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Related Experiment Videos

Defective insulin receptor function in down-regulated HepG2 cells.

J F Williams1, J M Olefsky

  • 1Department of Medicine, University of California, La Jolla 92037.

Endocrinology
|October 1, 1990
PubMed
Summary
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High insulin levels impair insulin receptors on HepG2 cells, reducing their number and function. This leads to kinase-incompetent receptors accumulating on the cell surface, causing insulin resistance.

Area of Science:

  • Cell biology
  • Endocrinology
  • Biochemistry

Background:

  • Insulin resistance is a major health concern.
  • Understanding insulin receptor (IR) function is crucial for metabolic disease research.
  • HepG2 cells are a valuable model for studying liver cell responses to insulin.

Purpose of the Study:

  • To investigate the functional defects of insulin receptors on HepG2 cells after insulin-induced down-regulation.
  • To characterize the abnormalities in insulin receptor internalization, degradation, and kinase activity.

Main Methods:

  • Down-regulation of insulin receptors in HepG2 cells using high insulin concentrations.
  • Quantification of cell surface receptors and ligand-mediated internalization.
  • Assessment of receptor autophosphorylation and tyrosine phosphorylation of substrate pp185.

Related Experiment Videos

  • Wheat germ affinity chromatography for receptor purification.

    • Main Results:

    • Insulin treatment decreased cell surface receptor number by 58%.
    • Remaining receptors showed reduced insulin internalization (40% decrease) and autophosphorylation (up to 70% decrease).
    • Down-regulated receptors exhibited impaired kinase activity and preferential degradation of functional receptors.

    Conclusions:

    • Insulin-induced down-regulation leads to accumulation of functionally defective insulin receptors on the cell surface.
    • These kinase-incompetent receptors may contribute to post-binding defects in insulin action.
    • The findings provide insights into molecular mechanisms underlying insulin resistance.