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dc.contributor.author | Seoane Collazo, Patricia |
dc.contributor.author | Rial Pensado, Eva |
dc.contributor.author | Estévez Salguero, Ánxela María |
dc.contributor.author | Milbank, Edward |
dc.contributor.author | García Caballero, Lucía |
dc.contributor.author | Ríos García, Marcos |
dc.contributor.author | Liñares Pose, Laura |
dc.contributor.author | Scotece, Morena |
dc.contributor.author | Gallego Gómez, María Rosalía |
dc.contributor.author | Fernández-Real, Jose Manuel |
dc.contributor.author | Nogueiras Pozo, Rubén |
dc.contributor.author | Diéguez González, Carlos |
dc.contributor.author | Gualillo, Oreste |
dc.contributor.author | López Pérez, Miguel Antonio |
dc.date.accessioned | 2022-08-24T11:49:10Z |
dc.date.available | 2022-08-24T11:49:10Z |
dc.date.issued | 2021 |
dc.identifier.citation | Arthritis & Rheumatology 74, 2, 2022, 212–222. https://doi.org/10.1002/art.41950 |
dc.identifier.uri | http://hdl.handle.net/10347/29137 |
dc.description.abstract | Objective: To investigate whether thermogenesis and the hypothalamus may be involved in the physiopathology of experimental arthritis (EA). Methods: EA was induced in male Lewis rats by intradermal injection of Freund's complete adjuvant (CFA). Food intake, body weight, plasma cytokines, thermographic analysis, gene and protein expression of thermogenic markers in brown adipose tissue (BAT) and white adipose tissue (WAT), and hypothalamic AMP-activated protein kinase (AMPK) were analyzed. Virogenetic activation of hypothalamic AMPK was performed. Results: We first demonstrated that EA was associated with increased BAT thermogenesis and browning of subcutaneous WAT leading to elevated energy expenditure. Moreover, rats experiencing EA showed inhibition of hypothalamic AMPK, a canonical energy sensor modulating energy homeostasis at the central level. Notably, specific genetic activation of AMPK in the ventromedial nucleus of the hypothalamus (a key site modulating energy metabolism) reversed the effect of EA on energy balance, brown fat, and browning, as well as promoting amelioration of synovial inflammation in experimental arthritis. Conclusion: Overall, these data indicate that EA promotes a central catabolic state that can be targeted and reversed by the activation of hypothalamic AMPK. This might provide new therapeutic alternatives to treat rheumatoid arthritis (RA)–associated metabolic comorbidities, improving the overall prognosis in patients with RA |
dc.description.sponsorship | The Centro Singular de Investigación en Medicina Molecular y Enfermedades Crónicas (CiMUS) is supported by the Xunta de Galicia (2016-2019, ED431G/05). The Centro de Investigación Biomédica en Red Fisiopatología de la Obesidad y Nutrición (CIBERobn) is an initiative of the Instituto de Salud Carlos III. Supported by the Xunta de Galicia (grants 2016-PG057 to Dr. Nogueiras, GPC IN607B2019/10 to Dr. Gualillo, and 2016-PG068 to Dr. López), the Ministerio de Economía y Competitividad (MINECO) co-funded by the FEDER Program of the European Union (grants BFU2017-90578-REDT/Adipoplast to Drs. Fernández-Real and López, RTI2018-099413-B-I00 to Dr. Nogueiras, BFU2017-87721-P to Dr. Diéguez, and RTI2018-101840-B-I00 to Dr. López), the Instituto de Salud Carlos III (grants PI15–01934 and PI18/0102224 to Dr. Fernández-Real and PI17/00409, PI20/00902, RD21/0002/0025, and RD16/0012/0014 to Dr. Gualillo), “la Caixa” Foundation (ID 100010434) (grant LCF/PR/HR19/52160022 to Dr. López), and the European Research Council (synergy grant-2019-WATCH- 810331 to Dr. Nogueiras). Dr. Seoane-Collazo's work was supported by the Xunta de Galicia (fellowship ED481B 2018/050) and the Horizon 2020 Research and Innovation Program of the European Union under the Marie Sklodowska-Curie actions. Drs. Nogueiras and López's work was supported in part by the Atresmedia Corporación. Dr. Nogueiras's work was supported in part by Fundación BBVA and the European Foundation for the Study of Diabetes. Dr. Gualillo's work was supported in part by the Horizon 2020 Research and Innovation Program of the European Union under the Marie Sklodowska-Curie actions (project no. 734899) and by the Xunta de Galicia through a research staff contract (ISCIII/SERGAS) |
dc.language.iso | eng |
dc.publisher | Wiley |
dc.rights | © 2021 The Authors. Arthritis & Rheumatology published by Wiley Periodicals LLC on behalf of American College of Rheumatology. This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made |
dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/4.0/ |
dc.title | Activation of hypothalamic AMP-activated protein kinase ameliorates metabolic complications of experimental arthritis |
dc.type | journal article |
dc.identifier.doi | 10.1002/art.41950 |
dc.relation.publisherversion | https://doi.org/10.1002/art.41950 |
dc.type.hasVersion | VoR |
dc.identifier.essn | 2326-5205 |
dc.rights.accessRights | open access |
dc.contributor.affiliation | Universidade de Santiago de Compostela. Centro de Investigación en Medicina Molecular e Enfermidades Crónicas |
dc.contributor.affiliation | Universidade de Santiago de Compostela. Departamento de Ciencias Morfolóxicas |
dc.contributor.affiliation | Universidade de Santiago de Compostela. Departamento de Fisioloxía |
dc.description.peerreviewed | SI |
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© 2021 The Authors. Arthritis & Rheumatology published by Wiley Periodicals LLC on behalf of American College of Rheumatology. This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made
© 2021 The Authors. Arthritis & Rheumatology published by Wiley Periodicals LLC on behalf of American College of Rheumatology. This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made