Fructose reprogrammes glutamine-dependent oxidative metabolism to support LPS-induced inflammation

Myeloid cells are able to utilize a variety of monosaccharides from our diet, including fructose. Here the authors show that when monocytes are reliant on fructose as a carbon energy source they are reprogrammed towards oxidative metabolism, glutamine anaplerosis and a pro-inflammatory phenotype owi...

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Autores principales:	Nicholas Jones, Julianna Blagih, Fabio Zani, April Rees, David G. Hill, Benjamin J. Jenkins, Caroline J. Bull, Diana Moreira, Azari I. M. Bantan, James G. Cronin, Daniele Avancini, Gareth W. Jones, David K. Finlay, Karen H. Vousden, Emma E. Vincent, Catherine A. Thornton
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Science Q
Acceso en línea:	https://doaj.org/article/e704cf7cb7a0484a9ad0d96a44d08b6a
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spelling	oai:doaj.org-article:e704cf7cb7a0484a9ad0d96a44d08b6a2021-12-02T11:02:37ZFructose reprogrammes glutamine-dependent oxidative metabolism to support LPS-induced inflammation10.1038/s41467-021-21461-42041-1723https://doaj.org/article/e704cf7cb7a0484a9ad0d96a44d08b6a2021-02-01T00:00:00Zhttps://doi.org/10.1038/s41467-021-21461-4https://doaj.org/toc/2041-1723Myeloid cells are able to utilize a variety of monosaccharides from our diet, including fructose. Here the authors show that when monocytes are reliant on fructose as a carbon energy source they are reprogrammed towards oxidative metabolism, glutamine anaplerosis and a pro-inflammatory phenotype owing to excess pro-inflammatory cytokine production.Nicholas JonesJulianna BlagihFabio ZaniApril ReesDavid G. HillBenjamin J. JenkinsCaroline J. BullDiana MoreiraAzari I. M. BantanJames G. CroninDaniele AvanciniGareth W. JonesDavid K. FinlayKaren H. VousdenEmma E. VincentCatherine A. ThorntonNature PortfolioarticleScienceQENNature Communications, Vol 12, Iss 1, Pp 1-13 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Science Q
spellingShingle	Science Q Nicholas Jones Julianna Blagih Fabio Zani April Rees David G. Hill Benjamin J. Jenkins Caroline J. Bull Diana Moreira Azari I. M. Bantan James G. Cronin Daniele Avancini Gareth W. Jones David K. Finlay Karen H. Vousden Emma E. Vincent Catherine A. Thornton Fructose reprogrammes glutamine-dependent oxidative metabolism to support LPS-induced inflammation
description	Myeloid cells are able to utilize a variety of monosaccharides from our diet, including fructose. Here the authors show that when monocytes are reliant on fructose as a carbon energy source they are reprogrammed towards oxidative metabolism, glutamine anaplerosis and a pro-inflammatory phenotype owing to excess pro-inflammatory cytokine production.
format	article
author	Nicholas Jones Julianna Blagih Fabio Zani April Rees David G. Hill Benjamin J. Jenkins Caroline J. Bull Diana Moreira Azari I. M. Bantan James G. Cronin Daniele Avancini Gareth W. Jones David K. Finlay Karen H. Vousden Emma E. Vincent Catherine A. Thornton
author_facet	Nicholas Jones Julianna Blagih Fabio Zani April Rees David G. Hill Benjamin J. Jenkins Caroline J. Bull Diana Moreira Azari I. M. Bantan James G. Cronin Daniele Avancini Gareth W. Jones David K. Finlay Karen H. Vousden Emma E. Vincent Catherine A. Thornton
author_sort	Nicholas Jones
title	Fructose reprogrammes glutamine-dependent oxidative metabolism to support LPS-induced inflammation
title_short	Fructose reprogrammes glutamine-dependent oxidative metabolism to support LPS-induced inflammation
title_full	Fructose reprogrammes glutamine-dependent oxidative metabolism to support LPS-induced inflammation
title_fullStr	Fructose reprogrammes glutamine-dependent oxidative metabolism to support LPS-induced inflammation
title_full_unstemmed	Fructose reprogrammes glutamine-dependent oxidative metabolism to support LPS-induced inflammation
title_sort	fructose reprogrammes glutamine-dependent oxidative metabolism to support lps-induced inflammation
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/e704cf7cb7a0484a9ad0d96a44d08b6a
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Fructose reprogrammes glutamine-dependent oxidative metabolism to support LPS-induced inflammation

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