Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/106368
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Type: Journal article
Title: MNK1 and MNK2 mediate adverse effects of high-fat feeding in distinct ways
Author: Moore, C.
Pickford, J.
Cagampang, F.
Stead, R.
Tian, S.
Zhao, X.
Tang, X.
Byrne, C.
Proud, C.
Citation: Scientific Reports, 2016; 6(1):23476-1-23476-15
Publisher: Nature Publishing Group
Issue Date: 2016
ISSN: 2045-2322
2045-2322
Statement of
Responsibility: 
C. E. J. Moore, J. Pickford, F. R. Cagampang, R. L. Stead, S. Tian, X. Zhao, X. Tang, C. D. Byrne and C. G. Proud
Abstract: The MAP kinase-interacting kinases (MNK1 and MNK2) are non-essential enzymes which are activated by MAP kinases. They are implicated in controlling protein synthesis. Here we show that mice in which the expression of either MNK1 or MNK2 has been knocked out (KO) are protected against adverse effects of high-fat feeding, and in distinct ways. High-fat diet (HFD)-fed MNK2-KO show less weight gain than wild-type animals, and improved glucose tolerance, better insulin sensitivity and markedly diminished adipose tissue inflammation. This suggests MNK2 plays a role in adipogenesis and/or lipogenesis and in macrophage biology. MNK1-KO/HFD mice show better glucose tolerance and insulin sensitivity, but gain weight and show similar adipose inflammation to WT animals. These data suggest MNK1 participates in mediating HFD-induced insulin resistance. Our findings reveal distinct roles for the MNKs in a novel area of disease biology, metabolic dysfunction, and suggests they are potential new targets for managing metabolic disease.
Keywords: Liver; Adipose Tissue; Cell Line; Adipocytes; Macrophages; Animals; Mice, Knockout; Mice; Insulin Resistance; Inflammation; Protein-Serine-Threonine Kinases; Glucose Tolerance Test; Cell Differentiation; Organ Specificity; Lipid Metabolism; Diet, High-Fat
Rights: This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
RMID: 0030047113
DOI: 10.1038/srep23476
Appears in Collections:Molecular and Biomedical Science publications

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