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Endotoxin and interleukin-1 decrease hepatic lipase mRNA levels.

K R Feingold1, R A Memon, A H Moser

  • 1Department of Medicine, University of California San Francisco, Department of Veterans Affairs Medical Center, 94121, USA. kfngld@itsa.ucsf.edu

Atherosclerosis
|February 25, 1999
PubMed
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Lipopolysaccharide (LPS) and interleukin-1 (IL-1) decrease hepatic lipase activity and mRNA levels during the acute phase response. This inhibition impacts lipoprotein metabolism and may contribute to atherosclerosis if prolonged.

Area of Science:

  • Lipid metabolism
  • Molecular biology
  • Immunology

Background:

  • The acute phase response significantly alters lipoprotein metabolism, leading to hypertriglyceridemia and changes in HDL and LDL composition.
  • Hepatic lipase plays a crucial role in lipoprotein remodeling and is implicated in these metabolic shifts.

Purpose of the Study:

  • To investigate the effect of endotoxin (LPS) and cytokines on hepatic lipase activity and gene expression in vivo and in vitro.
  • To elucidate the role of IL-1 and TNF in regulating hepatic lipase during the acute phase response.

Main Methods:

  • Administered LPS to Syrian hamsters and measured hepatic lipase activity in liver and plasma.
  • Quantified hepatic lipase mRNA levels in response to LPS, IL-1, and TNF.
  • Treated HepG2 cells with IL-1 to assess direct effects on hepatic lipase expression.

Related Experiment Videos

  • Utilized IL-1 receptor deficient mice to evaluate the necessity of IL-1 signaling.

    • Main Results:

    • LPS treatment significantly decreased hepatic lipase activity (56% in liver, 45% in plasma) and mRNA levels (>90% decrease at 1.0 μg/100 g BW).
    • IL-1 markedly reduced hepatic lipase mRNA levels, while TNF had no significant effect.
    • IL-1 decreased hepatic lipase mRNA in HepG2 cells, suggesting direct regulation.
    • LPS-induced decrease in hepatic lipase occurred independently of IL-1 receptor signaling.

    Conclusions:

    • Hepatic lipase inhibition is a sensitive host response to LPS during the acute phase.
    • IL-1 directly contributes to the downregulation of hepatic lipase expression.
    • Reduced hepatic lipase may impair triglyceride-rich lipoprotein clearance and alter HDL composition, potentially contributing to proatherogenic conditions with prolonged inflammation.