Bonjour J P, Trechsel U, Fleisch H, Schenk R, DeLuca H F, Baxter L A
Am J Physiol. 1975 Aug;229(2):402-8. doi: 10.1152/ajplegacy.1975.229.2.402.
The effect of 1,25-dihydroxycholecalciferol (1,25-(OH)2D3) on Ca balance, 45Ca kinetics, and bone morphology has been studied in control rats and rats given disodium ethane-1-hydroxy-1,1-diphosphonate (EHDP), 10 mg P/kg sc per day. This large dose of EHDP is known to inhibit bone mineralization and intestinal calcium absorption and to depress the endogenous production of 1,25-(OH)2D3. In conctrol rats, 1,25-(OH)2D3 increased intestinal calcium absorption. However, in contrast to the enhanced calcium absorption that results from an augmentation of dietary calcium, the 1,25(OH)2D3-induced augmentation of calcium absorption does not lead to a rise in calcium retention, the intestinal effect being matched by an increased excretion of urinary calcium. The EHDP-induced decrease of intestinal calcium absorption could be completely prevented by the concomitant administration of 1,25-(OH)2D3 but not the inhibition of bone mineralization. Therefore, in contrast to the impairment of calcium absorption, that of bone mineralization brought about by large doses of EHDP cannot be merely attributed to a decreased production of 1,25-(OH)2D3.
在对照大鼠和每天皮下注射10mg磷/千克乙烷-1-羟基-1,1-二膦酸二钠(EHDP)的大鼠中,研究了1,25-二羟基胆钙化醇(1,25-(OH)2D3)对钙平衡、45Ca动力学和骨形态的影响。已知这种大剂量的EHDP会抑制骨矿化和肠道钙吸收,并抑制1,25-(OH)2D3的内源性产生。在对照大鼠中,1,25-(OH)2D3增加了肠道钙吸收。然而,与因膳食钙增加而导致的钙吸收增强不同,1,25-(OH)2D3诱导的钙吸收增加并未导致钙潴留增加,肠道效应与尿钙排泄增加相匹配。同时给予1,25-(OH)2D3可完全防止EHDP诱导的肠道钙吸收减少,但不能防止骨矿化受到抑制。因此,与钙吸收受损不同,大剂量EHDP引起的骨矿化受损不能仅仅归因于1,25-(OH)2D3产生减少。