PKR is not obligatory for high-fat diet-induced obesity and its associated metabolic and inflammatory complications

PKR is not obligatory for high-fat diet-induced obesity and its associated metabolic and inflammatory complications

Protein kinase R (PKR) has been suggested to act as a mediator of ER stress and inflammation in obesity. Here, Lancaster et al. find that genetic loss of PKR does not alter the development of obesity, and suggest that the use of littermate controls may explain differences in mouse knockout phenotype...

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Main Authors: G. I. Lancaster, H. L. Kammoun, M. J. Kraakman, G. M. Kowalski, C. R. Bruce, M. A. Febbraio
Format: Article
Language:English
Published: Nature Publishing Group 2016-02-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/ncomms10626
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spelling doaj-33a5a266327947a0a8bd5841e6f424982021-05-11T11:11:24ZengNature Publishing GroupNature Communications2041-17232016-02-017111010.1038/ncomms10626PKR is not obligatory for high-fat diet-induced obesity and its associated metabolic and inflammatory complicationsG. I. Lancaster0H. L. Kammoun1M. J. Kraakman2G. M. Kowalski3C. R. Bruce4M. A. Febbraio5Cellular and Molecular Metabolism Laboratory, BakerIDI Heart and Diabetes InstituteCellular and Molecular Metabolism Laboratory, BakerIDI Heart and Diabetes InstituteCellular and Molecular Metabolism Laboratory, BakerIDI Heart and Diabetes InstituteCellular and Molecular Metabolism Laboratory, BakerIDI Heart and Diabetes InstituteCellular and Molecular Metabolism Laboratory, BakerIDI Heart and Diabetes InstituteCellular and Molecular Metabolism Laboratory, BakerIDI Heart and Diabetes InstituteProtein kinase R (PKR) has been suggested to act as a mediator of ER stress and inflammation in obesity. Here, Lancaster et al. find that genetic loss of PKR does not alter the development of obesity, and suggest that the use of littermate controls may explain differences in mouse knockout phenotypes.https://doi.org/10.1038/ncomms10626
collection DOAJ
language English
format Article
sources DOAJ
author G. I. Lancaster
H. L. Kammoun
M. J. Kraakman
G. M. Kowalski
C. R. Bruce
M. A. Febbraio
spellingShingle G. I. Lancaster
H. L. Kammoun
M. J. Kraakman
G. M. Kowalski
C. R. Bruce
M. A. Febbraio
PKR is not obligatory for high-fat diet-induced obesity and its associated metabolic and inflammatory complications
Nature Communications
author_facet G. I. Lancaster
H. L. Kammoun
M. J. Kraakman
G. M. Kowalski
C. R. Bruce
M. A. Febbraio
author_sort G. I. Lancaster
title PKR is not obligatory for high-fat diet-induced obesity and its associated metabolic and inflammatory complications
title_short PKR is not obligatory for high-fat diet-induced obesity and its associated metabolic and inflammatory complications
title_full PKR is not obligatory for high-fat diet-induced obesity and its associated metabolic and inflammatory complications
title_fullStr PKR is not obligatory for high-fat diet-induced obesity and its associated metabolic and inflammatory complications
title_full_unstemmed PKR is not obligatory for high-fat diet-induced obesity and its associated metabolic and inflammatory complications
title_sort pkr is not obligatory for high-fat diet-induced obesity and its associated metabolic and inflammatory complications
publisher Nature Publishing Group
series Nature Communications
issn 2041-1723
publishDate 2016-02-01
description Protein kinase R (PKR) has been suggested to act as a mediator of ER stress and inflammation in obesity. Here, Lancaster et al. find that genetic loss of PKR does not alter the development of obesity, and suggest that the use of littermate controls may explain differences in mouse knockout phenotypes.
url https://doi.org/10.1038/ncomms10626
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