Abstract:
:Hyp mice have a defective control system for the synthesis of 1,25-(OH)2-vitamin D that does not respond to a low phosphate stimulus. While the plasma levels of 25-OH-vitamin D are reduced somewhat, this seems to be not a serious defect since plasma 1,25-(OH)2-vitamin D levels are normal. Hyp kidneys synthesize and excrete elevated levels of cyclic AMP and cyclic GMP. The elevated tissue levels of trace minerals suggests increased food intake with normal intestinal absorption of the minerals. In addition there is the reduced renal tubular reabsorption of phosphate caused by a change in the brush border transport of phosphate. This leads to hypophosphatemia, osteomalacic bone disease and altered Mg metabolism. There is intestinal resistance to 1,25-(OH)2-vitamin D stimulation. Many of these defects seem unrelated to the reduced renal tubular reabsorption of phosphate. Yet all are derived from one mutation in the Hyp gene. The underlying explanation must account for all abnormalities by a single mutation in a single gene product. The near normal phosphate levels in soft tissues and the multiple defects argue against a genetic change in the phosphate pump as an ultimate explanation. Still to be explored are possible changes in a phosphate recognition site on a cell membrane or a change in an as yet unknown phosphate regulating system.
journal_name
Adv Exp Med Bioljournal_title
Advances in experimental medicine and biologyauthors
Meyer RA Jr,Gray RW,Kiebzak GM,Mish PMdoi
10.1007/978-1-4615-9167-2_40subject
Has Abstractpub_date
1980-01-01 00:00:00pages
351-9eissn
0065-2598issn
2214-8019journal_volume
128pub_type
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