Novel roles for JNK1 in metabolism.
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.
Belgardt
Bengt F
BF
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), 2nd Department for Internal Medicine University of Cologne 50674 Cologne, Germany.
Mauer
Jan
J
Brüning
Jens C
JC
D000818:Animals; D002490:Central Nervous System / Q000502:physiology; D004734:Energy Metabolism / Q000502:physiology*; D005947:Glucose / Q000378:metabolism; D018149:Glucose Intolerance / Q000503:physiopathology / Q000517:prevention & control; D006801:Humans; D007328:Insulin / Q000502:physiology; D007333:Insulin Resistance / Q000502:physiology; D050356:Lipid Metabolism / Q000502:physiology*; D024821:Metabolic Syndrome / Q000503:physiopathology*; D051379:Mice; D018345:Mice, Knockout; D048055:Mitogen-Activated Protein Kinase 8 / Q000502:physiology*; D023421:Models, Animal; D009765:Obesity / Q000503:physiopathology / Q000517:prevention & control; D015398:Signal Transduction / Q000502:physiology
D007328:Insulin; D048055:Mitogen-Activated Protein Kinase 8; D005947:Glucose