Parathyroid Function and Magnesium Depletion in the Rat*

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Abstract
Hypocalcemia is characteristically observed in Mg deficiency in a number of animal species. Previous studies demonstrated impaired release of PTH [parathyroid hormone] in Mg-depleted hypocalcemic humans. However, an enigma remains in that, unlike other animals, hypercalcemia, rather than hypocalcemia accompanies Mg-deficiency in the rat. Because intact parathyroids are necessary for the development of this hypercalcemia, it was postulated that Mg depletion stimulates, rather than impairs, PTH secretion in the rat. In an effort to more directly evaluate this thesis, sequential measurements of circulating immunoreactive PTH (iPTH) were made over a 30-day period in rats maintained on a Mg-deficient diet and in match-fed controls. In the control rats, serum Ca, Mg and iPTH remained relatively constant throughout the study. By contrast, during the first 4 days of a low Mg diet, serum Mg decreased to 1.0 mg/dl, serum Ca increased moderately, while serum iPTH increased to a mean level that was twice that in controls. After 5 days, when serum Mg progressively fell to levels less than 0.6 mg/dl and serum Ca continued to rise, serum iPTH fell to levels significantly lower than the control value. In a 2nd set of experiments, the effect of hypocalcemia on circulating iPTH in Mg deficiency was evaluated. Circulating iPTH was greatly increased and significantly different in Mg-deficient and Mg-replete animals who were rendered chronically hypocalcemic by diets deficient in either Ca or vitamin D. In the rat, an increase in PTH secretion occurs early in the genesis of Mg deficiency in the presence of a modest increase in serum Ca; however, the subsequent further increase in serum Ca counteracts the stimulatory effect of hypomagnesemia on PTH secretion; unlike the human parathyroid gland, the rat parathyroid gland responds appropriately to both hypo- and hypercalcemia in M deficiency; and the hypercalcemia that occurs in the Mg-deficient rat is not due to increased PTH secretion and must be accounted for by another mechanism.