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, Tania Paloma, Gavaldà i Navarro, Aleix, Morón-Ros, Samantha, Campderrós Traver, Laura, Iglesias Coll, María del Rosario, Giralt i Oms, Marta, Villarroya i Gombau, Francesc
Tipo de documento: artigo
Estado:Versión aceptada para publicación
Data de publicação:2019
País:España
Recursos:Universidad de Barcelona
Repositório:Dipòsit Digital de la UB
OAI Identifier:oai:diposit.ub.edu:2445/153987
Acesso em linha:https://hdl.handle.net/2445/153987
Access Level:Acceso aberto
Palavra-chave:Teixit adipós
Infants nadons
Adipose tissues
Newborn infants
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spelling GPR120 controls neonatal brown adipose tissue thermogenic inductionQuesada López, Tania PalomaGavaldà i Navarro, AleixMorón-Ros, SamanthaCampderrós Traver, LauraIglesias Coll, María del RosarioGiralt i Oms, MartaVillarroya i Gombau, FrancescTeixit adipósInfants nadonsAdipose tissuesNewborn infantsAdaptive 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 21ºC, but all such pups survived at 25ºC. 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.American Physiological Society2019info:eu-repo/semantics/articleinfo:eu-repo/semantics/acceptedVersionapplication/pdfhttps://hdl.handle.net/2445/153987Articles publicats en revistes (Bioquímica i Biomedicina Molecular)reponame:Dipòsit Digital de la UBinstname:Universidad de BarcelonaInglésVersió postprint del document publicat a: https://doi.org/10.1152/ajpendo.00081.2019American Journal of Physiology-Endocrinology and Metabolism, 2019, vol. 317, num. 5, p. 742-750https://doi.org/10.1152/ajpendo.00081.2019(c) American Physiological Society, 2019info:eu-repo/semantics/openAccessoai:diposit.ub.edu:2445/1539872026-05-27T06:46:51Z
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, Tania Paloma
Teixit adipós
Infants nadons
Adipose tissues
Newborn infants
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, Tania Paloma
Gavaldà i Navarro, Aleix
Morón-Ros, Samantha
Campderrós Traver, Laura
Iglesias Coll, María del Rosario
Giralt i Oms, Marta
Villarroya i Gombau, Francesc
author Quesada López, Tania Paloma
author_facet Quesada López, Tania Paloma
Gavaldà i Navarro, Aleix
Morón-Ros, Samantha
Campderrós Traver, Laura
Iglesias Coll, María del Rosario
Giralt i Oms, Marta
Villarroya i Gombau, Francesc
author_role author
author2 Gavaldà i Navarro, Aleix
Morón-Ros, Samantha
Campderrós Traver, Laura
Iglesias Coll, María del Rosario
Giralt i Oms, Marta
Villarroya i Gombau, Francesc
author2_role author
author
author
author
author
author
dc.subject.none.fl_str_mv Teixit adipós
Infants nadons
Adipose tissues
Newborn infants
topic Teixit adipós
Infants nadons
Adipose tissues
Newborn infants
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 21ºC, but all such pups survived at 25ºC. 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/acceptedVersion
format article
status_str acceptedVersion
dc.identifier.none.fl_str_mv https://hdl.handle.net/2445/153987
url https://hdl.handle.net/2445/153987
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.relation.none.fl_str_mv Versió postprint del document publicat a: https://doi.org/10.1152/ajpendo.00081.2019
American Journal of Physiology-Endocrinology and Metabolism, 2019, vol. 317, num. 5, p. 742-750
https://doi.org/10.1152/ajpendo.00081.2019
dc.rights.none.fl_str_mv (c) American Physiological Society, 2019
info:eu-repo/semantics/openAccess
rights_invalid_str_mv (c) American Physiological Society, 2019
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv American Physiological Society
publisher.none.fl_str_mv American Physiological Society
dc.source.none.fl_str_mv Articles publicats en revistes (Bioquímica i Biomedicina Molecular)
reponame:Dipòsit Digital de la UB
instname:Universidad de Barcelona
instname_str Universidad de Barcelona
reponame_str Dipòsit Digital de la UB
collection Dipòsit Digital de la UB
repository.name.fl_str_mv
repository.mail.fl_str_mv
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score 15,301603

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