| First Author | Duchow EG | Year | 2019 |
| Journal | Proc Natl Acad Sci U S A | Volume | 116 |
| Issue | 49 | Pages | 24527-24532 |
| PubMed ID | 31748273 | Mgi Jnum | J:282369 |
| Mgi Id | MGI:6380627 | Doi | 10.1073/pnas.1915442116 |
| Citation | Duchow EG, et al. (2019) Vitamin D binding protein is required to utilize skin-generated vitamin D. Proc Natl Acad Sci U S A 116(49):24527-24532 |
| abstractText | 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. |
