Articles producció científica> Medicina i Cirurgia

SUCNR1 signaling in adipocytes controls energy metabolism by modulating circadian clock and leptin expression

  • Dades identificatives

    Identificador: imarina:9295186
    Autors:
    Villanueva-Carmona, TCedó, LMadeira, ACeperuelo-Mallafré, VRodríguez-Peña, MMNúñez-Roa, CMaymó-Masip, ERepollés-de-Dalmau, MBadia, JKeiran, NMirasierra, MPimenta-Lopes, CSabadell-Basallote, JBosch, RCaubet, LEscolà-Gil, JCFernández-Real, JMVilarrasa, NVentura, FVallejo, MVendrell, JFernández-Veledo, S
    Resum:
    Adipose tissue modulates energy homeostasis by secreting leptin, but little is known about the factors governing leptin production. We show that succinate, long perceived as a mediator of immune response and lipolysis, controls leptin expression via its receptor SUCNR1. Adipocyte-specific deletion of Sucnr1 influences metabolic health according to nutritional status. Adipocyte Sucnr1 deficiency impairs leptin response to feeding, whereas oral succinate mimics nutrient-related leptin dynamics via SUCNR1. SUCNR1 activation controls leptin expression via the circadian clock in an AMPK/JNK-C/EBPα-dependent manner. Although the anti-lipolytic role of SUCNR1 prevails in obesity, its function as a regulator of leptin signaling contributes to the metabolically favorable phenotype in adipocyte-specific Sucnr1 knockout mice under standard dietary conditions. Obesity-associated hyperleptinemia in humans is linked to SUCNR1 overexpression in adipocytes, which emerges as the major predictor of adipose tissue leptin expression. Our study establishes the succinate/SUCNR1 axis as a metabolite-sensing pathway mediating nutrient-related leptin dynamics to control whole-body homeostasis.Copyright © 2023 Elsevier Inc. All rights reserved.
  • Altres:

    Autor segons l'article: Villanueva-Carmona, T; Cedó, L; Madeira, A; Ceperuelo-Mallafré, V; Rodríguez-Peña, MM; Núñez-Roa, C; Maymó-Masip, E; Repollés-de-Dalmau, M; Badia, J; Keiran, N; Mirasierra, M; Pimenta-Lopes, C; Sabadell-Basallote, J; Bosch, R; Caubet, L; Escolà-Gil, JC; Fernández-Real, JM; Vilarrasa, N; Ventura, F; Vallejo, M; Vendrell, J; Fernández-Veledo, S
    Departament: Bioquímica i Biotecnologia Medicina i Cirurgia Ciències Mèdiques Bàsiques
    Autor/s de la URV: Badia Aparicio, José María / Bosch Príncep, Ramon / CEDÓ GINÉ, LÍDIA / Ceperuelo Mallafré, Maria Victoria / Fernandez Veledo, Sonia / Keiran Fernandez, Noelia Elisabeth / Maymo Masip, Elsa / RODRIGUEZ PEÑA, MARIA DEL MAR / Vendrell Ortega, Juan José / Villanueva Carmona, Teresa
    Paraules clau: Sucnr1 Succinate Obesity Metabolite Metabolism Leptin Gpcr Circadian clock Adipose tissue Adipocyte Activated protein-kinase succinate stem-cells plasma leptin ob gene glucose-uptake gene-expression food-intake bone-formation ampk activation
    Resum: Adipose tissue modulates energy homeostasis by secreting leptin, but little is known about the factors governing leptin production. We show that succinate, long perceived as a mediator of immune response and lipolysis, controls leptin expression via its receptor SUCNR1. Adipocyte-specific deletion of Sucnr1 influences metabolic health according to nutritional status. Adipocyte Sucnr1 deficiency impairs leptin response to feeding, whereas oral succinate mimics nutrient-related leptin dynamics via SUCNR1. SUCNR1 activation controls leptin expression via the circadian clock in an AMPK/JNK-C/EBPα-dependent manner. Although the anti-lipolytic role of SUCNR1 prevails in obesity, its function as a regulator of leptin signaling contributes to the metabolically favorable phenotype in adipocyte-specific Sucnr1 knockout mice under standard dietary conditions. Obesity-associated hyperleptinemia in humans is linked to SUCNR1 overexpression in adipocytes, which emerges as the major predictor of adipose tissue leptin expression. Our study establishes the succinate/SUCNR1 axis as a metabolite-sensing pathway mediating nutrient-related leptin dynamics to control whole-body homeostasis.Copyright © 2023 Elsevier Inc. All rights reserved.
    Àrees temàtiques: Physiology Odontología Molecular biology Medicina ii Medicina i Interdisciplinar General medicine Endocrinology & metabolism Educação física Ciências biológicas ii Ciências biológicas i Cell biology
    Accès a la llicència d'ús: https://creativecommons.org/licenses/by/3.0/es/
    Adreça de correu electrònic de l'autor: josepmaria.badia@urv.cat sonia.fernandez@urv.cat teresa.villanueva@urv.cat ramon.bosch@urv.cat elsa.maymo@urv.cat victoria.ceperuelo@urv.cat ramon.bosch@urv.cat josepmaria.badia@urv.cat josepmaria.badia@urv.cat teresa.villanueva@urv.cat juanjose.vendrell@urv.cat
    Identificador de l'autor: 0000-0003-2906-3788 0000-0002-9133-3120 0000-0002-4460-9761 0000-0002-6994-6115
    Data d'alta del registre: 2024-08-31
    Versió de l'article dipositat: info:eu-repo/semantics/acceptedVersion
    Enllaç font original: https://www.cell.com/cell-metabolism/fulltext/S1550-4131(23)00082-7?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS1550413123000827%3Fshowall%3Dtrue
    URL Document de llicència: https://repositori.urv.cat/ca/proteccio-de-dades/
    Referència a l'article segons font original: Cell Metabolism. 35 (4): 601-619.e10
    Referència de l'ítem segons les normes APA: Villanueva-Carmona, T; Cedó, L; Madeira, A; Ceperuelo-Mallafré, V; Rodríguez-Peña, MM; Núñez-Roa, C; Maymó-Masip, E; Repollés-de-Dalmau, M; Badia, J; (2023). SUCNR1 signaling in adipocytes controls energy metabolism by modulating circadian clock and leptin expression. Cell Metabolism, 35(4), 601-619.e10. DOI: 10.1016/j.cmet.2023.03.004
    DOI de l'article: 10.1016/j.cmet.2023.03.004
    Entitat: Universitat Rovira i Virgili
    Any de publicació de la revista: 2023
    Tipus de publicació: Journal Publications
  • Paraules clau:

    Cell Biology,Endocrinology & Metabolism,Molecular Biology,Physiology
    Sucnr1
    Succinate
    Obesity
    Metabolite
    Metabolism
    Leptin
    Gpcr
    Circadian clock
    Adipose tissue
    Adipocyte
    Activated protein-kinase
    succinate
    stem-cells
    plasma leptin
    ob gene
    glucose-uptake
    gene-expression
    food-intake
    bone-formation
    ampk activation
    Physiology
    Odontología
    Molecular biology
    Medicina ii
    Medicina i
    Interdisciplinar
    General medicine
    Endocrinology & metabolism
    Educação física
    Ciências biológicas ii
    Ciências biológicas i
    Cell biology
  • Documents:

  • Cerca a google

    Search to google scholar