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1,25-二羟维生素D3对维生素D供应正常的大鼠肠道磷吸收的作用

Role of 1,25-dihydroxyvitamin D3 on intestinal phosphate absorption in rats with a normal vitamin D supply.

作者信息

Rizzoli R, Fleisch H, Bonjour J P

出版信息

J Clin Invest. 1977 Sep;60(3):639-47. doi: 10.1172/JCI108815.

Abstract

In vitamin D-deficient rats, impaired intestinal phosphorus (P) absorption can be corrected by 1,25-dihydroxyvitamin D(3)[1,25-(OH)(2)D(3)]. In the present study, it was investigated whether changes in 1,25-(OH)(2)D(3) production can influence intestinal P transport also in animals with a normal supply of vitamin D. The intestinal P absorption was evaluated in rats using both the in situ duodenal loop technique and the determination of the overall gastrointestinal absorption under three conditions known to influence the production of 1,25-(OH)(2)D(3): (a) variation in dietary P, (b) thyroparathyroidectomy (TPTX) with or without administration of parathyroid hormone (PTH), and (c) treatment with disodium ethane-1-hydroxy-1,1-diphosphonate (EHDP). In all circumstances changes in duodenal absorption paralleled the changes in the overall fractional absorption. (a) Lowering dietary P stimulated P absorption. (b) TPTX decreased P absorption. This effect was corrected either by the administration of PTH or by the administration of 1,25-(OH)(2)D(3). (c) EHDP, when given at a dose known to inhibit 1,25-(OH)(2)D(3) formation, decreased the duodenal P absorption in both intact and TPTX animals. This effect was corrected by 1,25-(OH)(2)D(3). In the TPTX-EHDP-treated animals, the administration of PTH did not rectify the low duodenal P absorption. These results support the thesis that, in rats with normal vitamin D supply, variations in the endogenous production of 1,25-(OH)(2)D(3) change the rate of P absorption. However, these changes are in such magnitude that they are of relatively small importance when compared to the effect of variation in the dietary intake of P. These results also strongly suggest that the action of PTH on duodenal P transport is mediated by its effect on 1,25-(OH)(2)D(3) production, inasmuch as the effect of the hormone is abolished after blocking the renal 1-hydroxylation with EHDP.

摘要

在维生素D缺乏的大鼠中,肠道磷(P)吸收受损可通过1,25 - 二羟基维生素D3 [1,25 - (OH)2D3]得到纠正。在本研究中,探讨了1,25 - (OH)2D3生成的变化是否也会在维生素D供应正常的动物中影响肠道磷转运。在三种已知会影响1,25 - (OH)2D3生成的条件下,使用原位十二指肠袢技术和测定胃肠道整体吸收情况来评估大鼠的肠道磷吸收:(a) 饮食中磷的变化,(b) 甲状腺甲状旁腺切除术(TPTX),伴或不伴甲状旁腺激素(PTH)给药,以及(c) 用乙烷 - 1 - 羟基 - 1,1 - 二膦酸钠(EHDP)治疗。在所有情况下,十二指肠吸收的变化与整体分数吸收的变化平行。(a) 降低饮食中的磷会刺激磷吸收。(b) TPTX会降低磷吸收。通过给予PTH或给予1,25 - (OH)2D3可纠正这种效应。(c) 当以已知可抑制1,25 - (OH)2D3形成的剂量给予EHDP时,完整动物和TPTX动物的十二指肠磷吸收均降低。这种效应可通过1,25 - (OH)2D3得到纠正。在TPTX - EHDP处理的动物中,给予PTH并不能纠正十二指肠磷吸收低下的情况。这些结果支持这样的论点,即在维生素D供应正常的大鼠中,1,25 - (OH)2D3内源性生成的变化会改变磷吸收的速率。然而,与饮食中磷摄入量变化的影响相比,这些变化的幅度较小,相对不太重要。这些结果还强烈表明,PTH对十二指肠磷转运的作用是通过其对1,25 - (OH)2D3生成的影响介导的,因为在用EHDP阻断肾脏1 - 羟化作用后,该激素的作用就消失了。

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