Kraut J A, Gordon E M, Ransom J C, Horst R, Slatopolsky E, Coburn J W, Kurokawa K
Kidney Int. 1983 Nov;24(5):644-8. doi: 10.1038/ki.1983.206.
Bone disease may occur in disorders associated with chronic metabolic acidosis. This has been attributed, in part, to reduced production of 1,25(OH)2D3. Although metabolic acidosis in the vitamin D deficient animal has been associated with a reduction in the conversion of radiolabeled 25(OH)D3 to 1,25(OH)2D3, studies in D-replete humans have revealed no effect of acidosis on 1,25(OH)2D3 metabolism. To examine this issue further, we measured serum 25(OH)D, 1,25(OH)2D, and 24,25(OH)2D levels in six healthy subjects before and after 9 days of metabolic acidosis induced by the ingestion of ammonium chloride. In four subjects, we measured the increment in serum levels of 1,25(OH)2D in response to the infusion of parathyroid extract both during control and acidosis. Serum levels of 1,25(OH)2D, 13.6 +/- 1.3 and 14.3 +/- 0.9 pg/ml, in control and acidosis, respectively, were not different. The serum 1,25(OH)2D levels in control and acidosis rose to a similar degree with the infusion of PTE. These data provide strong evidence that metabolic acidosis does not have a substantial impact on the synthesis of 1,25(OH)2D3 metabolism in vitamin D-replete humans.
骨病可能发生在与慢性代谢性酸中毒相关的病症中。这部分归因于1,25(OH)2D3生成减少。尽管维生素D缺乏动物的代谢性酸中毒与放射性标记的25(OH)D3向1,25(OH)2D3的转化减少有关，但在维生素D充足的人类中的研究表明酸中毒对1,25(OH)2D3代谢没有影响。为了进一步研究这个问题，我们测量了6名健康受试者在摄入氯化铵诱导代谢性酸中毒9天前后的血清25(OH)D、1,25(OH)2D和24,25(OH)2D水平。在4名受试者中，我们测量了在对照期和酸中毒期静脉输注甲状旁腺提取物后血清1,25(OH)2D水平的升高情况。对照期和酸中毒期的血清1,25(OH)2D水平分别为13.6±1.3和14.3±0.9 pg/ml，没有差异。在对照期和酸中毒期，静脉输注甲状旁腺提取物后血清1,25(OH)2D水平升高程度相似。这些数据提供了有力证据，表明代谢性酸中毒对维生素D充足的人类中1,25(OH)2D3代谢的合成没有实质性影响。
