Low protein-induced increases in FGF21 drive UCP1-dependent metabolic but not thermoregulatory endpoints

Abstract Dietary protein restriction increases adipose tissue uncoupling protein 1 (UCP1), energy expenditure and food intake, and these effects require the metabolic hormone fibroblast growth factor 21 (FGF21). Here we test whether the induction of energy expenditure during protein restriction requ...

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Autores principales:	Cristal M. Hill, Thomas Laeger, Diana C. Albarado, David H. McDougal, Hans-Rudolf Berthoud, Heike Münzberg, Christopher D. Morrison
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/4f8959552de94e438407d316dc830a05
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spelling	oai:doaj.org-article:4f8959552de94e438407d316dc830a052021-12-02T16:06:06ZLow protein-induced increases in FGF21 drive UCP1-dependent metabolic but not thermoregulatory endpoints10.1038/s41598-017-07498-w2045-2322https://doaj.org/article/4f8959552de94e438407d316dc830a052017-08-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-07498-whttps://doaj.org/toc/2045-2322Abstract Dietary protein restriction increases adipose tissue uncoupling protein 1 (UCP1), energy expenditure and food intake, and these effects require the metabolic hormone fibroblast growth factor 21 (FGF21). Here we test whether the induction of energy expenditure during protein restriction requires UCP1, promotes a resistance to cold stress, and is dependent on the concomitant hyperphagia. Wildtype, Ucp1-KO and Fgf21-KO mice were placed on control and low protein (LP) diets to assess changes in energy expenditure, food intake and other metabolic endpoints. Deletion of Ucp1 blocked LP-induced increases in energy expenditure and food intake, and exacerbated LP-induced weight loss. While LP diet increased energy expenditure and Ucp1 expression in an FGF21-dependent manner, neither LP diet nor the deletion of Fgf21 influenced sensitivity to acute cold stress. Finally, LP-induced energy expenditure occurred even in the absence of hyperphagia. Increased energy expenditure is a primary metabolic effect of dietary protein restriction, and requires both UCP1 and FGF21 but is independent of changes in food intake. However, the FGF21-dependent increase in UCP1 and energy expenditure by LP has no effect on the ability to acutely respond to cold stress, suggesting that LP-induced increases in FGF21 impact metabolic but not thermogenic endpoints.Cristal M. HillThomas LaegerDiana C. AlbaradoDavid H. McDougalHans-Rudolf BerthoudHeike MünzbergChristopher D. MorrisonNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-11 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Cristal M. Hill Thomas Laeger Diana C. Albarado David H. McDougal Hans-Rudolf Berthoud Heike Münzberg Christopher D. Morrison Low protein-induced increases in FGF21 drive UCP1-dependent metabolic but not thermoregulatory endpoints
description	Abstract Dietary protein restriction increases adipose tissue uncoupling protein 1 (UCP1), energy expenditure and food intake, and these effects require the metabolic hormone fibroblast growth factor 21 (FGF21). Here we test whether the induction of energy expenditure during protein restriction requires UCP1, promotes a resistance to cold stress, and is dependent on the concomitant hyperphagia. Wildtype, Ucp1-KO and Fgf21-KO mice were placed on control and low protein (LP) diets to assess changes in energy expenditure, food intake and other metabolic endpoints. Deletion of Ucp1 blocked LP-induced increases in energy expenditure and food intake, and exacerbated LP-induced weight loss. While LP diet increased energy expenditure and Ucp1 expression in an FGF21-dependent manner, neither LP diet nor the deletion of Fgf21 influenced sensitivity to acute cold stress. Finally, LP-induced energy expenditure occurred even in the absence of hyperphagia. Increased energy expenditure is a primary metabolic effect of dietary protein restriction, and requires both UCP1 and FGF21 but is independent of changes in food intake. However, the FGF21-dependent increase in UCP1 and energy expenditure by LP has no effect on the ability to acutely respond to cold stress, suggesting that LP-induced increases in FGF21 impact metabolic but not thermogenic endpoints.
format	article
author	Cristal M. Hill Thomas Laeger Diana C. Albarado David H. McDougal Hans-Rudolf Berthoud Heike Münzberg Christopher D. Morrison
author_facet	Cristal M. Hill Thomas Laeger Diana C. Albarado David H. McDougal Hans-Rudolf Berthoud Heike Münzberg Christopher D. Morrison
author_sort	Cristal M. Hill
title	Low protein-induced increases in FGF21 drive UCP1-dependent metabolic but not thermoregulatory endpoints
title_short	Low protein-induced increases in FGF21 drive UCP1-dependent metabolic but not thermoregulatory endpoints
title_full	Low protein-induced increases in FGF21 drive UCP1-dependent metabolic but not thermoregulatory endpoints
title_fullStr	Low protein-induced increases in FGF21 drive UCP1-dependent metabolic but not thermoregulatory endpoints
title_full_unstemmed	Low protein-induced increases in FGF21 drive UCP1-dependent metabolic but not thermoregulatory endpoints
title_sort	low protein-induced increases in fgf21 drive ucp1-dependent metabolic but not thermoregulatory endpoints
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/4f8959552de94e438407d316dc830a05
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Low protein-induced increases in FGF21 drive UCP1-dependent metabolic but not thermoregulatory endpoints

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