Evidence map›Paper›PMID 39545055›Full record

ArticleJournal of the Endocrine Society2024

Sexual Dimorphism in the Immunometabolic Role of Gpr183 in Mice.

Liv von Voss, Tulika Arora, Juliana Assis, Katharina B Kuentzel, Kristine N Arfelt, Mark K Nøhr, Trisha J Grevengoed, Manimozhiyan Arumugam, Thomas Mandrup-Poulsen, Mette M Rosenkilde

Abstract read
In one paragraph

Article in Journal of the Endocrine Society, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
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.

Liv von VossMolecular and Translational Pharmacology, Department of Biomedical Sciences, University of Copenhagen, DK 2200 Copenhagen, Denmark.ORCID https://orcid.org/0000-0002-0515-0345
Tulika AroraNovo Nordisk Foundation Center for Basic Metabolic Research and Medical Sciences, University of Copenhagen, DK 2200 Copenhagen, Denmark.ORCID https://orcid.org/0000-0001-8821-8191
Juliana AssisNovo Nordisk Foundation Center for Basic Metabolic Research and Medical Sciences, University of Copenhagen, DK 2200 Copenhagen, Denmark.ORCID https://orcid.org/0000-0001-5995-8684
Katharina B KuentzelMolecular and Translational Pharmacology, Department of Biomedical Sciences, University of Copenhagen, DK 2200 Copenhagen, Denmark.ORCID https://orcid.org/0000-0002-1445-5466
Kristine N ArfeltMolecular and Translational Pharmacology, Department of Biomedical Sciences, University of Copenhagen, DK 2200 Copenhagen, Denmark.ORCID https://orcid.org/0000-0002-7806-8502
Mark K NøhrMolecular and Translational Pharmacology, Department of Biomedical Sciences, University of Copenhagen, DK 2200 Copenhagen, Denmark.ORCID https://orcid.org/0000-0002-5536-654X
Trisha J GrevengoedMolecular and Translational Pharmacology, Department of Biomedical Sciences, University of Copenhagen, DK 2200 Copenhagen, Denmark.ORCID https://orcid.org/0000-0003-4433-3950
Manimozhiyan ArumugamNovo Nordisk Foundation Center for Basic Metabolic Research and Medical Sciences, University of Copenhagen, DK 2200 Copenhagen, Denmark.ORCID https://orcid.org/0000-0002-0886-9101
Thomas Mandrup-PoulsenMolecular and Translational Pharmacology, Department of Biomedical Sciences, University of Copenhagen, DK 2200 Copenhagen, Denmark.ORCID https://orcid.org/0000-0002-3215-9273
Mette M RosenkildeMolecular and Translational Pharmacology, Department of Biomedical Sciences, University of Copenhagen, DK 2200 Copenhagen, Denmark.ORCID https://orcid.org/0000-0001-9600-3254

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Context: Excessive eating and intake of a Western diet negatively affect the intestinal immune system, resulting in compromised glucose homeostasis and lower gut bacterial diversity. The G protein-coupled receptor GPR183 regulates immune cell migration and intestinal immune response and has been associated with tuberculosis, type 1 diabetes, and inflammatory bowel diseases. Objective: We hypothesized that with these implications, GPR183 has an important immunometabolic role and investigated this using a global Gpr183 knockout mouse model. Methods: Wild-type (WT) and Results: A sexual dimorphism was discovered, whereby female Gpr183 Conclusion: Gpr183 maintains metabolic homeostasis in female but not in male mice independent of diet. If confirmed in humans, future therapy targeting GPR183 should consider this sexual dimorphism.

Indexed as

GPR183Gpr183 knockout mouseG protein–coupled receptorhigh-fathigh-sucrose dietoxysterolssexual dimorphism

Identifiers

PMID39545055
PMCPMC11561910

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Registered trials

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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.