Toll-like receptor 4 knockout mice are protected against endoplasmic reticulum stress induced by a high-fat diet.

The purpose of this study was to investigate whether toll-like receptor 4 (TLR4) is implicated in the development of endoplasmic reticulum stress (ER stress) observed after a high-fat diet (HFD) in liver, skeletal muscle and adipose tissue. TLR4(-/-) and C57BL/6J wild-type mice (WT) were fed with ch...

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Autores principales:	Nicolas Pierre, Louise Deldicque, Caroline Barbé, Damien Naslain, Patrice D Cani, Marc Francaux
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2013
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/d571c57be9344477a87724e65751c369
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spelling	oai:doaj.org-article:d571c57be9344477a87724e65751c3692021-11-18T07:43:28ZToll-like receptor 4 knockout mice are protected against endoplasmic reticulum stress induced by a high-fat diet.1932-620310.1371/journal.pone.0065061https://doaj.org/article/d571c57be9344477a87724e65751c3692013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23741455/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203The purpose of this study was to investigate whether toll-like receptor 4 (TLR4) is implicated in the development of endoplasmic reticulum stress (ER stress) observed after a high-fat diet (HFD) in liver, skeletal muscle and adipose tissue. TLR4(-/-) and C57BL/6J wild-type mice (WT) were fed with chow or HFD (45% calories from fat) during 18 weeks. An oral glucose tolerance-test was performed. The animals were sacrificed in a fasted state and the tissues were removed. TLR4 deletion protected from body weight gain and glucose intolerance induced by HFD whereas energy intake was higher in transgenic mice suggesting larger energy expenditure. HFD induced an ER stress in skeletal muscle, liver and adipose tissue of WT mice as assessed by BiP, CHOP, spliced and unspliced XBP1 and phospho-eIF2α. TLR4(-/-) mice were protected against HFD-induced ER stress. Then, we investigated the main signaling downstream of TLR4 namely the NF-κB pathway, expecting to identify the mechanism by which TLR4 is able to activate ER stress. The mRNA levels of cytokines regulated by NF-κB namely TNFα, IL-1β and IL-6, were not changed after HFD and phospho-IκB-α (ser 32) was not changed. Our results indicate that TLR4 is essential for the development of ER stress related to HFD. Nevertheless, the NFκ-B pathway does not seem to be directly implicated. The reduced fat storage in TLR4(-/-) mice could explain the absence of an ER stress after HFD.Nicolas PierreLouise DeldicqueCaroline BarbéDamien NaslainPatrice D CaniMarc FrancauxPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 5, p e65061 (2013)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Nicolas Pierre Louise Deldicque Caroline Barbé Damien Naslain Patrice D Cani Marc Francaux Toll-like receptor 4 knockout mice are protected against endoplasmic reticulum stress induced by a high-fat diet.
description	The purpose of this study was to investigate whether toll-like receptor 4 (TLR4) is implicated in the development of endoplasmic reticulum stress (ER stress) observed after a high-fat diet (HFD) in liver, skeletal muscle and adipose tissue. TLR4(-/-) and C57BL/6J wild-type mice (WT) were fed with chow or HFD (45% calories from fat) during 18 weeks. An oral glucose tolerance-test was performed. The animals were sacrificed in a fasted state and the tissues were removed. TLR4 deletion protected from body weight gain and glucose intolerance induced by HFD whereas energy intake was higher in transgenic mice suggesting larger energy expenditure. HFD induced an ER stress in skeletal muscle, liver and adipose tissue of WT mice as assessed by BiP, CHOP, spliced and unspliced XBP1 and phospho-eIF2α. TLR4(-/-) mice were protected against HFD-induced ER stress. Then, we investigated the main signaling downstream of TLR4 namely the NF-κB pathway, expecting to identify the mechanism by which TLR4 is able to activate ER stress. The mRNA levels of cytokines regulated by NF-κB namely TNFα, IL-1β and IL-6, were not changed after HFD and phospho-IκB-α (ser 32) was not changed. Our results indicate that TLR4 is essential for the development of ER stress related to HFD. Nevertheless, the NFκ-B pathway does not seem to be directly implicated. The reduced fat storage in TLR4(-/-) mice could explain the absence of an ER stress after HFD.
format	article
author	Nicolas Pierre Louise Deldicque Caroline Barbé Damien Naslain Patrice D Cani Marc Francaux
author_facet	Nicolas Pierre Louise Deldicque Caroline Barbé Damien Naslain Patrice D Cani Marc Francaux
author_sort	Nicolas Pierre
title	Toll-like receptor 4 knockout mice are protected against endoplasmic reticulum stress induced by a high-fat diet.
title_short	Toll-like receptor 4 knockout mice are protected against endoplasmic reticulum stress induced by a high-fat diet.
title_full	Toll-like receptor 4 knockout mice are protected against endoplasmic reticulum stress induced by a high-fat diet.
title_fullStr	Toll-like receptor 4 knockout mice are protected against endoplasmic reticulum stress induced by a high-fat diet.
title_full_unstemmed	Toll-like receptor 4 knockout mice are protected against endoplasmic reticulum stress induced by a high-fat diet.
title_sort	toll-like receptor 4 knockout mice are protected against endoplasmic reticulum stress induced by a high-fat diet.
publisher	Public Library of Science (PLoS)
publishDate	2013
url	https://doaj.org/article/d571c57be9344477a87724e65751c369
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Toll-like receptor 4 knockout mice are protected against endoplasmic reticulum stress induced by a high-fat diet.

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