Primary hyperparathyroidism is associated with decreased insulin receptor binding and glucose intolerance.
We studied insulin receptor-binding and carbohydrate and metabolism in 15 patients with symptomatic primary hyperparathyroidism in comparison with 20 healthy controls. Insulin binding to monocytes and erythrocytes was measured by radioreceptor-ligand-assay. Furthermore, patients and controls were characterized by testing oral (100 g glucose load) glucose tolerance as well as insulin tolerance (0.1U insulin/kg body weight). Compared with controls, patients with primary hyperparathyroidism exhibited marked hyperinsulinemia (P less than 0.01) and significantly higher glucose levels (P less than 0.01) after an oral glucose load. The glucose lowering effect of intravenous insulin was significantly diminished in primary hyperparathyroidism compared with controls (P less than 0.01). Receptor studies revealed a significantly lower (P less than 0.01) insulin binding to monocytes and to erythrocytes in patients with primary hyperparathyroidism compared with controls. The present data indicate an insulin-resistant state in primary hyperparathyroidism, which is caused at least in part, by a downregulation of insulin receptors.
D000328:Adult; D001786:Blood Glucose / Q000032:analysis*; D004912:Erythrocytes / Q000378:metabolism; D005260:Female; D005951:Glucose Tolerance Test; D006801:Humans; D006934:Hypercalcemia / Q000209:etiology; D006946:Hyperinsulinism / Q000209:etiology; D006961:Hyperparathyroidism / Q000150:complications / Q000378:metabolism*; D007328:Insulin / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000378:metabolism; D011972:Receptor, Insulin / Q000378:metabolism*
D001786:Blood Glucose; D007328:Insulin; D011972:Receptor, Insulin