1. Mechanisms of chronic JAK-STAT3-SOCS3 signaling in obesity
- Author
-
Claudia M. Wunderlich, F. Thomas Wunderlich, and Nadine Hövelmeyer
- Subjects
medicine.medical_specialty ,IL-6 ,obesity ,biology ,business.industry ,Leptin ,Insulin ,medicine.medical_treatment ,General Medicine ,Review ,medicine.disease ,leptin resistance ,stat ,Endocrinology ,Insulin resistance ,Internal medicine ,insulin resistance ,biology.protein ,Medicine ,SOCS3 ,Signal transduction ,business ,Janus kinase ,STAT3 - 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.
- Published
- 2012