the obese and obese-GDM groups. Cell culture experiments identified TNF-alpha and leptin, but not glucose or insulin, as regulators of EL expression in ECs. Induction of EL expression by these mediators occurred in a para/endocrine manner, since only leptin and TNF-alpha receptors, but not the cytokines themselves, were expressed in ECs. Inhibitor experiments suggested that TNF-alpha and leptin-mediated upregulation of EL may occur via two different routes. Whereas TNF-alpha induced EL upregulation in ECs by activation of the NF-kappa B pathway, leptin did not stimulate NF-kappa B or MAP.K signaling pathways in these cells. CONCLUSIONS-Metabolic inflammation with high leptin and locally increased TNF-alpha concentrations at the fetal-placental interface regulates placental EL expression. Diabetes 60:2457-2464, 2011
Find related publications in this database (using NLM MeSH Indexing)
Adult -
Cells, Cultured -
Diabetes, Gestational - enzymology
Endothelial Cells - enzymology Endothelial Cells - metabolism
Female -
Gene Expression Profiling -
Gene Expression Regulation - physiology
Humans -
Leptin - metabolism
Lipase - genetics Lipase - metabolism
Obesity - complications Obesity - enzymology
Placenta - enzymology
Pregnancy -
Protein Array Analysis -
Receptors, Leptin -
Receptors, Tumor Necrosis Factor -
Tumor Necrosis Factor-alpha - metabolism
Up-Regulation -
Young Adult -

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