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

Lancaster, Graeme I., Kowalski, Greg M., Estevez, Emma, Kraakman, Michael J., Grigoriadis, George, Febbraio, Mark A., Gerondakis, Steve and Banerjee, Ashish 2012, Tumor progression locus 2 (Tpl2) deficiency does not protect against obesity-induced metabolic disease, PLoS one, vol. 7, no. 6, Article number e39100, pp. 1-7, doi: 10.1371/journal.pone.0039100.

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Title Tumor progression locus 2 (Tpl2) deficiency does not protect against obesity-induced metabolic disease
Author(s) Lancaster, Graeme I.
Kowalski, Greg M.ORCID iD for Kowalski, Greg M. orcid.org/0000-0002-1599-017X
Estevez, Emma
Kraakman, Michael J.
Grigoriadis, George
Febbraio, Mark A.
Gerondakis, Steve
Banerjee, Ashish
Journal name PLoS one
Volume number 7
Issue number 6
Season Article number e39100
Start page 1
End page 7
Total pages 7
Publisher Public Library of Science
Place of publication San Francisco, Calif.
Publication date 2012-06-11
ISSN 1932-6203
Keyword(s) tumor progression locus 2 (Tpl2)
obesity
metabolic dysfunction
insulin resistance
high fat (HF) diets
Summary 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 tpl22/2 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 tpl22/2 mice on any of these diets. Insulin tolerance was similar on both standard chow and 42% HF diets, but was slightly impaired in tpl22/2 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.
Language eng
DOI 10.1371/journal.pone.0039100
Field of Research 119999 Medical and Health Sciences not elsewhere classified
Socio Economic Objective 970111 Expanding Knowledge in the Medical and Health Sciences
HERDC Research category C1.1 Refereed article in a scholarly journal
Copyright notice ©2012, Public Library of Science
Free to Read? Yes
Persistent URL http://hdl.handle.net/10536/DRO/DU:30063102

Document type: Journal Article
Collections: School of Exercise and Nutrition Sciences
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Every reasonable effort has been made to ensure that permission has been obtained for items included in DRO. If you believe that your rights have been infringed by this repository, please contact drosupport@deakin.edu.au.