Evidence map›Paper›PMID 29166648›Full record

ArticlePloS one2017

Different response to hypoxia of adipose-derived multipotent cells from obese subjects with and without metabolic syndrome.

Wilfredo Oliva-Olivera, Isabel Moreno-Indias, Leticia Coín-Aragüez, Said Lhamyani, Juan Alcaide Torres, Sonia Fernández-Veledo, Joan Vendrell, Antonio Camargo, Rajaa El Bekay, Francisco José Tinahones

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

6 citing papers in PubMed, 11 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

10 authors at 2 institutions in 1 country.

Wilfredo Oliva-OliveraDepartment of Clinical Endocrinology and Nutrition, Institute of Biomedical Research of Málaga (IBIMA), Hospital of Málaga (Virgen de la Victoria), University of Málaga (UMA), Málaga, Spain.ORCID http://orcid.org/0000-0003-3473-7898
Isabel Moreno-IndiasDepartment of Clinical Endocrinology and Nutrition, Institute of Biomedical Research of Málaga (IBIMA), Hospital of Málaga (Virgen de la Victoria), University of Málaga (UMA), Málaga, Spain.
Leticia Coín-AragüezDepartment of Clinical Endocrinology and Nutrition, Institute of Biomedical Research of Málaga (IBIMA), Hospital of Málaga (Virgen de la Victoria), University of Málaga (UMA), Málaga, Spain.
Said LhamyaniResearch Laboratory, Science School, University of Málaga (UMA), Málaga, Spain.
Juan Alcaide TorresDepartment of Clinical Endocrinology and Nutrition, Institute of Biomedical Research of Málaga (IBIMA), Hospital of Málaga (Virgen de la Victoria), University of Málaga (UMA), Málaga, Spain.
Sonia Fernández-VeledoHospital Universitari de Tarragona Joan XXIII, Institut d'Investigació Sanitària Pere Virgili, Universitat Rovirai Virgili, Tarragona, Spain.
Joan VendrellHospital Universitari de Tarragona Joan XXIII, Institut d'Investigació Sanitària Pere Virgili, Universitat Rovirai Virgili, Tarragona, Spain.
Antonio CamargoCIBER Fisiopatología Obesidad y Nutrición, Instituto de Salud Carlos III, Madrid, Spain.
Rajaa El BekayDepartment of Clinical Endocrinology and Nutrition, Institute of Biomedical Research of Málaga (IBIMA), Hospital of Málaga (Virgen de la Victoria), University of Málaga (UMA), Málaga, Spain.
Francisco José TinahonesDepartment of Clinical Endocrinology and Nutrition, Institute of Biomedical Research of Málaga (IBIMA), Hospital of Málaga (Virgen de la Victoria), University of Málaga (UMA), Málaga, Spain.
Instituto de Salud Carlos III · ESUniversidad de Málaga · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

objectivesMultiple studies suggest that hypoxia, together with inflammation, could be one of the phenomena involved in the onset and progression of obesity-related insulin resistance. In addition, dysfunction of adipose tissue in obese subjects with metabolic syndrome is associated with decreased angiogenesis. However, some subjects with a high body mass index do not develop metabolic abnormalities associated with obesity. The aim of the current study was to examine the neovascular properties of visceral adipose tissue-derived multipotent mesenchymal cells subjected to hypoxia (hypox-visASCs) from normal-weight subjects (Nw) and obese patients with metabolic syndrome (MS) and without metabolic syndrome (NonMS).

methodsThis was a 2-year study to enroll subjects who underwent bariatric surgery or cholecystectomy. Eight patients who underwent either bariatric surgery or cholecystectomy (27 patients) participated in the study. Visceral adipose tissue samples from Nw, MS and NonMS subjects were processed by enzymatic digestion. VisASCs cultured under hypoxic conditions were characterized by tubule formation assay, ELISA, flow cytometry, migration rate, and qRT-PCR, and the effects of visASCs-conditioned medium on survival and endothelial cell tubule formation were evaluated.

resultsHypox-visASCs from NonMS subjects showed a greater capacity for tubule formation than hypox-visASCs from Nw and MS subjects. The lower percentage of CD140b+/CD44+ and CD140b+/CD184+ cells observed in hypox-visASCs from NonMS subjects compared to MS subjects was accompanied not only by a lower migration rate from the chemotactic effects of stromal cell derived factor 1α, but also by lower levels of NOX5 mRNA expression. While the levels of monocyte chemoattractant protein 1 mRNA expressed by hypox-visASCs correlated positively with the body mass index and waist circumference of the subjects, the concentration of vascular endothelial growth factor present in hypox-visASC-conditioned culture medium decreased significantly with increasing plasma glucose. The survival rate and tubules formed by endothelial cells cultured in hypox-visASC-conditioned medium decreased significantly with increasing homeostasis model assessment to quantify insulin resistance.

conclusionsOur results suggest that hypox-visASCs from NonMS subjects could promote healthy adipose tissue expansion, while hypox-visASCs from MS subjects appear to contribute to the decreased angiogenic potential and increased inflammation underlying adipose tissue dysfunction in obesity. Our results emphasize the importance of taking into account not only the BMI but also the metabolic profile of the subjects during the implementation of ASCs-based therapy to promote neovascularization.

Indexed as

Adipose TissueAdultAnthropometryCell CountCell MovementCells, CulturedChemokine CXCL12Culture Media, ConditionedGene Expression RegulationHepatocyte Growth FactorHumansHypoxiaImmunophenotypingInflammation MediatorsMetabolic SyndromeModels, BiologicalChemokine CXCL12Culture Media, ConditionedHepatocyte Growth FactorInflammation MediatorsNADPH OxidasesOxygenReceptor, Platelet-Derived Growth Factor betaVascular Endothelial Growth Factor A

Identifiers

PMID29166648
PMCPMC5699836
OpenAlexW2770268026

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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.