The influence of serum calcium and parathyroid hormone upon glucose metabolism in uremia.

The alterations in carbohydrate metabolism which attend the uremic syndrome have been recognized for some time. Recently, an interaction between hyperparathyroidism and these alterations in intermediary metabolism has been postulated. To further define any such interaction, 6 stable dialysis patients with significant secondary hyperparathyroidism were studied prior to and after subtotal parathyroidectomy. Glucose utilization and insulin secretion were estimated by use of a standard intravenous glucose tolerance test and the resistance of peripheral tissues to exogenous insulin was evaluated by insulin tolerance testing. All of peripheral tissues to exogenous insulin was evaluated by insulin tolerance testing. All patients were studied under baseline conditions, as well as induced hyper- and hypocalcemia, prior to and at least 2 months after surgery. Parathyroidectomy, per se, had no significant effect upon glucose utilization, insulin secretion, or the resistance of peripheral tissues to the action of exogenous insulin. Both induced hyper- and hypocalcemia, on the other hand, significantly diminished glucose utilization as judged by a reduced glucose disappearance rate during intravenous glucose tolerance testing. Hypocalcemia was associated with a markedly reduced insulin secretory response and normal tissue insulin sensitivity, while hypercalcemia was associated with a normal insulin response but reduced tissue sensitivity. The data suggest that calcium ion concentration may affect both glucose utilization and insulin secretion. As such, it must be adequately controlled in furture metabolic studies.