Normocalcemia without hyperparathyroidism in vitamin D-deficient rats.

Normocalcemia without hyperparathyroidism in vitamin D-deficient rats.
复制标题

维生素 D 缺乏大鼠的钙血症正常但无甲状旁腺功能亢进。

DOI:
10.1002/jbmr.5650060309
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发表时间:
1991
期刊:
Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research
影响因子:
--
通讯作者:
Walters,MR
Walters,MR
中科院分区:
--
文献类型:
--
作者:
Kollenkirchen,U;Fox,J;Walters,MR

文献摘要

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尽管进行了多次尝试,但没有可靠的饮食方案可以在不改变血浆甲状旁腺激素(PTH)、钙或磷酸盐的情况下实现大鼠维生素D缺乏症(‐D)。这是研究维生素D代谢物在1,25‐二羟基维生素D3[1,25‐(OH)2D3]靶组织功能中的生理作用的一个重要障碍。本文介绍了高钙含量、适当控制钙磷比和乳糖相结合的饲粮的成功开发。正常断奶大鼠饲喂含有A、0.8% Ca、0.5% P、+D3或含有B、0.8% Ca和0.5% P的‐D日粮;C, 2.0% Ca, 1.25% P;或D, 2.0% Ca, 1.25% P和20%乳糖。6周后,D组大鼠血钙和血磷水平保持正常,B组和C组低血钙水平(分别为6.9±0.8和7.2±0.4 mg/dl)。因此,在缺乏乳糖的情况下,高钙、高磷饲料不能维持正常的血浆钙水平。D组的正常钙血症不是通过PTH分泌升高来维持的,因为N端PTH水平也正常(14±3对20±5 pg/ml)。相比之下,低钙B组和C组PTH水平明显升高(分别为47±7和48±10 pg/ml)。在所有‐D组中,血浆25‐ohd3和1.25‐(OH) 2d3水平分别降至< 120和< 12 pg/ml。因此,高钙饮食和正常断奶仔猪的使用并没有阻碍维生素D缺乏症的发展。这种正常钙血症维生素D缺乏的大鼠模型将极大地促进阐明维生素D代谢物在125‐(OH) 2d3靶点正常功能中的生理作用。
Despite numerous attempts, no reliable dietary regimen exists to achieve vitamin D deficiency (‐D) in rats without attendant changes in plasma parathyroid hormone (PTH), Ca, or phosphate. This represents an important obstacle to proper investigations of the physiologic role(s) of vitamin D metabolites in the function of 1,25‐dihydroxyvitamin D3[1,25‐(OH)2D3] target tissues. This paper describes the successful development of such a diet, which uses a combination of high Ca content, properly controlled Ca/P ratio, and lactose. Normal weanling rats were fed diets containing A, 0.8% Ca, 0.5% P, +D3, or ‐D diets containing B, 0.8% Ca and 0.5% P; C, 2.0% Ca and 1.25% P; or D, 2.0% Ca, 1.25% P, and 20% lactose. After 6 diet weeks group D rats remained normocalcemic and normophosphatemic, but diet groups B and C became hypocalcemic (6.9 ± 0.8 and 7.2 ± 0.4 mg/dl, respectively). Thus high dietary Ca and P was incapable of maintaining normal plasma Ca levels in the absence of dietary lactose. The normocalcemia in group D was not maintained by elevated PTH secretion because N‐terminal PTH levels were also normal (14 ± 3 versus 20 ± 5 pg/ml). In contrast, PTH levels were markedly elevated in hypocalcemic groups B and C (47 ± 7 and 48 ± 10 pg/ml, respectively). Plasma 25‐OHD3and 1,25‐(OH)2D3levels were reduced to < 120 and < 12 pg/ml, respectively, in all ‐D groups. Thus the high‐Ca diet and the use of normal weanlings did not impede the development of vitamin D deficiency. This rat model of normocalcemic vitamin D deficiency will greatly facilitate elucidation of the physiologic role(s) of vitamin D metabolites in the normal functioning of 1,25‐(OH)2D3targets.