| Autor: |
Dr. Meyer, Ralph A., Meyer, Martha H., Tenenhouse, Harriet S., Klugerman, Abbey H. |
| Zdroj: |
Journal of Bone & Mineral Research; August 1989, Vol. 4 Issue: 4 p523-532, 10p |
| Abstrakt: |
The X‐linked hypophosphatemic (Hyp) mouse is a model for human X‐linked hypophosphatemia. Surgical joining of normal to Hypmice by parabiosis results in the normal mice developing low renal retention of phosphate and hypophosphatemia. These results suggest a humoral component to the renal defect. To test whether this component could be parathyroid hormone, surgical parathyroidectomy (PTX) or sham surgery was performed in mice 3 weeks after parabiotic union (n> 20 per group). After an overnight fast, PTX mice were hypocalcemic and hyperphosphatemic relative to sham‐operated control mice. PTX normal mice joined to PTX Hypmice were significantly lower in plasma phosphate and higher in fractional excretion of phosphate [U/P phosphate/(U/P creatinine)] when compared with PTX normal mice joined to other PTX normals. To test for more specific evidence of altered renal transport function, renal brush‐border membrane vesicles (BBMV) were prepared from these mice, and phosphate and glucose uptakes were measured. The phosphate/glucose transport ratio was lower in BBMV from Hypmice, joined to either normal mice or to Hypmice, when compared with that from normal‐normal pairs. Moreover, BBMV from normal mice joined to Hypmice had a significantly lower phosphate/glucose uptake ratio than BBMV from normal mice joined to other normal mice, and their activity approached that of BBMV derived from Hypmice. Glucose uptake in BBMV was unaffected by parabiosis or genotype. In summary, parabiosis of normal mice to Hypmice resulted in the development of phosphaturia and decreased BBMV phosphate transport in the normal mice. The persistence of the phosphate transport defect in parathyroidectomized mice suggests that parathyroid hormone is not the humoral factor contributing to these results. |
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