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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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
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spelling GPR120 controls neonatal brown adipose tissue thermogenic induction.Quesada-López TGavaldà-Navarro AMorón-Ros SCampderros LIglesias RGiralt MVillarroya FGPR120, brown adipose tissue, fibroblast growth factor-21, neonate, thermogenesisAdaptive 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.AMER PHYSIOLOGICAL SOC2019info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttps://fsjd.fundanetsuite.com/Publicaciones/ProdCientif/PublicacionFrw.aspx?id=16489AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISMISSN: 01931849ISSNe: 15221555reponame:r-FSJD. Repositorio Institucional de Producción Científica de la Fundació Sant Joan de Déuinstname:Fundació Sant Joan de DéuInglésinfo:eu-repo/semantics/openAccessoai:fsjd.fundanetsuite.com:p164892026-05-27T12:37:41Z
dc.title.none.fl_str_mv GPR120 controls neonatal brown adipose tissue thermogenic induction.
title GPR120 controls neonatal brown adipose tissue thermogenic induction.
spellingShingle GPR120 controls neonatal brown adipose tissue thermogenic induction.
Quesada-López T
GPR120, brown adipose tissue, fibroblast growth factor-21, neonate, thermogenesis
title_short GPR120 controls neonatal brown adipose tissue thermogenic induction.
title_full GPR120 controls neonatal brown adipose tissue thermogenic induction.
title_fullStr GPR120 controls neonatal brown adipose tissue thermogenic induction.
title_full_unstemmed GPR120 controls neonatal brown adipose tissue thermogenic induction.
title_sort GPR120 controls neonatal brown adipose tissue thermogenic induction.
dc.creator.none.fl_str_mv Quesada-López T
Gavaldà-Navarro A
Morón-Ros S
Campderros L
Iglesias R
Giralt M
Villarroya F
author Quesada-López T
author_facet Quesada-López T
Gavaldà-Navarro A
Morón-Ros S
Campderros L
Iglesias R
Giralt M
Villarroya F
author_role author
author2 Gavaldà-Navarro A
Morón-Ros S
Campderros L
Iglesias R
Giralt M
Villarroya F
author2_role author
author
author
author
author
author
dc.subject.none.fl_str_mv GPR120, brown adipose tissue, fibroblast growth factor-21, neonate, thermogenesis
topic GPR120, brown adipose tissue, fibroblast growth factor-21, neonate, thermogenesis
description 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.
publishDate 2019
dc.date.none.fl_str_mv 2019
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv https://fsjd.fundanetsuite.com/Publicaciones/ProdCientif/PublicacionFrw.aspx?id=16489
url https://fsjd.fundanetsuite.com/Publicaciones/ProdCientif/PublicacionFrw.aspx?id=16489
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.publisher.none.fl_str_mv AMER PHYSIOLOGICAL SOC
publisher.none.fl_str_mv AMER PHYSIOLOGICAL SOC
dc.source.none.fl_str_mv AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
ISSN: 01931849
ISSNe: 15221555
reponame:r-FSJD. Repositorio Institucional de Producción Científica de la Fundació Sant Joan de Déu
instname:Fundació Sant Joan de Déu
instname_str Fundació Sant Joan de Déu
reponame_str r-FSJD. Repositorio Institucional de Producción Científica de la Fundació Sant Joan de Déu
collection r-FSJD. Repositorio Institucional de Producción Científica de la Fundació Sant Joan de Déu
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