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Published on: August 14, 2013

Mechanism of insulin-induced paralysis of muscles from potassium-depleted rats

I Kao, A M Gordon

    Science (New York, N.Y.)
    |May 16, 1975
    PubMed

    Insights

    Zinc-free insulin causes paralysis by reducing muscle potassium, leading to depolarization and blocked action potentials. This suggests a mechanism for insulin-induced paralysis in hypokalemic periodic paralysis patients, possibly via insulin receptors.

    Area of Science:

    • Endocrinology
    • Neurophysiology
    • Muscle Physiology

    Background:

    • Hypokalemic periodic paralysis (HPP) is characterized by episodic muscle weakness.
    • Insulin administration can trigger paralysis in some HPP patients.
    • The precise mechanism of insulin-induced paralysis remains unclear.

    Purpose of the Study:

    • To investigate the effect of zinc-free insulin on muscle electrophysiology.
    • To elucidate the mechanism underlying insulin-induced paralysis in HPP.
    • To explore the role of insulin receptors in this process.

    Main Methods:

    • Studied the effect of zinc-free insulin on potassium conductance in muscle fibers from potassium-depleted muscle.
    • Examined changes in membrane potential and action potential propagation.
    • Compared the effects of zinc-free insulin with concanavalin A.

    Main Results:

    • Zinc-free insulin significantly reduced potassium conductance in muscle fibers.
    • This reduction led to muscle fiber depolarization and blockage of action potentials.
    • Concanavalin A produced similar effects, suggesting receptor-mediated action.

    Conclusions:

    • Insulin-induced paralysis in HPP may result from reduced potassium conductance, leading to depolarization and impaired action potential conduction.
    • The findings suggest that insulin receptors play a crucial role in mediating these effects.

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