Research Perspective Volume 2, Issue 9 pp 621—626
Novel roles for JNK1 in metabolism
- 1 Institute for Genetics, Department of Mouse Genetics and Metabolism, Center for Molecular Medicine, University of Cologne (CMMC), Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), 2 Department for Internal Medicine University of Cologne 50674 Cologne, Germany
- 2 Max Planck Institute for the Biology of Ageing, 50674 Cologne, Germany
received: July 5, 2010 ; accepted: August 29, 2010 ; published: August 31, 2010 ;https://doi.org/10.18632/aging.100192
How to Cite
Activation of stress-kinase signaling has recently been recognized as an important pathophysiological mechanism in the development of diet-induced obesity, type 2 diabetes mellitus and other aging-related pathologies. Here, c-Jun N-terminal Kinase (JNK) 1 knockout mice have been shown to exhibit protection from diet-induced obesity, glucose intolerance, and insulin resistance. Nonetheless, the tissue-specific role of JNK1-activation in the development of the metabolic syndrome has been poorly defined so far. Recently, it was demonstrated that JNK1 signaling plays a crucial role in the central nervous system (CNS) and in the pituitary to control systemic glucose and lipid metabolism partially through regulation of hormones involved in growth and energy expenditure.