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Related Experiment Videos

Endotoxin, tumor necrosis factor, and interleukin-1 decrease hepatic squalene synthase activity, protein, and mRNA

R A Memon1, I Shechter, A H Moser

  • 1Department of Medicine, University of California San Francisco, and Department of Veterans Affairs Medical Center, 94121, USA.

Journal of Lipid Research
|August 1, 1997
PubMed
Summary

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Endotoxin (LPS) administration significantly reduces squalene synthase, a key enzyme in cholesterol biosynthesis, in hamsters. This rapid decrease impacts cholesterol metabolism during infection and inflammation.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Metabolic Regulation

Background:

  • Endotoxin (LPS) administration increases hepatic HMG-CoA reductase but only modestly affects cholesterol synthesis.
  • This suggests LPS influences other key enzymes in cholesterol metabolism, like squalene synthase.

Purpose of the Study:

  • To investigate the effect of LPS and cytokines on squalene synthase, the first committed enzyme in cholesterol biosynthesis.
  • To understand the regulation of the mevalonate pathway during infection and inflammation.

Main Methods:

  • Administered LPS and cytokines to Syrian hamsters.
  • Measured squalene synthase activity, protein mass, and mRNA levels.
  • Utilized colestipol to increase basal squalene synthase expression.

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Main Results:

  • LPS markedly decreased squalene synthase mRNA levels rapidly and at low doses.
  • LPS significantly reduced squalene synthase activity and protein mass.
  • LPS decreased squalene synthase expression even when upregulated by colestipol; cytokines also reduced expression.

Conclusions:

  • LPS and cytokines downregulate squalene synthase during infection/inflammation.
  • Discordant regulation of HMG-CoA reductase and squalene synthase affects mevalonate pathway substrate flux.
  • This highlights a complex regulatory response impacting cholesterol and non-sterol biosynthesis.