SECONDARY HYPERPARATHYROIDISM IN X-LINKED HYPOPHOSPHATEMIC MICE
SECONDARY HYPERPARATHYROIDISM IN X-LINKED HYPOPHOSPHATEMIC MICE
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DOI：
10.1210/endo-111-2-650
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发表时间：
1982-01-01
期刊：
影响因子：
4.8
通讯作者：
MEYER, RA
中科院分区：
文献类型：
--
作者：
KIEBZAK, GM;ROOS, BA;MEYER, RA
测定成年、年龄匹配、正常成年小鼠和Hyp雄性小鼠(11只/基因型)血浆甲状旁腺激素(PTH)水平。Hyp小鼠是人类疾病X连锁低磷血症的动物模型。用放射免疫分析法检测甲状旁腺素的完整片段和羧基末端片段。Hyp小鼠的血浆甲状旁腺素水平显著升高(0.21。+-。0.03 ng牛甲状旁腺素eq/ml)，正常小鼠(0.04±-)。0.03 ng/ml；P<0.01)。这种甲状旁腺机能亢进可能是骨骼对内源性甲状旁腺素抵抗的结果，也可能是其肾脏磷酸盐和尿环磷酸腺苷排泄显著增加的原因。
Plasma parathyroid hormone (PTH) was measured in adult, age-matched, intact normal mice and Hyp male mice (11/genotype). Hyp mice are an animal model for the human disease X-linked hypophosphatemia. A radioimmunoassay was used which detects intact and carboxyl-terminal fragments of PTH. Hyp mice had significantly higher plasma PTH levels (0.21 .+-. 0.03 ng bovine PTH eq/ml) than normal mice (0.04 .+-. 0.03 ng/ml; P < 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.