Forbes R M, Parker H M
J Nutr. 1980 Aug;110(8):1610-7. doi: 10.1093/jn/110.8.1610.
A series of six experiments was conducted to investigate the effects of Mg deficiency in the young rat on parathyroid hormone (PTH) activity and on response to parathyroid extract (PTE) and to endogenously produced PTH stimulated by dietary Ca deficiency. Major criteria employed were 45Ca release from pre-labeled bone and urinary excretion of cAMP. Mg deficiency was accompanied by lowered 45Ca mobilization and urinary cAMP excretion, indicating either a depression in PTH secretion or tissue insensitivity to it. Administration of PTE resulted in equivalent increases in 45Ca mobilization irrespective of Mg status but increased cAMP excretion only in Mg-adequate animals, thus indicating a depressed sensitivity of kidney to PTH in the Mg-deficient animal. In vitro response of kidney cortex from Mg-deficient animals to PTE added to incubation medium indicated no defect in the adenyl cyclase system. Endogenous stimulation of PTH by low Ca diet increased cAMP in Mg-adequate animals but not in rats with pre-existing Mg deficiency. Mg deficiency did not reduce cAMP previously stimulated by Ca deficiency.
进行了一系列六项实验，以研究幼鼠镁缺乏对甲状旁腺激素（PTH）活性、对甲状旁腺提取物（PTE）的反应以及对因饮食缺钙刺激内源性产生的PTH的反应的影响。采用的主要标准是预标记骨中45Ca的释放和尿中cAMP的排泄。镁缺乏伴随着45Ca动员和尿中cAMP排泄的降低，这表明要么是PTH分泌减少，要么是组织对其不敏感。无论镁状态如何，给予PTE都会使45Ca动员等量增加，但仅在镁充足的动物中cAMP排泄增加，因此表明镁缺乏动物的肾脏对PTH的敏感性降低。来自镁缺乏动物的肾皮质对添加到孵育培养基中的PTE的体外反应表明腺苷酸环化酶系统没有缺陷。低钙饮食对PTH的内源性刺激在镁充足的动物中增加了cAMP，但在先前存在镁缺乏的大鼠中没有增加。镁缺乏并没有降低先前由缺钙刺激产生的cAMP。
