INSULIN RECEPTORS, INSULIN SECRETION, AND GLUCOSE DISAPPEARANCE RATE IN PATIENTS WITH PERIODIC HYPOKALAEMIC PARALYSIS

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Abstract
In a study of 6 male patients with periodic hypokalemic paralysis (PHP), reduced insulin binding to monocytes was found as compared with a group of 25 normal subjects (P < 0.1). The decreased insulin binding was caused by the decreased binding affinity. During induction of paralysis by a prolonged oral glucose load, 1 patient showed 24 h variations in the insulin binding to monocytes not differing from those observed in normals. After i.v. administration of glucose, these patients showed an elevated initial insulin response compared with the normals (P < 0.1). The i.v. glucose tolerance tests revealed normal glucose disappearance rates. Changes in insulin receptor binding do not appear to be of pathophysiological significance for eliciting the paretic attacks in PHP. The increased insulin response, following carbohydrate intake, might be of significance in the generation of paralytic attacks in patients with PHP.

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