Evidence map›Paper›PMID 23744028›Full record

ArticleNature communications2013

The orphan receptor Gpr83 regulates systemic energy metabolism via ghrelin-dependent and ghrelin-independent mechanisms.

Timo D Müller, Anne Müller, Chun-Xia Yi, Kirk M Habegger, Carola W Meyer, Bruce D Gaylinn, Brian Finan, Kristy Heppner, Chitrang Trivedi, Maximilian Bielohuby and 25 more

Open access · hybridAbstract read
In one paragraph

Article in Nature communications, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

47 citing papers in PubMed, 79 citations in OpenAlex.

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  15. Article
  16. Is the Neuropeptide PEN a Ligand of GPR83?International journal of molecular sciences · 2023
    Article
  17. Article
  18. Gpr83 Tunes Nociceptor Function, Controlling Pain.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023
    Article
  19. Article
  20. Molecular pharmacology · 2022
    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

35 authors at 8 institutions in 2 countries.

Timo D MüllerInstitute for Diabetes and Obesity, Helmholtz Center Munich and Division of Metabolic Diseases, Department of Medicine, Technical University Munich, Munich, Germany.
Anne Müller
Chun-Xia Yi
Kirk M Habegger
Carola W Meyer
Bruce D Gaylinn
Brian Finan
Kristy Heppner
Chitrang Trivedi
Maximilian Bielohuby
William Abplanalp
Franziska Meyer
Carolin L Piechowski
Juliane Pratzka
Kerstin Stemmer
Jenna Holland
Jazzmin Hembree
Nakul Bhardwaj
Christine Raver
Nickki Ottaway
Radha Krishna
Renu Sah
Floyd R Sallee
Stephen C Woods
Diego Perez-Tilve
Martin Bidlingmaier
Michael O Thorner
Heiko Krude
David Smiley
Richard DiMarchi
Susanna Hofmann
Paul T Pfluger
Gunnar Kleinau
Heike Biebermann
Matthias H Tschöp
University of Cincinnati · USCharité - Universitätsmedizin Berlin · DEHelmholtz Zentrum München · DEIndiana University Bloomington · USUniversity of Cincinnati Medical Center · USUniversity of Virginia · USLMU Klinikum · DELudwig-Maximilians-Universität München · DE

Funding

Ghrelin Regulation: Implications for Understanding ObesityR01DK076037 · NIDDK · UNIVERSITY OF VIRGINIA · PI THORNER, MICHAEL O · 2008 to 2012
$2.7M
NIDDK NIH HHS R01 DK076037
6 · The paper itself

Abstract

The G protein-coupled receptor 83 (Gpr83) is widely expressed in brain regions regulating energy metabolism. Here we report that hypothalamic expression of Gpr83 is regulated in response to nutrient availability and is decreased in obese mice compared with lean mice. In the arcuate nucleus, Gpr83 colocalizes with the ghrelin receptor (Ghsr1a) and the agouti-related protein. In vitro analyses show heterodimerization of Gpr83 with Ghsr1a diminishes activation of Ghsr1a by acyl-ghrelin. The orexigenic and adipogenic effect of ghrelin is accordingly potentiated in Gpr83-deficient mice. Interestingly, Gpr83 knock-out mice have normal body weight and glucose tolerance when fed a regular chow diet, but are protected from obesity and glucose intolerance when challenged with a high-fat diet, despite hyperphagia and increased hypothalamic expression of agouti-related protein, Npy, Hcrt and Ghsr1a. Together, our data suggest that Gpr83 modulates ghrelin action but also indicate that Gpr83 regulates systemic metabolism through other ghrelin-independent pathways.

Indexed as

Energy MetabolismAgouti-Related ProteinAnimalsArcuate Nucleus of HypothalamusBody CompositionBody WeightDiet, High-FatFeeding BehaviorGene Expression ProfilingGhrelinHumansMaleMiceMice, Inbred C57BLMice, KnockoutObesityAgouti-Related ProteinGhrelinGpr83 protein, mouseMC3R protein, humanReceptor, Melanocortin, Type 3Receptors, GhrelinReceptors, G-Protein-Coupled

Identifiers

PMID23744028
PMCPMC3709495
OpenAlexW2021439125

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.