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Related Experiment Video

Updated: Jun 13, 2026

Measurement of Insulin- and Contraction-Stimulated Glucose Uptake in Isolated and Incubated Mature Skeletal Muscle from Mice
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Published on: May 16, 2021

SPARC interacts with AMPK and regulates GLUT4 expression.

Haiyan Song1, Yuanyuan Guan, Liping Zhang

  • 1Department of Endocrinology and Metabolism, The Second Affiliated Hospital of Harbin Medical University, Xuefu Road 246, Harbin 150080, China. songhy@ems.hrbmu.edu.cn

Biochemical and Biophysical Research Communications
|May 13, 2010
PubMed
Summary

Secreted protein acidic and rich in cysteine (SPARC) interacts with AMP-activated protein kinase (AMPK), enhancing its function. This interaction regulates glucose metabolism by influencing Glut4 expression, offering new insights into metabolic regulation.

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Area of Science:

  • Biochemistry
  • Molecular Biology
  • Metabolic Regulation

Background:

  • AMP-activated protein kinase (AMPK) is a key regulator of cellular energy homeostasis, particularly glucose and fat metabolism.
  • Understanding the molecular mechanisms and interacting partners of AMPK is crucial for elucidating its role in metabolic diseases.

Purpose of the Study:

  • To identify novel interacting partners of AMPK alpha 1 using a yeast two-hybrid screen.
  • To investigate the functional relationship between AMPK and its identified interacting partner in regulating glucose metabolism.

Main Methods:

  • Yeast two-hybrid screening of a mouse embryo cDNA library to identify AMPK alpha 1 binding partners.
  • Co-immunoprecipitation assays in HepG2 cells and various rat tissues to confirm endogenous protein interactions.
  • Western blotting and siRNA knockdown experiments to assess the impact of SPARC on AMPK activation and vice versa.
  • Analysis of Glut4 expression in L6 myocytes to evaluate the effect on glucose metabolism.

Main Results:

  • Secreted protein acidic and rich in cysteine (SPARC) was identified as an interacting partner of AMPK alpha 1.
  • AMPK activation enhances SPARC expression, while SPARC influences AMPK phosphorylation and activity.
  • SPARC modulates AMPK-mediated glucose metabolism through the regulation of Glut4 expression in L6 myocytes.

Conclusions:

  • SPARC and AMPK form a functional complex that mutually enhances their activity.
  • SPARC plays a role in regulating glucose metabolism, potentially via AMPK activation and modulation of Glut4 expression.
  • This study establishes a novel link between SPARC and AMPK, providing a foundation for further research into their roles in metabolic regulation.