Vitamin D binding protein is required to utilize skin-generated vitamin D
Autor: | Hector F. DeLuca, Jeremy Seeman, Nancy E. Cooke, Lori A. Plum, Elizabeth G. Duchow |
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Rok vydání: | 2019 |
Předmět: |
0301 basic medicine
Vitamin medicine.medical_specialty genetic structures Ultraviolet Rays Vitamin D-binding protein chemistry.chemical_element Calcium law.invention 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine law Internal medicine medicine Vitamin D and neurology Animals cardiovascular diseases Vitamin D Skin Mice Knockout Sunlight Multidisciplinary Hypocalcemia Chemistry Vitamin D-Binding Protein Biological Sciences Vitamin D Deficiency Recombinant Proteins 030104 developmental biology Endocrinology Injections Intravenous Recombinant DNA 030217 neurology & neurosurgery circulatory and respiratory physiology |
Zdroj: | Proc Natl Acad Sci U S A |
ISSN: | 1091-6490 0027-8424 |
DOI: | 10.1073/pnas.1915442116 |
Popis: | Vitamin D is produced in the skin following exposure to sunlight. Ultraviolet (UV) B (UVB, 280–310 nm) results in isomerization of 7-dehydrocholesterol to previtamin D that spontaneously isomerizes to vitamin D. This pool of skin-derived vitamin D is the major source of vitamin D for animals. However, the mechanisms by which it becomes available remain undefined. It has been assumed that cutaneous vitamin D is transported into the circulation by vitamin D binding protein (DBP), but experimental evidence is lacking. To determine whether cutaneous vitamin D is transported by DBP, we utilized DBP(−/−) mice that were made vitamin D-deficient. These animals lack measurable 25(OH)D in blood and are hypocalcemic. As controls, DBP(+/+) animals were vitamin D depleted and made equally hypocalcemic. UV irradiation of DBP(+/+) animals restored serum calcium and serum 25(OH)D while the same treatment of DBP(−/−) animals failed to show either a serum calcium or 25(OH)D response despite having normal vitamin D production in skin. Intravenous injection of small amounts of recombinant DBP to the vitamin D-deficient DBP(−/−) mice restored the response to UV light. These results demonstrate a requirement for DBP to utilize cutaneously produced vitamin D. |
Databáze: | OpenAIRE |
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