Journal article

Alteration of JNK-1 Signaling in Skeletal Muscle Fails to Affect Glucose Homeostasis and Obesity-Associated Insulin Resistance in Mice

Martin Pal, Claudia M Wunderlich, Gabriele Spohn, Hella S Broenneke, Marc Schmidt-Supprian, F Thomas Wunderlich

PLoS One | PUBLIC LIBRARY SCIENCE | Published : 2013

Abstract

Obesity and associated metabolic disturbances, such as increased circulating fatty acids cause prolonged low grade activation of inflammatory signaling pathways in liver, skeletal muscle, adipose tissue and even in the CNS. Activation of inflammatory pathways in turn impairs insulin signaling, ultimately leading to obesity-associated type 2 diabetes mellitus. Conventional JNK-1 knock out mice are protected from high fat diet-induced insulin resistance, characterizing JNK-1-inhibition as a potential approach to improve glucose metabolism in obese patients. However, the cell type-specific role of elevated JNK-1 signaling as present during the course of obesity has not been fully elucidated yet..

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University of Melbourne Researchers

Grants

Awarded by DFG


Awarded by Center for Molecular Medicine Cologne (CMMC)


Awarded by European Union


Awarded by Federal Ministry of Education and Research


Funding Acknowledgements

This work was supported by the DFG through SFB 832 A15 to FTW and Z3 to JCB, the Center for Molecular Medicine Cologne (CMMC) (D1 to JCB, B2 to FTW), the Cluster of Excellence Cellular Stress Responses in Aging-Associated Diseases (CECAD), the European Union (FP7-HEALTH-2009-241592, EurOCHIP, to JCB), the DFG (BR 1492/7-1 to JCB), and the Competence Network for Adipositas (Neurotarget) funded by the Federal Ministry of Education and Research (FKZ01GIO845 to JCB). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.