Mechanisms of chronic JAK-STAT3-SOCS3 signaling in obesity.
Janus kinase (JAK)-signal transducers and activators of transcription (STAT) signaling pathways are critical for the maintenance of homeostatic and developmental processes; however, deregulation and chronic activation of JAK-STAT3 results in numerous diseases. Among others, obesity is currently being intensively studied. In obesity, chronic JAK-STAT3 is activated by the CNS by increased circulating leptin levels leading to the development of leptin resistance, whereas in the peripheral organs chronic IL-6-induced JAK-STAT3 impairs insulin action. We report the consequences of chronic JAK-STAT3 induced signaling as present under obese conditions in the main metabolic organs.
Max Planck Institute for Neurological Research; Institute for Genetics; University of Cologne and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD) and Center of Molecular Medicine Cologne (CMMC); Cologne, Germany.
Claudia M
CM
Wunderlich
Nadine
N
Hövelmeyer
F Thomas
FT
Wunderlich
IL-6; SOCS3; insulin resistance; leptin resistance; obesity