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X连锁低磷血症小鼠中的继发性甲状旁腺功能亢进

Secondary hyperparathyroidism in X-linked hypophosphatemic mice.

作者信息

Kiebzak G M, Roos B A, Meyer R A

出版信息

Endocrinology. 1982 Aug;111(2):650-2. doi: 10.1210/endo-111-2-650.

Abstract

Plasma parathyroid hormone (PTH) was measured in adult, age-matched, intact normal mice and Hyp male mice (n = 11/genotype). Hyp mice are an animal model for the human disease X-linked hypophosphatemia. A RIA was used which detects intact and carboxyl-terminal fragments of PTH. Hyp mice were found to have significantly higher plasma PTH levels (0.21 +/- 0.03 ng bovine PTH eq/ml) than normal mice (0.04 +/- 0.03 ng/ml; P less than 0.01). This hyperparathyroidism in the slightly hypocalcemic, osteomalacic Hyp mice may be the result of skeletal resistance to endogenous PTH and may contribute to their characteristically elevated renal excretion of phosphate and urinary cAMP

摘要

在成年、年龄匹配的完整正常小鼠和Hyp雄性小鼠(每种基因型n = 11)中测量了血浆甲状旁腺激素(PTH)。Hyp小鼠是人类疾病X连锁低磷血症的动物模型。使用了一种放射免疫分析法(RIA),该方法可检测PTH的完整片段和羧基末端片段。发现Hyp小鼠的血浆PTH水平(0.21±0.03 ng牛PTH当量/ml)显著高于正常小鼠(0.04±0.03 ng/ml;P<0.01)。轻度低钙血症、患骨软化症的Hyp小鼠出现的这种甲状旁腺功能亢进可能是骨骼对内源性PTH抵抗的结果,并且可能导致它们典型的磷酸盐肾排泄增加和尿cAMP升高。

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