RT Journal Article
T1 Obestatin: canonical and unexpected functions
A1 Santos Zas, Icía
A1 Gurriarán Rodríguez, Uxía
A1 Cid Díaz, Tania
A1 Leal López, Saúl
A1 Casanueva Freijo, Felipe
A1 Pazos Randulfe, Yolanda
A1 Pérez Camiña, Jesús
K1 Obestatin
K1 GPR39
K1 Skeletal muscle
K1 Atrophy
K1 Wasting muscle
AB The 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.
PB Springer
YR 2026
FD 2026-03-05
LK https://hdl.handle.net/10347/46825
UL https://hdl.handle.net/10347/46825
LA eng
NO Santos-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
NO Open 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).
DS Minerva
RD 24 abr 2026