Goulding A, Gold E
Endocrinology. 1986 Nov;119(5):2148-54. doi: 10.1210/endo-119-5-2148.
The effects of dietary sodium chloride supplements (8 g/100 g diet) on parathyroid function, serum 1,25-dihydroxyvitamin D [1,25-(OH)2D], calcium balance, bone metabolism, and bone composition were studied in rats treated with prednisolone (2 mg/kg w X day) for 12 weeks. Animals on a low calcium diet (0.1% Ca) received the following treatments: group 1, control; group 2, NaCl; group 3, prednisolone; group 4, NaCl plus prednisolone. Parathyroid function was assessed indirectly from urinary cAMP excretion: bone resorption was estimated by studying urinary hydroxyproline excretion and mobilization of 45Ca from bone. Dietary salt loading increased the urinary excretion of calcium, 45Ca, cAMP, and hydroxyproline and raised serum 1,25-(OH)2D and net calcium absorption, but lowered calcium retention, femoral calcium, and total body calcium. Prednisolone slowed body growth and lowered net calcium absorption, calcium retention, femoral calcium, and total body calcium. Urinary calcium excretion was higher in rats receiving salt and prednisolone in combination than in animals taking salt without prednisolone, but other responses to salt and prednisolone were independent. Thus, salt and prednisolone each elicit osteopenia, and salt causes bone loss in rats receiving prednisolone. The osteopenic effect of salt is attributed to primary augmentation of urinary calcium excretion and secondary increases in PTH-medicated bone resorption. Although salt-treated rats have higher blood levels of 1,25-(OH)2D, bone loss occurs because alimentary calcium absorption is not elevated sufficiently to offset urinary calcium losses. Prednisolone lowers bone formation and net calcium absorption without lowering serum 1,25-(OH)2D values. The parathyroid-vitamin D axis remains intact in prednisolone-treated rats, as they show increases in PTH and 1,25-(OH)2D after salt treatment.
研究了氯化钠补充剂（8克/100克饮食）对用泼尼松龙（2毫克/千克体重×天）治疗12周的大鼠甲状旁腺功能、血清1,25 - 二羟基维生素D [1,25-(OH)₂D]、钙平衡、骨代谢和骨成分的影响。低钙饮食（0.1%钙）的动物接受以下处理：第1组，对照组；第2组，氯化钠；第3组，泼尼松龙；第4组，氯化钠加泼尼松龙。通过尿中环磷酸腺苷（cAMP）排泄间接评估甲状旁腺功能：通过研究尿羟脯氨酸排泄和骨中⁴⁵钙的动员来估计骨吸收。饮食中加盐增加了钙、⁴⁵钙、cAMP和羟脯氨酸的尿排泄，提高了血清1,25-(OH)₂D和净钙吸收，但降低了钙潴留、股骨钙和全身钙。泼尼松龙减缓了身体生长，降低了净钙吸收、钙潴留、股骨钙和全身钙。联合接受盐和泼尼松龙的大鼠尿钙排泄高于仅接受盐而未接受泼尼松龙的动物，但对盐和泼尼松龙的其他反应是独立的。因此，盐和泼尼松龙各自都会引起骨质减少，并且盐会导致接受泼尼松龙的大鼠出现骨质流失。盐的骨质减少作用归因于尿钙排泄的原发性增加以及甲状旁腺激素介导的骨吸收的继发性增加。尽管用盐处理的大鼠血液中1,25-(OH)₂D水平较高，但由于肠道钙吸收没有充分升高以抵消尿钙损失，所以仍会发生骨质流失。泼尼松龙降低了骨形成和净钙吸收，但未降低血清1,25-(OH)₂D值。在接受泼尼松龙治疗的大鼠中，甲状旁腺 - 维生素D轴保持完整，因为它们在盐处理后甲状旁腺激素和1,25-(OH)₂D增加。
