Evidence map›Paper›PMID 37080971›Full record

ArticleNature communications2023

Glucocorticoid activation of anti-inflammatory macrophages protects against insulin resistance.

Giorgio Caratti, Ulrich Stifel, Bozhena Caratti, Ali J M Jamil, Kyoung-Jin Chung, Michael Kiehntopf, Markus H Gräler, Matthias Blüher, Alexander Rauch, Jan P Tuckermann

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
9.2field-weighted citation impact, top 1% 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

34 citing papers in PubMed, 43 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 6 institutions in 3 countries.

Giorgio Caratti *Institute of Comparative Molecular Endocrinology, University of Ulm, Ulm, Germany.
Ulrich Stifel *Institute of Comparative Molecular Endocrinology, University of Ulm, Ulm, Germany.
Bozhena CarattiInstitute of Comparative Molecular Endocrinology, University of Ulm, Ulm, Germany.
Ali J M JamilMolecular Endocrinology & Stem Cell Research Unit, Department of Endocrinology and Metabolism, Odense University Hospital, Odense, Denmark.ORCID 0000-0002-8745-5483
Kyoung-Jin ChungInstitute for Clinical Chemistry and Laboratory Medicine, University Hospital and Faculty of Medicine, Technical University Dresden, Dresden, Germany.ORCID 0000-0001-6584-5352
Michael KiehntopfSG Sepsis Research Clinic for Anesthesiology and Intensive Care, Jena University Hospital, Jena, Germany.
Markus H GrälerDepartment of Anesthesiology and Intensive Care Medicine, Jena University Hospital, Jena, Germany.ORCID 0000-0001-6650-7849
Matthias BlüherDepartment of Endocrinology and Nephrology, University of Leipzig, Leipzig, Germany.ORCID 0000-0003-0208-2065
Alexander RauchMolecular Endocrinology & Stem Cell Research Unit, Department of Endocrinology and Metabolism, Odense University Hospital, Odense, Denmark. arauch@health.sdu.dk.ORCID 0000-0002-9429-7356
Jan P TuckermannInstitute of Comparative Molecular Endocrinology, University of Ulm, Ulm, Germany. jan.tuckermann@uni-ulm.de.ORCID 0000-0003-3691-275X
Universität Ulm · DEJena University Hospital · DELeipzig University · DESteno Diabetes Centers · DKTechnische Universität Dresden · DEUniversity of Southern Denmark · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Insulin resistance (IR) during obesity is linked to adipose tissue macrophage (ATM)-driven inflammation of adipose tissue. Whether anti-inflammatory glucocorticoids (GCs) at physiological levels modulate IR is unclear. Here, we report that deletion of the GC receptor (GR) in myeloid cells, including macrophages in mice, aggravates obesity-related IR by enhancing adipose tissue inflammation due to decreased anti-inflammatory ATM leading to exaggerated adipose tissue lipolysis and severe hepatic steatosis. In contrast, GR deletion in Kupffer cells alone does not alter IR. Co-culture experiments show that the absence of GR in macrophages directly causes reduced phospho-AKT and glucose uptake in adipocytes, suggesting an important function of GR in ATM. GR-deficient macrophages are refractory to alternative ATM-inducing IL-4 signaling, due to reduced STAT6 chromatin loading and diminished anti-inflammatory enhancer activation. We demonstrate that GR has an important function in macrophages during obesity by limiting adipose tissue inflammation and lipolysis to promote insulin sensitivity.

Indexed as

GlucocorticoidsInsulin ResistanceAdipose TissueAnimalsAnti-Inflammatory AgentsInflammationMacrophagesMiceMice, Inbred C57BLObesityAnti-Inflammatory AgentsGlucocorticoids

Identifiers

PMID37080971
PMCPMC10119112
OpenAlexW4366547977

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.