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Vitamin D action
Author(s) -
Goltzman David
Publication year - 2010
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2009.05226.x
Subject(s) - action (physics) , vitamin d and neurology , vitamin , chemistry , medicine , biochemistry , physics , quantum mechanics
Mouse models with targeted deletion of the genes encoding the enzyme 25‐hydroxyvitamin D 1alpha‐hydroxylase [1α(OH)ase], and the vitamin D receptor (VDR), have provided considerable insight into the regulation of mineral and skeletal physiology by 1,25‐dihydroxyvitamin D [1,25(OH) 2 D]. Dietary manipulation induced different phenotypic changes and demonstrated that parathyroid gland function is coordinately regulated by calcium and 1,25(OH) 2 D, but that mineralization of bone reflects ambient calcium (and phosphorus) levels rather than direct actions of the 1,25(OH) 2 D/VDR system. In contrast, increased calcium absorption and optimal osteoblastogenesis and bone formation is modulated by the 1,25(OH) 2 D/VDR system. Similar models have also been employed to study extraskeletal vitamin D actions. For example, increased blood pressure, activation of the renin/angiotensin system, myocardial hypertrophy, and cardiac dysfunction were observed in 1αOHase −/− mice, and could be prevented by 1,25(OH) 2 D 3 administration. These models allow controlled examination of the pathophysiology associated with1,25(OH) 2 D deficiency and intervention to prevent and treat these disorders.