Rayssiguier Y, Thomasset M, Garel J M, Barlet J P
Horm Metab Res. 1982 Jul;14(7):379-82. doi: 10.1055/s-2007-1019021.
Rats were pair fed a magnesium deficient or control diet. Plasma parathyroid hormone (PTH) was estimated by radioimmunoassay using synthetic 1-34 PTH and intestinal calcium-binding protein (CaBP) was quantified directly by RIA in proximal duodenum, distal ileum and medium jejunum. In magnesium depleted rats, plasma magnesium levels were significantly decreased, a fall in plasma phosphate paralleled the decrease in plasma magnesium and plasma calcium levels were significantly increased after 14 days of magnesium deficiency. A significant rise in plasma PTH was observed on day 7 and 14 after magnesium deficiency. This increase disappeared on day 20. During the whole experimental period, no significant differences in CaBP levels were observed between the two groups of rats. Thus it is difficult to postulate an increase in vitamin D-dependent calcium absorption to explain the hypercalcemia found in magnesium deficient rats. Neither can the hypercalcemia be readily explained by an increased bone calcium mobilisation due to transient PTH increase since previous results have reported decreased bone resorption in magnesium deficient rats under similar experimental conditions.
将大鼠分为两组,分别喂饲缺镁饮食或对照饮食。使用合成的1-34甲状旁腺激素通过放射免疫测定法估算血浆甲状旁腺激素(PTH),并通过放射免疫分析法直接对近端十二指肠、回肠末端和空肠中段的肠钙结合蛋白(CaBP)进行定量分析。在缺镁大鼠中,血浆镁水平显著降低,血浆磷酸盐的下降与血浆镁的降低平行,缺镁14天后血浆钙水平显著升高。缺镁后第7天和第14天观察到血浆PTH显著升高。这种升高在第20天消失。在整个实验期间,两组大鼠的CaBP水平未观察到显著差异。因此,很难假设维生素D依赖性钙吸收增加来解释缺镁大鼠中发现的高钙血症。高钙血症也不能轻易地用由于短暂的PTH增加导致骨钙动员增加来解释,因为先前的结果报道在类似实验条件下缺镁大鼠的骨吸收减少。