Elevated circulating immunoreactive calcitonin in the magnesium-deficient normocalcemic rat.

Previous studies indicate that magnesium, like calcium, stimulates the release of calcitonin (CT) from the thyroid gland. On the other hand, C-cell hyperplasia has been noted in magnesium-deficient dogs and rats. To explore further possible interrelationships between magnesium and CT, 21-day-old Sprague-Dawley male rats fed a control diet (0.043% Mg and 0.47 Ca) were match-fed with rats given either a control low calcium diet (0.043% Mg and 0.15% Ca) or a low magnesium-low calcium diet (0.001% Mg and 0.15% Ca). The low calcium content in the magnesium-deficient diet prevented the development of hypercalcemia characteristic of the magnesium-deficient rat. After 17 days, animals were killed by decapitation. Blood was obtained from some animals in the basal state and in other animals 1 min postpentagastrin or 1 min postmagnesium chloride infusion. No significant difference was found in the serum calcium level in the three groups, while the mean serum immunoreactive CT (iCT) level was significantly higher in magnesium-deficient rats both before and after pentagastrin. An acute iv infusion of MgCl2 resulted in significant increases in serum iCT in both the control and magnesium-deficient animals. The results of this study demonstrate that basal serum iCT levels and their response to pentagastrin are increased in magnesium-deficient, normocalcemic animals. The further increase in serum iCT after magnesium infusion in magnesium-depleted animals appears paradoxical and indicates that the relationship between extracellular magnesium and iCT release is not a simple feedback mechanism. It is possible that the increase in circulating iCT may be a response to extracellular-intracellular differences in magnesium concentration. Alternatively, the increased C-cell activity may be secondary to some unknown metabolic alteration induced by magnesium deficiency, rather than to magnesium deficiency per se.