Evidence map›Paper›PMID 37277610›Full record

ArticleNature metabolism2023

CaMK1D signalling in AgRP neurons promotes ghrelin-mediated food intake.

Karl Vivot, Gergö Meszaros, Evanthia Pangou, Zhirong Zhang, Mengdi Qu, Eric Erbs, Gagik Yeghiazaryan, Mar Quiñones, Erwan Grandgirard, Anna Schneider and 10 more

Open access · greenAbstract read
PubMed Publisher
In one paragraph

Article in Nature metabolism, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

16 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
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  10. Foods (Basel, Switzerland) · 2025
    Article
  11. Article
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  13. The ARCNature communications · 2025
    Article
  14. Article
  15. Review
  16. CAMK1D required for ghrelin-mediated food intake.Nature reviews. Endocrinology · 2023
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

20 authors at 8 institutions in 4 countries.

Karl VivotInstitut de Génétique et de Biologie Moléculaire et Cellulaire, Illkirch, France. vivotk@igbmc.fr.ORCID http://orcid.org/0000-0003-4617-0016
Gergö MeszarosInstitut de Génétique et de Biologie Moléculaire et Cellulaire, Illkirch, France.
Evanthia PangouInstitut de Génétique et de Biologie Moléculaire et Cellulaire, Illkirch, France.ORCID http://orcid.org/0000-0002-1266-2699
Zhirong ZhangInstitut de Génétique et de Biologie Moléculaire et Cellulaire, Illkirch, France.ORCID http://orcid.org/0000-0002-7331-783X
Mengdi QuInstitut de Génétique et de Biologie Moléculaire et Cellulaire, Illkirch, France.
Eric ErbsInstitut de Génétique et de Biologie Moléculaire et Cellulaire, Illkirch, France.ORCID http://orcid.org/0009-0008-6447-7154
Gagik YeghiazaryanBiocenter, Institute for Zoology, and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, (CECAD), University of Cologne, Cologne, Germany.
Mar QuiñonesInstituto de Investigación Sanitaria de Santiago de Compostela, Complexo Hospitalario Universitario de Santiago (CHUS/SERGAS), Santiago de Compostela, Spain.ORCID http://orcid.org/0000-0003-0180-2147
Erwan GrandgirardInstitut de Génétique et de Biologie Moléculaire et Cellulaire, Illkirch, France.ORCID http://orcid.org/0000-0002-5263-2144
Anna SchneiderInstitut de Génétique et de Biologie Moléculaire et Cellulaire, Illkirch, France.
Etienne Clauss-CreusotUniversité de Strasbourg, Strasbourg, France.
Alexandre CharletUniversité de Strasbourg, Strasbourg, France.ORCID http://orcid.org/0000-0003-4837-3706
Maya FaourUniversité Paris Cité, CNRS, Unité de Biologie Fonctionnelle et Adaptative, Paris, France.
Claire MartinUniversité Paris Cité, CNRS, Unité de Biologie Fonctionnelle et Adaptative, Paris, France.ORCID http://orcid.org/0000-0001-5340-8323
Fedor BerditchevskiInstitute of Cancer and Genomic Sciences, The University of Birmingham, Birmingham, UK.ORCID http://orcid.org/0000-0003-0911-834X
Izabela SumaraInstitut de Génétique et de Biologie Moléculaire et Cellulaire, Illkirch, France.
Serge LuquetUniversité Paris Cité, CNRS, Unité de Biologie Fonctionnelle et Adaptative, Paris, France.
Peter KloppenburgBiocenter, Institute for Zoology, and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, (CECAD), University of Cologne, Cologne, Germany.ORCID http://orcid.org/0000-0002-4554-404X
Ruben NogueirasInstituto de Investigación Sanitaria de Santiago de Compostela, Complexo Hospitalario Universitario de Santiago (CHUS/SERGAS), Santiago de Compostela, Spain.ORCID http://orcid.org/0000-0002-9976-9930
Romeo RicciInstitut de Génétique et de Biologie Moléculaire et Cellulaire, Illkirch, France. romeo.ricci@igbmc.fr.ORCID http://orcid.org/0000-0002-9766-4369
Centre National de la Recherche Scientifique · FRUniversity of Cologne · DEInstitut de génétique et de biologie moléculaire et cellulaire · FRInstitut des Neurosciences Cellulaires et Intégratives · FRInstituto de Salud Carlos III · ESUniversidade de Santiago de Compostela · ESUniversité de Strasbourg · FRUniversity of Birmingham · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypothalamic AgRP/NPY neurons are key players in the control of feeding behaviour. Ghrelin, a major orexigenic hormone, activates AgRP/NPY neurons to stimulate food intake and adiposity. However, cell-autonomous ghrelin-dependent signalling mechanisms in AgRP/NPY neurons remain poorly defined. Here we show that calcium/calmodulin-dependent protein kinase ID (CaMK1D), a genetic hot spot in type 2 diabetes, is activated upon ghrelin stimulation and acts in AgRP/NPY neurons to mediate ghrelin-dependent food intake. Global Camk1d-knockout male mice are resistant to ghrelin, gain less body weight and are protected against high-fat-diet-induced obesity. Deletion of Camk1d in AgRP/NPY, but not in POMC, neurons is sufficient to recapitulate above phenotypes. In response to ghrelin, lack of CaMK1D attenuates phosphorylation of CREB and CREB-dependent expression of the orexigenic neuropeptides AgRP/NPY in fibre projections to the paraventricular nucleus (PVN). Hence, CaMK1D links ghrelin action to transcriptional control of orexigenic neuropeptide availability in AgRP neurons.

Indexed as

Diabetes Mellitus, Type 2GhrelinAgouti-Related ProteinAnimalsCalcium-Calmodulin-Dependent Protein Kinase Type 1EatingMaleMiceMice, KnockoutNeuronsNeuropeptide YObesityAgouti-Related ProteinCalcium-Calmodulin-Dependent Protein Kinase Type 1Camk1d protein, mouseGhrelinNeuropeptide Y

Identifiers

PMID37277610
OpenAlexW4379390393

What OpenQuestion holds

Textmetadata
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.