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Abnormal parathyroid function in the X-linked hypophosphatemic mouse.

作者信息

Posillico J T, Lobaugh B, Muhlbaier L H, Drezner M K

出版信息

Calcif Tissue Int. 1985 Jul;37(4):418-22. doi: 10.1007/BF02553712.

DOI:10.1007/BF02553712
PMID:3930040
Abstract

Employing a cytochemical bioassay, we compared parathyroid function in normal and X-linked hypophosphatemic (Hyp) mice. Under basal conditions Hyp mice manifested hypocalcemia and, in accord, had a plasma bioactive parathyroid hormone concentration (3.04 +/- 0.14 pg/ml) significantly greater than that of normals (2.16 +/- 0.14 pg/ml). We confirmed the validity of the bioassay by demonstrating that the plasma collected from both mouse models diluted parallel to the assay standard curve. Moreover, after parathyroidectomy, normal and Hyp mice had plasma bioactive parathyroid hormone levels approximately 90% less than those obtained under basal conditions and indistinguishable from one another. In further studies we observed that dietary calcium and/or vitamin D deprivation in both animal models resulted in a comparable decline of the plasma calcium concentration. However, the concordant increase of the circulating bioactive parathyroid hormone level was greater in the normal mice. Thus, the bioactive parathyroid hormone concentration obtained in response to a low calcium challenge in normals was significantly greater than that in Hyp mice. In contrast, in response to dietary calcium loading, the plasma bioactive parathyroid hormone levels did not decrease significantly from basal values in either animal model. These data illustrate that the bioactive parathyroid hormone concentration in both normal and Hyp mice is inversely correlated with the plasma calcium. However, while the Hyp mice maintain an elevated plasma parathyroid hormone concentration under basal conditions (in response to a decreased plasma calcium), the parathyroid activity of the mutants after a more severe hypocalcemic challenge is attenuated, resulting in a significantly different model of linear correlation. Thus, these data indicate that Hyp mice manifested abnormal regulation of parathyroid function.

摘要

相似文献

1
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2
X-linked hypophosphatemic mice are not hypersensitive to parathyroid hormone.
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3
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J Bone Miner Res. 1989 Aug;4(4):523-32. doi: 10.1002/jbmr.5650040411.
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Increased plasma 1,25-dihydroxyvitamin D after low calcium challenge in X-linked hypophosphatemic mice.X连锁低磷血症小鼠低钙刺激后血浆1,25-二羟基维生素D升高。
Endocrinology. 1982 Jul;111(1):174-7. doi: 10.1210/endo-111-1-174.
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Increased bone volume and correction of HYP mouse hypophosphatemia in the Klotho/HYP mouse.Klotho/HYP 小鼠骨量增加及纠正低血磷。
Endocrinology. 2010 Feb;151(2):492-501. doi: 10.1210/en.2009-0564. Epub 2009 Dec 1.
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Abnormal parathyroid hormone stimulation of 25-hydroxyvitamin D-1 alpha-hydroxylase activity in the hypophosphatemic mouse. Evidence for a generalized defect of vitamin D metabolism.低磷血症小鼠中甲状旁腺激素对25-羟维生素D-1α-羟化酶活性的异常刺激。维生素D代谢普遍缺陷的证据。
J Clin Invest. 1986 Jan;77(1):181-7. doi: 10.1172/JCI112274.
3
Primary cultures of renal epithelial cells from X-linked hypophosphatemic (Hyp) mice express defects in phosphate transport and vitamin D metabolism.

本文引用的文献

1
Secondary hyperparathyroidism in X-linked hypophosphatemic mice.X连锁低磷血症小鼠中的继发性甲状旁腺功能亢进
Endocrinology. 1982 Aug;111(2):650-2. doi: 10.1210/endo-111-2-650.
2
Abnormal regulation of renal 25-hydroxyvitamin D-1 alpha-hydroxylase activity in the X-linked hypophosphatemic mouse.X连锁低磷血症小鼠中肾25-羟维生素D-1α-羟化酶活性的异常调节
J Clin Invest. 1983 Feb;71(2):400-3. doi: 10.1172/jci110783.
3
Abnormal 24-hydroxylation of 25-hydroxyvitamin D in the X-linked hypophosphatemic mouse.X连锁低磷血症小鼠中25-羟基维生素D的异常24-羟化作用。
来自X连锁低磷血症(Hyp)小鼠的肾上皮细胞原代培养物表现出磷酸盐转运和维生素D代谢缺陷。
Am J Hum Genet. 1988 Sep;43(3):293-303.
4
Crosstransplantation of kidneys in normal and Hyp mice. Evidence that the Hyp mouse phenotype is unrelated to an intrinsic renal defect.正常小鼠和Hyp小鼠之间的肾脏交叉移植。证据表明Hyp小鼠的表型与内在肾脏缺陷无关。
J Clin Invest. 1992 May;89(5):1453-9. doi: 10.1172/JCI115735.
Endocrinology. 1983 Feb;112(2):633-8. doi: 10.1210/endo-112-2-633.
4
X-linked hypophosphatemic mice are not hypersensitive to parathyroid hormone.
Endocrinology. 1982 Mar;110(3):1030-6. doi: 10.1210/endo-110-3-1030.
5
Increased urinary excretion of cyclic nucleotides in X-linked hypophosphatemic (Hyp) mice.
Experientia. 1981;37(9):978-9. doi: 10.1007/BF01971790.
6
Serum parathyroid hormone levels in acquired vitamin D deficiency of infancy.婴儿期获得性维生素D缺乏症的血清甲状旁腺激素水平
Pediatrics. 1972 Jun;49(6):837-40.
7
Serum parathyroid hormone concentrations in hypophosphataemic vitamin D resistant rickets.低磷性维生素D抵抗性佝偻病患者的血清甲状旁腺激素浓度
Helv Paediatr Acta. 1974 Aug;29(3):187-94.
8
Parathyroid hormone secretion in familial vitamin-D-resistant rickets.家族性维生素D抵抗性佝偻病中的甲状旁腺激素分泌
N Engl J Med. 1973 Nov 1;289(18):941-5. doi: 10.1056/NEJM197311012891804.
9
Nature of defect responsible for familial vitamin D-resistant rickets (VDRR) based on radioimmunoassay for parathyroid hormone (PTH).基于甲状旁腺激素(PTH)放射免疫测定法的家族性维生素D抵抗性佝偻病(VDRR)相关缺陷的性质
Trans Assoc Am Physicians. 1972;85:172-80.
10
Serum parathyroid hormone in hypophosphatemic vitamin D-resistant rickets.低磷性维生素D抵抗性佝偻病患者的血清甲状旁腺激素
J Pediatr. 1972 Aug;81(2):294-300. doi: 10.1016/s0022-3476(72)80298-1.