Regulation of calcium metabolism in streptozotocin-induced diabetes

Abstract
Sixty-nine-day-old female Wistar rats that had been made diabetic 9 days earlier by an intraperitoneal injection of streptozotocin were studied by a combination radioisotope and balance technique that evaluates calcium absorption, excretion, and bone calcium deposition and resorption rates. Streptozotocin-induced diabetes was associated with a marked drop in calcium absorption and a threefold rise in urinary calcium excretion, changes that greatly exceeded the expected effects from the hyperphagia and increased calcium intake of the experimental animals. Bone calcium deposition was halved in the diabetic rats, with bone resorption unchanged and ewqual to the deposition rate. As a result, the bone and body calcium balances were zero in the experimental animals. To maintain plasma calcium near normal under these circumstances, the diabetic animals turned over their skeletal calcium in relationship to the central pool much more rapidly than the controls. Although the skeleton in the normal animals serves as both storehouse and regulator of the plasma calcium, in short-term streptozotocin-induced diabetes there is no calcium storage in bone, with the skeleton only playing the role of regulator of calcium homeostasis.