GPR120 controls neonatal brown adipose tissue thermogenic induction.

Adaptive induction of thermogenesis in brown adipose tissue (BAT) is essential for the survival of mammals after birth. We herein show that G-coupled receptor protein-120 (GPR120) expression is dramatically induced after birth in mouse BAT. GPR120 expression in neonatal BAT is the highest among GPR1...

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Detalles Bibliográficos
Autores: Quesada-López T, Gavaldà-Navarro A, Morón-Ros S, Campderros L, Iglesias R, Giralt M, Villarroya F
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2019
País:España
Institución:Fundació Sant Joan de Déu
Repositorio:r-FSJD. Repositorio Institucional de Producción Científica de la Fundació Sant Joan de Déu
OAI Identifier:oai:fsjd.fundanetsuite.com:p16489
Acceso en línea:https://fsjd.fundanetsuite.com/Publicaciones/ProdCientif/PublicacionFrw.aspx?id=16489
Access Level:acceso abierto
Palabra clave:GPR120, brown adipose tissue, fibroblast growth factor-21, neonate, thermogenesis
Descripción
Sumario:Adaptive induction of thermogenesis in brown adipose tissue (BAT) is essential for the survival of mammals after birth. We herein show that G-coupled receptor protein-120 (GPR120) expression is dramatically induced after birth in mouse BAT. GPR120 expression in neonatal BAT is the highest among GPR120-expressing tissues in mouse at any developmental stage tested. The induction of GPR120 in neonatal BAT is caused by the postnatal thermal stress rather than by the initiation of suckling. GPR120-null neonates were found to be relatively intolerant to cold: close to one-third did not survive at 21C, but all such pups survived at 25C. Heat production in BAT was significantly impaired in GPR120-null pups. Deficiency in GPR120 did not modify brown adipocyte morphology or the anatomical architecture of BAT, as assessed by electron microscopy, but instead impaired the expression of UCP1 and the fatty acid oxidation capacity of neonatal BAT. Moreover, GPR120 deficiency impaired FGF21 gene expression in BAT and reduced plasma FGF21 levels. These results indicate that GPR120 is essential for neonatal adaptive thermogenesis through the control of the FGF21 system.