Hypercalcemic and Calcium‐Antagonistic Effects on Insulin Release and Oral Glucose Tolerance in Man

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Abstract
The acute effects of hypercalcemia on the carbohydrate metabolism were studied in healthy subjects and in patients with non-insulin-dependent diabetes mellitus (NIDDM). The combined effect of hypercalcemia and a Ca-antagonistic agent (verapamil) was also studied in healthy subjects, in patients with NIDDM, and in patients with chronic hypercalcemia, e.g., primary hyperparathyroidism (PHPT). Ca, infused i.v. to fasting diabetic patients, induced a singificant decline in the blood glucose concentration. This was not the case in healthy individuals. When glucose was administered orally during exogenous hypercalcemia, glucose tolerance decreased significantly in the diabetic as well as in the healthy individuals. Verapamil, however, abolished this hypercalcemia effect, and even improved the tolerance for oral glucose when administered i.v. together with Ca in the patients with NIDDM. No such effect of verapamil was seen in the healthy subjects or in the patients with PHPT. Insulin activity was left unaffected by hypercalcemia and/or verapamil in all experimental situations. Apparently, hypercalcemia decreases the tolerance for oral glucose in normoglycemic subjects, and further deteriorates the glucose tolerance in patients with an already impaired carbohydrate metabolism. Verapamil appears to counteract this effect of hypercalcemia in diabetic patients. Since insulin remains unaffected by Ca and verapamil in the above mentioned situations, it is reasonable to assume that the Ca and verapamil-induced effects on the glucose tolerance are due to glucose-regulatory factors other than insulin.