Analysis Tools
homeostasis/metabolism
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• on a vitamin D-depleted diet, mutant mice exhibit an appropriate increase in circulating PTH levels in reponse to hypocalcemia
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• on a vitamin D-depleted diet, mutant mice exhibit hypocalcemia due to hypovitaminosis D
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• on a normal (vitamin D-repleted) diet, urinary loss of 25-OH vitamin D3 coincides with a 50% reduction in the plasma levels of 25-OH vitamin D3 and of 1,25-(OH)2 D3 while serum calcium, phosphorus, and PTH levels remain unchanged relative to homozygous Lrp2tm1Tew control mice
• on a vitamin D-depleted diet, the plasma levels of 25-OH vitamin D3 and of 1,25-(OH)2 D3 are reduced to the lowest detection levels along with a marked reduction in serum calcium levels and an increase in PTH levels
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• a 5- to 6-fold increase in urinary excretion of 125I-labeled vitamin D-binding protein (DBP) and 3H-25-OH vitamin D3 is observed relative to homozygous Lrp2tm1Tew control mice
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• mutant kidneys display impaired retrieval of plasma proteins from the glomerular filtrate and excrete increased amounts of low molecular weight proteins into the urine, including vitamin D-binding protein (DBP) and retinol-binding protein (RBP)
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skeleton
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• the total bone mineral content in femur and tibia is drastically decreased relative to control mice
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• on a vitamin D-deficient chow, mutant verebrates exhibit a highly abnormal and unmineralized bone surface that is mostly covered by osteoid (uncalcified matrix)
• a significant increase in osteoid surface, osteoid width, and osteoid volume and a concomittant reduction in the mineralizing bone surfaces are observed
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osteomalacia
(
J:81496
)
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• after 6 weeks on a vitamin D-deficient chow, mutant mice exhibit true severe osteomalacia (softening of the bones) as a result of hypovitaminosis D
• osteopathy is characterized by a reduction in bone mineral content, an increase in osteoid surfaces, and a lack of mineralizing activity
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• on a normal diet, mutant lumbar vertebral bodies show a moderate but consistent increase in resorptive cavities and osteoid-covered surfaces, indicating increased resorption and remodeling activity
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• a modest increase in resorptive surface area is observed, as 67% of osteoid surfaces block access of osteoclasts to the bones
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renal/urinary system
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• a 5- to 6-fold increase in urinary excretion of 125I-labeled vitamin D-binding protein (DBP) and 3H-25-OH vitamin D3 is observed relative to homozygous Lrp2tm1Tew control mice
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• mutant kidneys display impaired retrieval of plasma proteins from the glomerular filtrate and excrete increased amounts of low molecular weight proteins into the urine, including vitamin D-binding protein (DBP) and retinol-binding protein (RBP)
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