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Related Experiment Videos

Oleate-induced decrease in hepatocyte insulin binding is mediated by PKC-delta.

Shu Chen1, Tony K T Lam, Edward Park

  • 1Department of Physiology, University of Toronto, Toronto, Ont., Canada M5S 1A8.

Biochemical and Biophysical Research Communications
|June 20, 2006
PubMed
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Free fatty acids (FFA) reduce insulin binding in liver cells, contributing to hyperinsulinemia. Protein kinase C delta (PKC-delta) activation is identified as the mechanism behind this effect.

Area of Science:

  • Metabolism and Endocrinology
  • Cellular Biology
  • Molecular Medicine

Background:

  • Free fatty acids (FFA) are known to impair hepatic insulin extraction in vivo.
  • This impairment can lead to hyperinsulinemia, a condition linked to atherosclerosis and cancer.
  • Hepatic insulin extraction relies on hepatocyte insulin binding, a receptor-mediated process.

Purpose of the Study:

  • To investigate the direct effect of FFA on insulin binding in isolated rat hepatocytes.
  • To elucidate the molecular mechanisms underlying FFA-induced changes in hepatocyte insulin binding.

Main Methods:

  • Isolated rat hepatocytes were exposed to varying concentrations of oleate (a free fatty acid).
  • Insulin binding was measured after FFA exposure.
  • The role of FFA oxidation and protein kinase C (PKC) signaling was assessed using specific inhibitors (methylpalmoxirate and bisindolylmaleimide).

Related Experiment Videos

  • Subcellular fractionation and immunoblotting were used to analyze PKC isoform translocation.

    • Main Results:

    • Oleate significantly decreased hepatocyte insulin binding in a concentration-dependent manner.
    • Inhibition of FFA oxidation did not prevent the reduction in insulin binding.
    • The PKC inhibitor bisindolylmaleimide abolished the oleate-induced decrease in insulin binding.
    • Oleate specifically induced the membrane translocation of PKC-delta, but not other tested PKC isoforms.

    Conclusions:

    • PKC-delta activation mediates the reduction in hepatocyte insulin binding caused by FFA.
    • This finding provides a mechanistic link between FFA, impaired insulin binding, and hyperinsulinemia.