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Mechanisms of chronic JAK-STAT3-SOCS3 signaling in obesity

Claudia M Wunderlich1, Nadine Hövelmeyer, F Thomas Wunderlich

  • 1Max 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.

JAK-STAT
|September 24, 2013
PubMed

Insights

Chronic Janus kinase (JAK)-signal transducers and activators of transcription (STAT) pathway activation, particularly JAK-STAT3, contributes to obesity by causing leptin resistance in the brain and impairing insulin action in peripheral organs.

Area of Science:

  • Molecular Biology
  • Physiology
  • Endocrinology

Background:

  • Janus kinase (JAK)-signal transducers and activators of transcription (STAT) pathways are essential for normal bodily functions.
  • Dysregulation and chronic activation of the JAK-STAT3 pathway are implicated in various diseases, including obesity.
  • Obesity involves chronic JAK-STAT3 activation in both the central nervous system (CNS) and peripheral organs.

Purpose of the Study:

  • To investigate the consequences of chronic JAK-STAT3 signaling in metabolic organs under obese conditions.
  • To elucidate the role of JAK-STAT3 in leptin resistance and insulin impairment in obesity.

Main Methods:

  • The study focuses on analyzing the effects of chronic JAK-STAT3 signaling.
  • The research examines conditions associated with obesity, including elevated leptin levels and IL-6 induction.
  • The investigation targets key metabolic organs.

Main Results:

  • Chronic JAK-STAT3 activation in the CNS, driven by increased leptin, leads to leptin resistance.
  • In peripheral organs, chronic IL-6-induced JAK-STAT3 activation negatively impacts insulin action.
  • The study details the specific consequences of this signaling in major metabolic organs.

Conclusions:

  • Chronic JAK-STAT3 signaling plays a significant role in the pathophysiology of obesity.
  • Targeting JAK-STAT3 pathways may offer therapeutic strategies for obesity-related metabolic dysfunction.
Keywords:
IL-6SOCS3insulin resistanceleptin resistanceobesity

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