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Chemerin-induced mitochondrial dysfunction in skeletal muscle.

Qihai Xie1, Yujie Deng, Chenglin Huang

  • 1State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Department of Hypertension Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.

Journal of Cellular and Molecular Medicine
|March 11, 2015
PubMed
Summary
This summary is machine-generated.

Chemerin, a factor inducing insulin resistance, impairs skeletal muscle mitochondrial function by increasing autophagy and oxidative stress. Restoring mitochondrial function can be achieved by targeting its signaling pathways.

Keywords:
autophagychemerinmitochondrial dysfunctionskeletal muscle

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Area of Science:

  • Metabolism
  • Molecular Biology
  • Cell Biology

Background:

  • Chemerin is an adipocyte-derived factor linked to insulin resistance in skeletal muscle.
  • The impact of chemerin on skeletal muscle mitochondrial function remains largely unexplored.

Purpose of the Study:

  • To investigate the role of mitochondrial dysfunction in chemerin-mediated insulin resistance.
  • To elucidate the mechanisms underlying chemerin's effects on skeletal muscle mitochondria.

Main Methods:

  • Overexpression of murine chemerin in C57BL/6 mice and cultured C2C12 myotubes.
  • Assessment of mitochondrial function, structure, autophagy markers (LC3-I/II, Beclin1, ATG5/7), reactive oxygen species (ROS) generation, mitochondrial membrane potential, protein carbonyls, and DNA deletions.
  • Analysis of signaling pathways involving protein kinase B (AKT) and forkhead box O3α (FoxO3α).
  • Intervention with chemokine-like receptor 1 (CMKLR1) knockdown and Mito-TEMPO.

Main Results:

  • Chemerin overexpression reduced mitochondrial content and increased mitochondrial autophagy in mouse skeletal muscle.
  • Chemerin treatment in myotubes elevated mitochondrial ROS, decreased mitochondrial membrane potential, and increased oxidative damage (protein carbonyls, DNA deletions).
  • Knockdown of CMKLR1 or use of Mito-TEMPO reversed chemerin-induced mitochondrial dysfunction.
  • Chemerin reduced insulin-stimulated AKT phosphorylation and dephosphorylated FoxO3α, suggesting involvement of an AKT-FoxO3α pathway in chemerin-induced mitochondrial autophagy.

Conclusions:

  • Chemerin induces skeletal muscle insulin resistance, at least partly, through mitochondrial dysfunction.
  • Chemerin promotes mitochondrial autophagy and oxidative stress in skeletal muscle.
  • The AKT-FoxO3α signaling pathway mediates chemerin-induced mitochondrial dysfunction and autophagy.