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Related Experiment Videos

Studies of endotoxin-induced decrease in lipoprotein lipase activity

M Kawakami, A Cerami

    The Journal of Experimental Medicine
    |September 1, 1981
    PubMed
    Summary
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    Endotoxin causes hyperlipidemia by suppressing lipoprotein lipase (LPL) activity. A transferable factor produced by exudate cells in response to endotoxin mediates this suppression in adipose tissue.

    Area of Science:

    • Biochemistry
    • Immunology
    • Metabolic Research

    Background:

    • Invasive stimuli, including endotoxin, can trigger hyperlipidemia.
    • Endotoxin exposure impairs triglyceride clearance by reducing lipoprotein lipase (LPL) activity.

    Purpose of the Study:

    • To investigate the mechanism by which endotoxin suppresses LPL activity.
    • To identify the source of the factor responsible for LPL suppression.

    Main Methods:

    • Comparing LPL activity in endotoxin-sensitive (C3H/HeN) and endotoxin-resistant (C3H/HeJ) mice after endotoxin administration.
    • Detecting and transferring blood factors from endotoxin-treated mice.
    • Culturing peritoneal exudate cells and testing conditioned medium.

    Main Results:

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    • Endotoxin markedly suppressed adipose tissue LPL activity in C3H/HeN mice.
    • A transferable factor in the blood of endotoxin-treated C3H/HeN mice suppressed LPL activity in both mouse strains.
    • Conditioned medium from endotoxin-stimulated exudate cells also suppressed LPL activity.

    Conclusions:

    • Exudate cells produce a humoral factor in response to endotoxin.
    • This factor suppresses adipose tissue LPL activity, contributing to endotoxin-induced hyperlipidemia.