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Abstract
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.
Disclosure of Potential Conflicts of Interest
No potential conflicts of interest were disclosed.
Acknowledgments
We are grateful for intensive discussions with members of the Wunderlich and Brüning labs and for manuscript proofreading by Linda Koch. C.M.W. was funded from grants of CECAD and CMMC attributed to F.T.W. who received additional support from the DFG (SFB832 A15 and Z3, CRU286 RP5). N.H. obtained funding from the DFG (grant HO 4440/1-1)