Vitamin D and Health: Perspectives From Mice and Man
Abstract
The discovery of the dual origin of vitamin D either by synthesis in the skin from 7-dehydrocholesterol under the influence of UVB sunlight or from dietary origin quickly enabled the eradication of endemic rickets. It then took about one century to unravel the complex metabolism of vitamin D into a large number of metabolites and a key hormone, 1,25(OH)2D, that acts as a ligand for a nuclear transcription factor, VDR, which like all other nuclear receptors, regulates gene transcription and cell function. The vitamin D endocrine system undoubtedly plays a key role in calcium and bone homeostasis. The widespread presence of VDR and the key activating (1α-hydroxylase, CYP27B1) and inactivating (24-hydroxylase, CYP24A1) enzymes in most mammalian cells and the data that 1,25(OH)2D regulates ∼3% of the mouse and human genome suggest that vitamin D metabolites may also function as a hormone or cytokine for many other cellular functions. The development of mice lacking either VDR or 1α-hydroxylase provided the tools for a more careful examination of the global physiologic role of vitamin D. The phenotype of these mice can then also be used to explore whether similar consequences of vitamin D deficiency or excess can be observed in humans. As for other ligands of nuclear receptors, the spectrum of activities of the vitamin D hormone not only covers a primary target system (calcium and bone homeostasis) but also modifies nearly all cells or tissues including skin and muscle, the…
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Evidence Hub reads this as a randomized trial, done in people. Its evidence level is 2 of 5 (High · randomized trial). Randomized trials of a reasonable size are the strongest single-study design. Reported size: 13,432 participants or records.
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