Insulin receptors, insulin secretion, and glucose disappearance rate in patients with periodic hypokalaemic paralysis.
In a study of 6 male patients with periodic hypokalaemic paralysis (PHP), we found reduced insulin binding to monocytes as compared with a group of 25 normal subjects (P less than 0.1). The decreased insulin binding was caused by the decreased binding affinity. During induction of paralysis by a prolonged oral glucose load, one patient showed 24-h variations in the insulin binding to monocytes not differing from those observed in normals. After iv administration of glucose, these patients showed an elevated initial insulin response compared with the normals (P less than 0.1). However, the iv glucose tolerance tests revealed normal glucose disappearance rates. We conclude that changes in insulin receptor binding do not appear to be of pathophysiological significance for eliciting the parese attacks in PHP. However, the increased insulin response, following carbohydrate intake, might be of significance in the generation of paralytic attacks in patients with PHP.
D000293:Adolescent; D000328:Adult; D001786:Blood Glucose / Q000378:metabolism; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005260:Female; D005947:Glucose / Q000378:metabolism*; D005951:Glucose Tolerance Test; D006801:Humans; D007008:Hypokalemia / Q000378:metabolism* / Q000503:physiopathology; D007328:Insulin / Q000097:blood / Q000378:metabolism*; D000078790:Insulin Secretion; D007657:Ketone Bodies / Q000097:blood; D008297:Male; D009000:Monocytes / Q000378:metabolism; D010245:Paralyses, Familial Periodic / Q000097:blood / Q000378:metabolism* / Q000503:physiopathology; D011972:Receptor, Insulin / Q000378:metabolism*
D001786:Blood Glucose; D005230:Fatty Acids, Nonesterified; D007328:Insulin; D007657:Ketone Bodies; D011972:Receptor, Insulin; D005947:Glucose