Evidence map›Paper›PMID 30143607›Full record

ArticleNature communications2018

p53 in AgRP neurons is required for protection against diet-induced obesity via JNK1.

Mar Quiñones, Omar Al-Massadi, Cintia Folgueira, Stephan Bremser, Rosalía Gallego, Leonardo Torres-Leal, Roberta Haddad-Tóvolli, Cristina García-Caceres, Rene Hernandez-Bautista, Brian Y H Lam and 19 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
4.0field-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

36 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Primary cilia dysfunction: A critical driver of metabolic diseases (Review).International journal of molecular medicine · 2026
    Review
  5. Article
  6. Article
  7. Review
  8. Attack of the kinases: JNK signaling in metabolism.American journal of physiology. Regulatory, integrative and comparative physiology · 2026
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Ghrelin regulating liver activity and its potential effects on liver fibrosis andFrontiers in cellular and infection microbiology · 2023
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

29 authors at 8 institutions in 4 countries.

Mar QuiñonesDepartment of Physiology, CIMUS, University of Santiago de Compostela-Instituto de Investigación Sanitaria, 15782, Santiago de Compostela, Spain.
Omar Al-MassadiDepartment of Physiology, CIMUS, University of Santiago de Compostela-Instituto de Investigación Sanitaria, 15782, Santiago de Compostela, Spain.
Cintia FolgueiraDepartment of Physiology, CIMUS, University of Santiago de Compostela-Instituto de Investigación Sanitaria, 15782, Santiago de Compostela, Spain.
Stephan BremserBiocenter, Institute for Zoology, University of Cologne, 50923, Cologne, Germany.
Rosalía GallegoDepartment of Morphological Sciences, School of Medicine, University of Santiago de Compostela-Instituto de Investigación Sanitaria, 15782, Santiago de Compostela, Spain.
Leonardo Torres-LealDepartment of Physiology, CIMUS, University of Santiago de Compostela-Instituto de Investigación Sanitaria, 15782, Santiago de Compostela, Spain.
Roberta Haddad-TóvolliNeuronal Control of Metabolism (NeuCoMe) Laboratory, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), 08036, Barcelona, Spain.
Cristina García-CaceresInstitute for Diabetes and Obesity, Helmholtz Diabetes Center, Helmholtz Zentrum München, 85764, Neuherberg, Germany.
Rene Hernandez-BautistaDepartment of Physiology, CIMUS, University of Santiago de Compostela-Instituto de Investigación Sanitaria, 15782, Santiago de Compostela, Spain.
Brian Y H LamMRC Metabolic Diseases Unit, University of Cambridge Metabolic Research Laboratories, Wellcome Trust-MRC Institute of Metabolic Science, Addenbrooke's Hospital, Cambridge, CB2 0QQ, UK.
Daniel BeiroaDepartment of Physiology, CIMUS, University of Santiago de Compostela-Instituto de Investigación Sanitaria, 15782, Santiago de Compostela, Spain.
Estrella Sanchez-RebordeloDepartment of Physiology, CIMUS, University of Santiago de Compostela-Instituto de Investigación Sanitaria, 15782, Santiago de Compostela, Spain.
Ana SenraDepartment of Physiology, CIMUS, University of Santiago de Compostela-Instituto de Investigación Sanitaria, 15782, Santiago de Compostela, Spain.
Jose A MalagonDepartment of Physiology, CIMUS, University of Santiago de Compostela-Instituto de Investigación Sanitaria, 15782, Santiago de Compostela, Spain.
Patricia ValerioDepartment of Physiology, CIMUS, University of Santiago de Compostela-Instituto de Investigación Sanitaria, 15782, Santiago de Compostela, Spain.
Marcos F FondevilaDepartment of Physiology, CIMUS, University of Santiago de Compostela-Instituto de Investigación Sanitaria, 15782, Santiago de Compostela, Spain.
Johan FernøKG Jebsen Center for Diabetes Research, Department of Clinical Science, University of Bergen, 5007, Bergen, Norway.
Maria M MalagonCIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn), 15706, Santiago de Compostela, Spain.
Raian ContrerasInstitute for Diabetes and Obesity, Helmholtz Diabetes Center, Helmholtz Zentrum München, 85764, Neuherberg, Germany.
Paul PflugerInstitute for Diabetes and Obesity, Helmholtz Diabetes Center, Helmholtz Zentrum München, 85764, Neuherberg, Germany.ORCID http://orcid.org/0000-0002-8118-7588
Jens C BrüningDepartment of Mouse Genetics and Metabolism, Institute for Genetics and Center for Molecular Medicine (CMMC), University of Cologne, Zülpicher Strasse 47b, 50674, Cologne, Germany.
Giles YeoMRC Metabolic Diseases Unit, University of Cambridge Metabolic Research Laboratories, Wellcome Trust-MRC Institute of Metabolic Science, Addenbrooke's Hospital, Cambridge, CB2 0QQ, UK.
Matthias TschöpInstitute for Diabetes and Obesity, Helmholtz Diabetes Center, Helmholtz Zentrum München, 85764, Neuherberg, Germany.
Carlos DiéguezDepartment of Physiology, CIMUS, University of Santiago de Compostela-Instituto de Investigación Sanitaria, 15782, Santiago de Compostela, Spain.
Miguel LópezDepartment of Physiology, CIMUS, University of Santiago de Compostela-Instituto de Investigación Sanitaria, 15782, Santiago de Compostela, Spain.
Marc ClaretNeuronal Control of Metabolism (NeuCoMe) Laboratory, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), 08036, Barcelona, Spain.
Peter KloppenburgBiocenter, Institute for Zoology, University of Cologne, 50923, Cologne, Germany.
Guadalupe SabioFundación Centro Nacional de Investigaciones Cardiovasculares Carlos III, 28029, Madrid, Spain.
Ruben NogueirasDepartment of Physiology, CIMUS, University of Santiago de Compostela-Instituto de Investigación Sanitaria, 15782, Santiago de Compostela, Spain. ruben.nogueiras@usc.es.ORCID http://orcid.org/0000-0002-9976-9930
Universidade de Santiago de Compostela · ESHelmholtz Zentrum München · DEUniversity of Cologne · DECentro de Investigación Biomédica en Red Diabetes y Enfermedades Metabólicas Asociadas · ESUniversity of Cambridge · GBHaukeland University Hospital · NOInstituto Maimónides de Investigación Biomédica de Córdoba · ESSpanish National Centre for Cardiovascular Research · ES

Funding

Medical Research Council MC_UU_12012/1Medical Research Council MC_UU_12012/5Ministry of Economy and Competitiveness | Consejo Superior de Investigaciones Científicas (Spanish National Research Council) BFU2015-70664RNIMHD NIH HHS L60 MD003733
6 · The paper itself

Abstract

p53 is a well-known tumor suppressor that has emerged as an important player in energy balance. However, its metabolic role in the hypothalamus remains unknown. Herein, we show that mice lacking p53 in agouti-related peptide (AgRP), but not proopiomelanocortin (POMC) or steroidogenic factor-1 (SF1) neurons, are more prone to develop diet-induced obesity and show reduced brown adipose tissue (BAT) thermogenic activity. AgRP-specific ablation of p53 resulted in increased hypothalamic c-Jun N-terminal kinase (JNK) activity before the mice developed obesity, and central inhibition of JNK reversed the obese phenotype of these mice. The overexpression of p53 in the ARC or specifically in AgRP neurons of obese mice decreased body weight and stimulated BAT thermogenesis, resulting in body weight loss. Finally, p53 in AgRP neurons regulates the ghrelin-induced food intake and body weight. Overall, our findings provide evidence that p53 in AgRP neurons is required for normal adaptations against diet-induced obesity.

Indexed as

Adipose Tissue, BrownAgouti-Related ProteinAnimalsDietHypothalamusMaleMiceMice, Inbred C57BLMitogen-Activated Protein Kinase 8NeuronsObesityPro-OpiomelanocortinRats, Sprague-DawleySteroidogenic Factor 1Tumor Suppressor Protein p53Agouti-Related ProteinMitogen-Activated Protein Kinase 8Pro-OpiomelanocortinSteroidogenic Factor 1steroidogenic factor 1, mouseTumor Suppressor Protein p53

Identifiers

PMID30143607
PMCPMC6109113
OpenAlexW2888053157

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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.