Anast C S, Forte L F
Endocrinology. 1983 Jul;113(1):184-9. doi: 10.1210/endo-113-1-184.
Hypocalcemia is characteristically observed in magnesium deficiency in a number of animal species. Previous studies demonstrated impaired release of PTH in magnesium-depleted hypocalcemic humans. However, an enigma remains in that, unlike in other animals, hypercalcemia, rather than hypocalcemia, accompanies magnesium deficiency in the rat. Because intact parathyroids are necessary for the development of this hypercalcemia, it has been postulated that magnesium 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 magnesium-deficient diet and in match-fed controls. In the control rats, serum calcium, magnesium, and iPTH remained relatively constant throughout the study. By contrast, during the first 4 days of a low magnesium diet, serum magnesium decreased to 1.0 mg/dl, serum calcium increased moderately, while serum iPTH increased to a mean level that was twice that in controls. After 5 days, when serum magnesium progressively fell to levels less than 0.6 mg/dl and serum calcium continued to rise, serum iPTH fell to levels significantly lower than the control value. In a second set of experiments, the effect of hypocalcemia on circulating iPTH in magnesium deficiency was evaluated. Circulating iPTH was greatly increased and not significantly different in magnesium-deficient and magnesium-replete animals who were rendered chronically hypocalcemic by diets deficient in either calcium or vitamin D. The results of this study indicate that: 1) in the rat, an increase in PTH secretion occurs early in the genesis of magnesium deficiency in the presence of a modest increase in serum calcium; however, the subsequent further increase in serum calcium counteracts the stimulatory effect of hypomagnesemia on PTH secretion; 2) unlike the human parathyroid gland, the rat parathyroid gland responds appropriately to both hypo- and hypercalcemia in magnesium deficiency; and 3) the hypercalcemia that occurs in the magnesium-deficient rat is not due to increased PTH secretion and must be accounted for by another mechanism.
在许多动物物种中，低钙血症是镁缺乏的典型表现。先前的研究表明，缺镁的低钙血症患者甲状旁腺激素（PTH）释放受损。然而，一个谜仍然存在，即与其他动物不同，大鼠缺镁时伴随的是高钙血症，而非低钙血症。由于完整的甲状旁腺对于这种高钙血症的发生是必需的，因此有人推测，缺镁刺激而非损害大鼠的PTH分泌。为了更直接地评估这一论点，在以缺镁饮食喂养的大鼠和配对喂养的对照大鼠中，在30天内连续测量循环免疫反应性PTH（iPTH）。在对照大鼠中，整个研究过程中血清钙、镁和iPTH保持相对稳定。相比之下，在低镁饮食的前4天，血清镁降至1.0mg/dl，血清钙适度升高，而血清iPTH升高至平均水平，是对照组的两倍。5天后，当血清镁逐渐降至低于0.6mg/dl且血清钙持续升高时，血清iPTH降至明显低于对照值的水平。在第二组实验中，评估了低钙血症对缺镁时循环iPTH的影响。通过钙或维生素D缺乏饮食导致长期低钙血症的缺镁和补镁动物，其循环iPTH大幅增加且无显著差异。本研究结果表明：1）在大鼠中，缺镁初期血清钙适度升高时PTH分泌增加；然而，随后血清钙的进一步升高抵消了低镁血症对PTH分泌的刺激作用；2）与人类甲状旁腺不同，大鼠甲状旁腺在缺镁时对低钙血症和高钙血症均有适当反应；3）缺镁大鼠中出现的高钙血症并非由于PTH分泌增加，而必须由另一种机制来解释。
