Obestatin: canonical and unexpected functions

dc.contributor.authorSantos Zas, Icía
dc.contributor.authorGurriarán Rodríguez, Uxía
dc.contributor.authorCid Díaz, Tania
dc.contributor.authorLeal López, Saúl
dc.contributor.authorCasanueva Freijo, Felipe
dc.contributor.authorPazos Randulfe, Yolanda
dc.contributor.authorPérez Camiña, Jesús
dc.date.accessioned2026-04-20T11:57:44Z
dc.date.available2026-04-20T11:57:44Z
dc.date.issued2026-03-05
dc.description.abstractThe functions of appetite-regulating hormones have been studied for decades with the aim of finding a solution to the problem of obesity. Among these molecules, a small peptide called obestatin has emerged as an anorexigenic hormone, with an antagonistic effect to the hunger hormone ghrelin. After years of controversy regarding its function in food intake and the establishment of its receptor, GPR39, obestatin is currently being proposed as a powerful therapeutic candidate for pathologies associated with skeletal muscle. Several studies have demonstrated its key role as a regulatory peptide in myogenesis, thereby increasing regeneration in acute muscle damage. Obestatin promotes vascularization and reduces fibrosis in regenerated tissue, while also increasing muscle strength in muscle atrophy pathologies associated with glucocorticoid treatment and Duchenne muscular dystrophy. This review describes the main mechanisms and signaling pathways regulated by the obestatin peptide in muscle pathology.
dc.description.peerreviewedSI
dc.description.sponsorshipOpen Access funding provided thanks to the CRUE-CSIC agreement with Springer Nature. This work was supported by grants from Instituto de Salud Carlos III in co-financing with FEDER (ISCIIIFEDER; MINECO, Spain; PI21/01639, PI22/00155 and PI24/01602), La Caixa Foundation (LCF/BQ/PI22/11910038) and Axencia Galega de Innovación (Xunta de Galicia; IN607D-2023/04, IN607D-2024/05).
dc.identifier.citationSantos-Zas, I., Gurriaran-Rodriguez, U., Cid-Diaz, T., Leal-López, S., Casanueva, F., Pazos-Randulfe, Y., & P. Camiña, J. (2026) Obestatin: canonical and unexpected functions. Reviews in Endocrine and Metabolic Disorders. https://doi.org/10.1007/s11154-026-10021-0
dc.identifier.doi10.1007/s11154-026-10021-0
dc.identifier.essn1573-2606
dc.identifier.urihttps://hdl.handle.net/10347/46825
dc.journal.titleReviews in Endocrine and Metabolic Disorders
dc.language.isoeng
dc.page.final14
dc.page.initial1
dc.publisherSpringer
dc.relation.publisherversionhttps://doi.org/10.1007/s11154-026-10021-0
dc.rightsThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.
dc.rightsAttribution 4.0 Internationalen
dc.rights.accessRightsopen access
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectObestatin
dc.subjectGPR39
dc.subjectSkeletal muscle
dc.subjectAtrophy
dc.subjectWasting muscle
dc.titleObestatin: canonical and unexpected functions
dc.typejournal article
dc.type.hasVersionVoR
dspace.entity.typePublication
relation.isAuthorOfPublication97168138-a5c3-44f4-b4ea-71e3ef68a1bf
relation.isAuthorOfPublication.latestForDiscovery97168138-a5c3-44f4-b4ea-71e3ef68a1bf

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