Evidence map›Paper›PMID 38821174›Full record

ArticleMolecular metabolism2024

Differential cell type-specific function of the aryl hydrocarbon receptor and its repressor in diet-induced obesity and fibrosis.

Frederike J Graelmann, Fabian Gondorf, Yasmin Majlesain, Birte Niemann, Katarina Klepac, Dominic Gosejacob, Marlene Gottschalk, Michelle Mayer, Irina Iriady, Philip Hatzfeld and 14 more

Abstract read
In one paragraph

Article in Molecular metabolism, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
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

11 citing papers in PubMed.

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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

24 authors.

Frederike J GraelmannImmunology and Environment, Life and Medical Sciences (LIMES) Institute, University of Bonn, Germany.
Fabian GondorfImmunology and Environment, Life and Medical Sciences (LIMES) Institute, University of Bonn, Germany.
Yasmin MajlesainImmunology and Environment, Life and Medical Sciences (LIMES) Institute, University of Bonn, Germany.
Birte NiemannInstitute of Pharmacology and Toxicology, University Hospital Bonn, University of Bonn, Germany.
Katarina KlepacInstitute of Pharmacology and Toxicology, University Hospital Bonn, University of Bonn, Germany.
Dominic GosejacobInstitute of Pharmacology and Toxicology, University Hospital Bonn, University of Bonn, Germany.
Marlene GottschalkImmunology and Environment, Life and Medical Sciences (LIMES) Institute, University of Bonn, Germany.
Michelle MayerImmunology and Environment, Life and Medical Sciences (LIMES) Institute, University of Bonn, Germany.
Irina IriadyImmunology and Environment, Life and Medical Sciences (LIMES) Institute, University of Bonn, Germany.
Philip HatzfeldImmunology and Environment, Life and Medical Sciences (LIMES) Institute, University of Bonn, Germany.
Sophie K LindenbergImmunology and Environment, Life and Medical Sciences (LIMES) Institute, University of Bonn, Germany.
Klaus WunderlingBiochemistry & Cell Biology of Lipids, Life and Medical Sciences (LIMES) Institute, University of Bonn, Germany.
Christoph ThieleBiochemistry & Cell Biology of Lipids, Life and Medical Sciences (LIMES) Institute, University of Bonn, Germany.
Zeinab AbdullahInstitute of Molecular Medicine and Experimental Immunology, University Hospital Bonn, University of Bonn, Germany.
Wei HeBraunschweig Integrated Centre of Systems Biology (BRICS), Technische Universität Braunschweig, Braunschweig, Germany.
Karsten HillerBraunschweig Integrated Centre of Systems Biology (BRICS), Technische Universität Braunschweig, Braunschweig, Germany.
Kristian HändlerPRECISE Platform for Single cell Genomics and Epigenomics at the German Center for Neurodegenerative Diseases and the University of Bonn and West German Genome Center, Bonn, Germany; Genomics and Immunoregulation, Life and Medical Sciences (LIMES) Institute, University of Bonn, Germany; Institute of Human Genetics, Universitätsklinikum Schleswig-Holstein, University of Lübeck and University of Kiel, 23562 Lübeck, Germany.
Marc D BeyerPRECISE Platform for Single cell Genomics and Epigenomics at the German Center for Neurodegenerative Diseases and the University of Bonn and West German Genome Center, Bonn, Germany; Immunogenomics & Neurodegeneration, German Center for Neurodegenerative Diseases, Bonn, Germany.
Thomas UlasPRECISE Platform for Single cell Genomics and Epigenomics at the German Center for Neurodegenerative Diseases and the University of Bonn and West German Genome Center, Bonn, Germany; Genomics and Immunoregulation, Life and Medical Sciences (LIMES) Institute, University of Bonn, Germany.
Alexander PfeiferInstitute of Pharmacology and Toxicology, University Hospital Bonn, University of Bonn, Germany.
Charlotte EsserIUF-Leibniz Research Institute for Environmental Medicine gGmbH, Düsseldorf, Germany.
Heike WeighardtImmunology and Environment, Life and Medical Sciences (LIMES) Institute, University of Bonn, Germany; IUF-Leibniz Research Institute for Environmental Medicine gGmbH, Düsseldorf, Germany.
Irmgard FörsterImmunology and Environment, Life and Medical Sciences (LIMES) Institute, University of Bonn, Germany. Electronic address: irmgard.foerster@uni-bonn.de.
Laia Reverte-SalisaImmunology and Environment, Life and Medical Sciences (LIMES) Institute, University of Bonn, Germany. Electronic address: laia@uni-bonn.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThe aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor regulating xenobiotic responses as well as physiological metabolism. Dietary AhR ligands activate the AhR signaling axis, whereas AhR activation is negatively regulated by the AhR repressor (AhRR). While AhR-deficient mice are known to be resistant to diet-induced obesity (DIO), the influence of the AhRR on DIO has not been assessed so far.

methodsIn this study, we analyzed AhRR

resultsWe demonstrate that global AhRR deficiency leads to a robust, but not as profound protection from DIO and hepatosteatosis as AhR deficiency. Under conditions of DIO, AhRR

conclusionsAhRR-deficient mice are resistant to diet-induced metabolic syndrome. Although conditional ablation of either the AhR or AhRR in myeloid cells did not recapitulate the phenotype of the global knockout, our findings suggest that enhanced AhR signaling in myeloid cells deficient for AhRR protects from diet-induced liver damage and fibrosis, whereas myeloid cell-specific AhR deficiency is detrimental.

Indexed as

Basic Helix-Loop-Helix ProteinsDiet, High-FatMice, Inbred C57BLMice, KnockoutObesityReceptors, Aryl HydrocarbonAnimalsFibrosisLiverMacrophagesMaleMiceMyeloid CellsRepressor ProteinsSignal TransductionAhr protein, mouseAhrr protein, mouseBasic Helix-Loop-Helix ProteinsReceptors, Aryl HydrocarbonRepressor ProteinsCollagen depositionEnergy expenditureHepatic steatosisIndole-3-carbinolMacrophage metabolismMetabolic dysfunction

Identifiers

PMID38821174
PMCPMC11214421

What OpenQuestion holds

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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.