The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.
Osteopathy and resistance to vitamin D toxicity in mice null for vitamin D binding protein
Open accessAbstract
A line of mice deficient in vitamin D binding protein (DBP) was generated by targeted mutagenesis to establish a model for analysis of DBP's biological functions in vitamin D metabolism and action. On vitamin D-replete diets, DBP-/- mice had low levels of total serum vitamin D metabolites but were otherwise normal. When maintained on vitamin D-deficient diets for a brief period, the DBP-/-, but not DBP+/+, mice developed secondary hyperparathyroidism and the accompanying bone changes associated with vitamin D deficiency. DBP markedly prolonged the serum half-life of 25(OH)D and less dramatically prolonged the half-life of vitamin D by slowing its hepatic uptake and increasing the efficiency of its conversion to 25(OH)D in the liver. After an overload of vitamin D, DBP-/- mice were unexpectedly less susceptible to hypercalcemia and its toxic effects. Peak steady-state mRNA levels of the vitamin D-dependent calbindin-D9K gene were induced by 1,25(OH)2D more rapidly in the DBP-/- mice. Thus, the role of DBP is to maintain stable serum stores of vitamin D metabolites and modulate the rates of its bioavailability, activation, and end-organ responsiveness. These properties may have evolved to stabilize and maintain serum levels of vitamin D in environments with variable vitamin D availability.
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Cites
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Metadata
- Authors
- Safadi, F. F., Thornton, P., Magiera, H., Hollis, B. W., Gentile, M., Haddad, J. G., Liebhaber, S. A., & Cooke, N. E.
- Venue
- Journal of Clinical Investigation
- Published
- 1999-01-15
- Volume
- 103
- Issue
- 2
- Pages
- 239-251
- ISSN
- 0021-9738 (ISSN-L)
- OpenAlex
- W1970536654
- Cited by
- 402
- References
- 1
- FWCI
- 6.72
- Type
- journal article
- Language
- en
- Open access
- bronze
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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