Termed vitamin due to its source from diet, but it is highly similar to a hormone. It can be produced by human organism in small amounts from 7-dehydrocholesterol present in the skin with high consumption of ultraviolet light. It also has to undergo metabolic transitions before becoming active in the body.
Synthesis and metabolism
Vitamin D comes in two forms – as vitamin D3 and vitamin D2. The former one can be synthesized by human body as described before (large amounts of this vitamin come from diet, e.g. eggs), while the later one has to be ingested. The difference between two is a single side chain. Absorption of either form of vitamin D depends on bile salts, since vitamin D is hydrophobic and lipid soluble. That is why it is found associated with chylomicrons or vitamin-D-binding protein (plasma binding protein) in the circulation. Body fat plays a role of storage for vitamin D. While in the circulation, either form of vitamin has to undergo 25-hydroxylation by cytochrome P-450 mixed-function oxidase, found primarily in the liver. Second round of hydroxylation at position 1 occurs in the kidneys and is tightly controlled by PTH and 1,25-dihydroxyvitamin D, the product of reaction, providing negative feedback loop. 1,25-dihydroxyvitamin D has much higher affinity compared to 25-hydroxyvitamin D, yet both play important role due to the higher concentration of the later.
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Vitamin D inhibits PTH synthesis and secretion as described in detail in Hormones section. Besides inhibiting action, vitamin D acts on small intestine, kidneys and bone. As described in Hormones section, vitamin D acts on a nuclear receptor which acts as a transcription modifying factor, when combined with another molecule.
In duodenum, vitamin D induces synthesis of Ca2+ channels, pumps and Ca2+-binding proteins, promoting increased Ca2+ absorption. Phosphate absorption increase is mediated by inducing synthesis of NaPi cotransporter, which appears to be rete limiting.
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In kidneys, vitamin D induces reabsorption of Ca2+ and phosphate, however it is not as potent as PTH. This causes net excretion of phosphate.
In bone, vitamin D acts on both, osteoblasts and osteoclast precursors, having a double effect. On one hand, stimulates osteoclastic precursors to differentiate, increasing the number of osteoclasts and promoting bone resporption. On the other hand, osteoblasts are stimulated to secrete osteoid proteins. It is currently believed that vitamin D promotes mobilization of Ca2+ and phosphate out of the bone in short run, but promotes bone mineralization in the long run.