Tumor progression locus 2 (Tpl2) deficiency does not protect against obesity-induced metabolic disease.

Obesity is associated with a state of chronic low grade inflammation that plays an important role in the development of insulin resistance. Tumor progression locus 2 (Tpl2) is a serine/threonine mitogen activated protein kinase kinase kinase (MAP3K) involved in regulating responses to specific infla...

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Autores principales:	Graeme I Lancaster, Greg M Kowalski, Emma Estevez, Michael J Kraakman, George Grigoriadis, Mark A Febbraio, Steve Gerondakis, Ashish Banerjee
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2012
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/2e31a491233e4894a1717b561203ebd5
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spelling	oai:doaj.org-article:2e31a491233e4894a1717b561203ebd52021-11-18T07:15:47ZTumor progression locus 2 (Tpl2) deficiency does not protect against obesity-induced metabolic disease.1932-620310.1371/journal.pone.0039100https://doaj.org/article/2e31a491233e4894a1717b561203ebd52012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22701749/?tool=EBIhttps://doaj.org/toc/1932-6203Obesity is associated with a state of chronic low grade inflammation that plays an important role in the development of insulin resistance. Tumor progression locus 2 (Tpl2) is a serine/threonine mitogen activated protein kinase kinase kinase (MAP3K) involved in regulating responses to specific inflammatory stimuli. Here we have used mice lacking Tpl2 to examine its role in obesity-associated insulin resistance. Wild type (wt) and tpl2(-/-) mice accumulated comparable amounts of fat and lean mass when fed either a standard chow diet or two different high fat (HF) diets containing either 42% or 59% of energy content derived from fat. No differences in glucose tolerance were observed between wt and tpl2(-/-) mice on any of these diets. Insulin tolerance was similar on both standard chow and 42% HF diets, but was slightly impaired in tpl2(-/-) mice fed the 59% HFD. While gene expression markers of macrophage recruitment and inflammation were increased in the white adipose tissue of HF fed mice compared with standard chow fed mice, no differences were observed between wt and tpl2(-/-) mice. Finally, a HF diet did not increase Tpl2 expression nor did it activate Extracellular Signal-Regulated Kinase 1/2 (ERK1/2), the MAPK downstream of Tpl2. These findings argue that Tpl2 does not play a non-redundant role in obesity-associated metabolic dysfunction.Graeme I LancasterGreg M KowalskiEmma EstevezMichael J KraakmanGeorge GrigoriadisMark A FebbraioSteve GerondakisAshish BanerjeePublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 6, p e39100 (2012)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Graeme I Lancaster Greg M Kowalski Emma Estevez Michael J Kraakman George Grigoriadis Mark A Febbraio Steve Gerondakis Ashish Banerjee Tumor progression locus 2 (Tpl2) deficiency does not protect against obesity-induced metabolic disease.
description	Obesity is associated with a state of chronic low grade inflammation that plays an important role in the development of insulin resistance. Tumor progression locus 2 (Tpl2) is a serine/threonine mitogen activated protein kinase kinase kinase (MAP3K) involved in regulating responses to specific inflammatory stimuli. Here we have used mice lacking Tpl2 to examine its role in obesity-associated insulin resistance. Wild type (wt) and tpl2(-/-) mice accumulated comparable amounts of fat and lean mass when fed either a standard chow diet or two different high fat (HF) diets containing either 42% or 59% of energy content derived from fat. No differences in glucose tolerance were observed between wt and tpl2(-/-) mice on any of these diets. Insulin tolerance was similar on both standard chow and 42% HF diets, but was slightly impaired in tpl2(-/-) mice fed the 59% HFD. While gene expression markers of macrophage recruitment and inflammation were increased in the white adipose tissue of HF fed mice compared with standard chow fed mice, no differences were observed between wt and tpl2(-/-) mice. Finally, a HF diet did not increase Tpl2 expression nor did it activate Extracellular Signal-Regulated Kinase 1/2 (ERK1/2), the MAPK downstream of Tpl2. These findings argue that Tpl2 does not play a non-redundant role in obesity-associated metabolic dysfunction.
format	article
author	Graeme I Lancaster Greg M Kowalski Emma Estevez Michael J Kraakman George Grigoriadis Mark A Febbraio Steve Gerondakis Ashish Banerjee
author_facet	Graeme I Lancaster Greg M Kowalski Emma Estevez Michael J Kraakman George Grigoriadis Mark A Febbraio Steve Gerondakis Ashish Banerjee
author_sort	Graeme I Lancaster
title	Tumor progression locus 2 (Tpl2) deficiency does not protect against obesity-induced metabolic disease.
title_short	Tumor progression locus 2 (Tpl2) deficiency does not protect against obesity-induced metabolic disease.
title_full	Tumor progression locus 2 (Tpl2) deficiency does not protect against obesity-induced metabolic disease.
title_fullStr	Tumor progression locus 2 (Tpl2) deficiency does not protect against obesity-induced metabolic disease.
title_full_unstemmed	Tumor progression locus 2 (Tpl2) deficiency does not protect against obesity-induced metabolic disease.
title_sort	tumor progression locus 2 (tpl2) deficiency does not protect against obesity-induced metabolic disease.
publisher	Public Library of Science (PLoS)
publishDate	2012
url	https://doaj.org/article/2e31a491233e4894a1717b561203ebd5
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Tumor progression locus 2 (Tpl2) deficiency does not protect against obesity-induced metabolic disease.

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