Evidence map›Paper›PMID 29031722›Full record

ArticleMolecular metabolism2017

Activated macrophages control human adipocyte mitochondrial bioenergetics via secreted factors.

Michaela Keuper, Stephan Sachs, Ellen Walheim, Lucia Berti, Bernhard Raedle, Daniel Tews, Pamela Fischer-Posovszky, Martin Wabitsch, Martin Hrabě de Angelis, Gabi Kastenmüller and 4 more

Open access · goldAbstract read
In one paragraph

Article in Molecular metabolism, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

21 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
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  6. AnJournal of biosciences · 2024
    Article
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  8. White adipose tissue mitochondrial bioenergetics in metabolic diseases.Reviews in endocrine & metabolic disorders · 2023
    Review
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  16. Inflammatory Signaling and Brown Fat Activity.Frontiers in endocrinology · 2020
    Review
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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

14 authors at 2 institutions in 1 country.

Michaela KeuperInstitute of Diabetes and Regeneration Research, Helmholtz Zentrum Muenchen, German Research Center for Environmental Health (GmbH), Neuherberg, Germany; German Center for Diabetes Research (DZD), Neuherberg, Germany; Institute of Experimental Genetics, Helmholtz Zentrum Muenchen, German Research Center for Environmental Health (GmbH), Neuherberg, Germany. Electronic address: michaela.keuper@helmholtz-muenchen.de.
Stephan SachsInstitute of Diabetes and Regeneration Research, Helmholtz Zentrum Muenchen, German Research Center for Environmental Health (GmbH), Neuherberg, Germany; German Center for Diabetes Research (DZD), Neuherberg, Germany.
Ellen WalheimGerman Center for Diabetes Research (DZD), Neuherberg, Germany; Institute for Diabetes and Obesity, Helmholtz Zentrum Muenchen, German Research Center for Environmental Health (GmbH), Neuherberg, Germany.
Lucia BertiGerman Center for Diabetes Research (DZD), Neuherberg, Germany; Institute for Diabetes Research and Metabolic Diseases of the Helmholtz Center Munich at the University of Tübingen, Tübingen, Germany.
Bernhard RaedleGerman Center for Diabetes Research (DZD), Neuherberg, Germany; Institute of Experimental Genetics, Helmholtz Zentrum Muenchen, German Research Center for Environmental Health (GmbH), Neuherberg, Germany.
Daniel TewsDivision of Pediatric Endocrinology and Diabetes, Department of Pediatrics and Adolescent Medicine, University Medical Center, Ulm, Germany.
Pamela Fischer-PosovszkyDivision of Pediatric Endocrinology and Diabetes, Department of Pediatrics and Adolescent Medicine, University Medical Center, Ulm, Germany.
Martin WabitschDivision of Pediatric Endocrinology and Diabetes, Department of Pediatrics and Adolescent Medicine, University Medical Center, Ulm, Germany.
Martin Hrabě de AngelisGerman Center for Diabetes Research (DZD), Neuherberg, Germany; Institute of Experimental Genetics, Helmholtz Zentrum Muenchen, German Research Center for Environmental Health (GmbH), Neuherberg, Germany; Chair of Experimental Genetics, School of Life Science Weihenstephan, Technische Universität München, Alte Akademie 8, 85354 Freising, Germany.
Gabi KastenmüllerInstitute of Bioinformatics and Systems Biology, Helmholtz Zentrum Muenchen, German Research Center for Environmental Health (GmbH), Neuherberg, Germany.
Matthias H TschöpGerman Center for Diabetes Research (DZD), Neuherberg, Germany; Institute for Diabetes and Obesity, Helmholtz Zentrum Muenchen, German Research Center for Environmental Health (GmbH), Neuherberg, Germany.
Martin JastrochGerman Center for Diabetes Research (DZD), Neuherberg, Germany; Institute for Diabetes and Obesity, Helmholtz Zentrum Muenchen, German Research Center for Environmental Health (GmbH), Neuherberg, Germany.
Harald StaigerGerman Center for Diabetes Research (DZD), Neuherberg, Germany; Institute for Diabetes Research and Metabolic Diseases of the Helmholtz Center Munich at the University of Tübingen, Tübingen, Germany; Institute of Pharmaceutical Sciences, Department of Pharmacy and Biochemistry, Eberhard Karls University Tübingen, Germany.
Susanna M HofmannInstitute of Diabetes and Regeneration Research, Helmholtz Zentrum Muenchen, German Research Center for Environmental Health (GmbH), Neuherberg, Germany; German Center for Diabetes Research (DZD), Neuherberg, Germany; Medizinische Klinik und Poliklinik IV, Klinikum der LMU, 80336 München, Germany.
Helmholtz Zentrum München · DEDeutsches Diabetes-Zentrum e.V. · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveObesity-associated WAT inflammation is characterized by the accumulation and local activation of macrophages (MΦs), and recent data from mouse studies suggest that macrophages are modifiers of adipocyte energy metabolism and mitochondrial function. As mitochondrial dysfunction has been associated with obesity and the metabolic syndrome in humans, herein we aimed to delineate how human macrophages may affect energy metabolism of white adipocytes.

methodsHuman adipose tissue gene expression analysis for markers of macrophage activation and tissue inflammation (CD11c, CD40, CD163, CD206, CD80, MCP1, TNFα) in relationship to mitochondrial complex I (NDUFB8) and complex III (UQCRC2) was performed on subcutaneous WAT of 24 women (BMI 20-61 kg/m

resultsStepwise regression analysis of human WAT gene expression data revealed that a linear combination of CD40 and CD163 was the strongest predictor for mitochondrial complex I (NDUFB8) and complex III (UQCRC2) levels, independent of BMI. IL10/TGFβ-activated MΦs displayed high CD163 and low CD40 expression and secreted factors that decreased UQCRC2 gene/protein expression and ATP-linked respiration in human white adipocytes. In contrast, LPS/IFNγ-activated MΦs showed high CD40 and low CD163 expression and secreted factors that enhanced adipocyte mitochondrial activity resulting in a total difference of 37% in ATP-linked respiration of white adipocytes (p = 0.0024) when comparing the effect of LPS/IFNγ- vs IL10/TGFβ-activated MΦs.

conclusionOur data demonstrate that macrophages modulate human adipocyte energy metabolism via an activation-dependent paracrine mechanism.

Indexed as

Adipocytes, WhiteAdipose Tissue, WhiteAdultAgedAntigens, CDCytokinesEnergy MetabolismFemaleHumansMacrophage ActivationMacrophagesMiddle AgedMitochondriaObesitySignal TransductionTumor Necrosis Factor-alphaAntigens, CDCytokinesTumor Necrosis Factor-alphaCellular metabolismCytokinesGlycolysisOxidative phosphorylation

Identifiers

PMID29031722
PMCPMC5641636
OpenAlexW2739427432

What OpenQuestion holds

Textmetadata
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.