Evidence map›Paper›PMID 21852675›Full record

ArticleDiabetes2011

Dysregulation of placental endothelial lipase in obese women with gestational diabetes mellitus.

Martin Gauster, Ursula Hiden, Mireille van Poppel, Sasa Frank, Christian Wadsack, Sylvie Hauguel-de Mouzon, Gernot Desoye

Open access · hybridAbstract read
In one paragraph

Article in Diabetes, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
7.0field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

52 citing papers in PubMed, 1 synthesis or guideline pooled it, 101 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 3 countries.

Martin GausterInstitute of Cell Biology, Histology and Embryology, Center for Molecular Medicine, Medical University of Graz, Graz, Austria. martin.gauster@medunigraz.at
Ursula Hiden
Mireille van Poppel
Sasa Frank
Christian Wadsack
Sylvie Hauguel-de Mouzon
Gernot Desoye
Medical University of Graz · ATEMGO Institute for Health and Care Research · NLMetroHealth Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThis 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

methodsEL 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)-α, and EL expression was measured. Inhibitors of nuclear factor (NF)-κB or mitogen-activated protein kinase (MAPK) signaling were used to detect potential pathways of EL regulation in primary placental endothelial cells (ECs).

resultsIn 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-α values in the obese and obese-GDM groups. Cell culture experiments identified TNF-α 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-α receptors, but not the cytokines themselves, were expressed in ECs. Inhibitor experiments suggested that TNF-α and leptin-mediated upregulation of EL may occur via two different routes. Whereas TNF-α induced EL upregulation in ECs by activation of the NF-κB pathway, leptin did not stimulate NF-κB or MAPK signaling pathways in these cells.

conclusionsMetabolic inflammation with high leptin and locally increased TNF-α concentrations at the fetal-placental interface regulates placental EL expression.

Indexed as

AdultCells, CulturedDiabetes, GestationalEndothelial CellsFemaleGene Expression ProfilingGene Expression RegulationHumansLeptinLipaseObesityPlacentaPregnancyProtein Array AnalysisReceptors, LeptinReceptors, Tumor Necrosis FactorLeptinLipaseLIPG protein, humanReceptors, LeptinReceptors, Tumor Necrosis FactorTumor Necrosis Factor-alpha

Identifiers

PMID21852675
PMCPMC3178285
OpenAlexW2143142730

What OpenQuestion holds

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LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.