Evidence map›Paper›PMID 31530579›Full record

ArticleDiabetes2019

MCH Regulates SIRT1/FoxO1 and Reduces POMC Neuronal Activity to Induce Hyperphagia, Adiposity, and Glucose Intolerance.

Omar Al-Massadi, Mar Quiñones, Jerome Clasadonte, René Hernandez-Bautista, Amparo Romero-Picó, Cintia Folgueira, Donald A Morgan, Imre Kalló, Violeta Heras, Ana Senra and 18 more

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

25 citing papers in PubMed, 41 citations in OpenAlex.

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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

28 authors at 8 institutions in 5 countries.

Omar Al-MassadiDepartment of Physiology, CIMUS, Universidad de Santiago de Compostela-Instituto de Investigación Sanitaria, Santiago de Compostela, Spain.
Mar QuiñonesDepartment of Physiology, CIMUS, Universidad de Santiago de Compostela-Instituto de Investigación Sanitaria, Santiago de Compostela, Spain.
Jerome ClasadonteINSERM, U1172, Laboratory of Development and Plasticity of the Neuroendocrine Brain, Jean-Pierre Aubert Research Center, Lille, France.
René Hernandez-BautistaDepartment of Physiology, CIMUS, Universidad de Santiago de Compostela-Instituto de Investigación Sanitaria, Santiago de Compostela, Spain.
Amparo Romero-PicóDepartment of Physiology, CIMUS, Universidad de Santiago de Compostela-Instituto de Investigación Sanitaria, Santiago de Compostela, Spain.
Cintia FolgueiraDepartment of Physiology, CIMUS, Universidad de Santiago de Compostela-Instituto de Investigación Sanitaria, Santiago de Compostela, Spain.
Donald A MorganDepartment of Pharmacology, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, and Iowa City VA Health Care System, Iowa City, IA.
Imre KallóLaboratory of Endocrine Neurobiology, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest, Hungary.
Violeta HerasDepartment of Physiology, CIMUS, Universidad de Santiago de Compostela-Instituto de Investigación Sanitaria, Santiago de Compostela, Spain.
Ana SenraDepartment of Physiology, CIMUS, Universidad de Santiago de Compostela-Instituto de Investigación Sanitaria, Santiago de Compostela, Spain.
Samuel C FunderburkDiabetes, Endocrinology, and Obesity Branch, National Institutes of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD.
Michael J KrashesDiabetes, Endocrinology, and Obesity Branch, National Institutes of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD.
Yara SoutoDepartment of Physiology, CIMUS, Universidad de Santiago de Compostela-Instituto de Investigación Sanitaria, Santiago de Compostela, Spain.
Miguel FidalgoDepartment of Physiology, CIMUS, Universidad de Santiago de Compostela-Instituto de Investigación Sanitaria, Santiago de Compostela, Spain.
Serge LuquetUnité de Biologie Fonctionnelle et Adaptative, CNRS UMR 8251, Université Paris Diderot, Sorbonne Paris Cité, Paris, France.
Melissa J CheeDivision of Endocrinology, Beth Israel Deaconess Medical Center, Department of Medicine, Harvard Medical School, Boston, MA.
Monica ImbernonDepartment of Physiology, CIMUS, Universidad de Santiago de Compostela-Instituto de Investigación Sanitaria, Santiago de Compostela, Spain.
Daniel BeiroaDepartment of Physiology, CIMUS, Universidad de Santiago de Compostela-Instituto de Investigación Sanitaria, Santiago de Compostela, Spain.
Lucía García-CaballeroDepartment of Morphological Sciences, School of Medicine, Universidad de Santiago de Compostela-Instituto de Investigación Sanitaria, Santiago de Compostela, Spain.
Rosalia GallegoDepartment of Morphological Sciences, School of Medicine, Universidad de Santiago de Compostela-Instituto de Investigación Sanitaria, Santiago de Compostela, Spain.
Brian Y H LamMRC Metabolic Diseases Unit, Wellcome-MRC Institute of Metabolic Science-Metabolic Research Laboratories, University of Cambridge, and Addenbrooke's Hospital, Cambridge, U.K.
Giles YeoMRC Metabolic Diseases Unit, Wellcome-MRC Institute of Metabolic Science-Metabolic Research Laboratories, University of Cambridge, and Addenbrooke's Hospital, Cambridge, U.K.
Miguel LopezDepartment of Physiology, CIMUS, Universidad de Santiago de Compostela-Instituto de Investigación Sanitaria, Santiago de Compostela, Spain.ORCID 0000-0002-7823-1648
Zsolt LipositsLaboratory of Endocrine Neurobiology, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest, Hungary.
Kamal RahmouniDepartment of Pharmacology, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, and Iowa City VA Health Care System, Iowa City, IA.ORCID 0000-0001-5136-6748
Vincent PrevotINSERM, U1172, Laboratory of Development and Plasticity of the Neuroendocrine Brain, Jean-Pierre Aubert Research Center, Lille, France.
Carlos DieguezDepartment of Physiology, CIMUS, Universidad de Santiago de Compostela-Instituto de Investigación Sanitaria, Santiago de Compostela, Spain carlos.dieguez@usc.es ruben.nogueiras@usc.es.ORCID 0000-0002-0919-4337
Ruben NogueirasDepartment of Physiology, CIMUS, Universidad de Santiago de Compostela-Instituto de Investigación Sanitaria, Santiago de Compostela, Spain carlos.dieguez@usc.es ruben.nogueiras@usc.es.ORCID 0000-0002-9976-9930
Universidade de Santiago de Compostela · ESInserm · FRCentre National de la Recherche Scientifique · FRHUN-REN Institute of Experimental Medicine · HUNational Institutes of Health · USUniversity of Iowa · USWellcome/MRC Institute of Metabolic Science · GBBeth Israel Deaconess Medical Center · US

Funding

Role of the brain Renin-Angiotensin Sys. in Cardiovas and Metabolic RegulationP01HL084207 · NHLBI · UNIVERSITY OF IOWA · PI GROBE, JUSTIN L · 2007 to 2022
$30.2M
Neuronal Mechanisms of Obesity-Induced HypertensionI01BX004249 · VA · IOWA CITY VA MEDICAL CENTER · PI KAMAL RAHMOUNI · 2019 to 2026
–
BLRD VA I01 BX004249Medical Research Council MC_UU_00014/5Medical Research Council MC_UU_12012/5NHLBI NIH HHS P01 HL084207
6 · The paper itself

Abstract

Melanin-concentrating hormone (MCH) is an important regulator of food intake, glucose metabolism, and adiposity. However, the mechanisms mediating these actions remain largely unknown. We used pharmacological and genetic approaches to show that the sirtuin 1 (SIRT1)/FoxO1 signaling pathway in the hypothalamic arcuate nucleus (ARC) mediates MCH-induced feeding, adiposity, and glucose intolerance. MCH reduces proopiomelanocortin (POMC) neuronal activity, and the SIRT1/FoxO1 pathway regulates the inhibitory effect of MCH on POMC expression. Remarkably, the metabolic actions of MCH are compromised in mice lacking SIRT1 specifically in POMC neurons. Of note, the actions of MCH are independent of agouti-related peptide (AgRP) neurons because inhibition of γ-aminobutyric acid receptor in the ARC did not prevent the orexigenic action of MCH, and the hypophagic effect of MCH silencing was maintained after chemogenetic stimulation of AgRP neurons. Central SIRT1 is required for MCH-induced weight gain through its actions on the sympathetic nervous system. The central MCH knockdown causes hypophagia and weight loss in diet-induced obese wild-type mice; however, these effects were abolished in mice overexpressing SIRT1 fed a high-fat diet. These data reveal the neuronal basis for the effects of MCH on food intake, body weight, and glucose metabolism and highlight the relevance of SIRT1/FoxO1 pathway in obesity.

Indexed as

AdiposityAnimalsForkhead Box Protein O1Glucose IntoleranceHyperphagiaHypothalamic HormonesHypothalamusMaleMelaninsMiceMice, KnockoutNeuronsPatch-Clamp TechniquesPituitary HormonesPro-OpiomelanocortinRats, Sprague-DawleyForkhead Box Protein O1Hypothalamic Hormonesmelanin-concentrating hormoneMelaninsPituitary HormonesPro-OpiomelanocortinSirtuin 1

Identifiers

PMID31530579
PMCPMC6868473
OpenAlexW2974898673

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.