Zinc-free insulin elicited a reduction in the potassium conductance of muscle fibers from potassium-depleted muscle, which led to depolarization, blockage of action-poteintial mechanism, and paralysis. These changes are proposed as the mechanism of insulin-induced paralysis in patients with hypokalemic periodic paralysis. A similar effect by concanavalin a suggests that the effect may be mediated through the insulin receptors.