Abstract
Synthesis of vitamin D in the skin in response to ultraviolet light is the main determinant of vitamin D status in man1 and it is therefore surprising that rickets and osteomalacia, clinical signs of vitamin D deficiency, remain common in tropical and subtropical countries2. Skin pigmentation can reduce vitamin D formation3 but this is a negligible limitation in people exposed to abundant ultraviolet light4,5. Earlier studies in animals6 and man7 suggested that another environmental factor, the low calcium/high cereal diet typical of susceptible populations2, might affect the efficiency of vitamin D utilization. We show here in rats that the rate of inactivation of vitamin D in the liver is increased by calcium deprivation. The effect is mediated by 1,25-dihydroxyvitamin D, produced in response to secondary hyperparathyroidism8,9, which promotes hepatic conversion of vitamin D to polar inactivation products that are excreted in bile. This finding has widespread implications both for understanding the pathogenesis of endemic rickets and in that it provides a unifying mechanism for the development of vitamin D deficiency in many clinical disorders.
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Clements, M., Johnson, L. & Fraser, D. A new mechanism for induced vitamin D deficiency in calcium deprivation . Nature 325, 62–65 (1987). https://doi.org/10.1038/325062a0
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DOI: https://doi.org/10.1038/325062a0
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