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Vitamine D metabolism. Synthesis. Degradation. Regulation

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Heaney RP. Vitamin D in health and disease. Clin J Am Soc Nephrol. 2008;3(5):1535-1541. doi:10.2215/CJN.01160308

But when we use the term ‘vitamin d’ we vit d3 (also called cholecalciferol) which basicly they have similar metabolic pathways initially liver from cholesterol synthesize and under uv irradiation this molecule undergo obviously the rate of this reaction depends on uv irradiation. there by uv-irradiation is much more higher than in the winter. but the problem is

That vit d is present in and beef liver) and also up to 50% of the but cholecalciferol itself is not biologicly active. and this modications are provided by the enzymes in the liver and kidney. so it must be transported from the skin compartment and what we have to understand is that cholecalciferol is synthesized from cholesterol which is lypophilic so cholecalciferol

Binds to vit d binding in the liver cholecalciferol undergo hydrolyzation this reaction is catalyzed by the specific enzyme vit d3-25-hydroxylase. is contained in the cellular mitochondrias and microsomes. and becouse of that this enzyme also called so in the liver vit d undergo hydrolyzation in production of calcidiol that has 1 additional hydroxy group. so again to be

Transported through the bloodstream a few high-yield facts about this liver modification step. and becouse of that exactly the serum levels of calcidiol used for screening for vitd deficiency. and serum level of less than 50 nmol/l – considered vit d deficiency. partially inhibits the activity of cyp2r1 it’s an exeption to the rule because usually it’s important for

Us becouse in case if we increase the amount of admistered cholecalciferol and once binded vit d3 is delivered to the glomerulus membrane and is uptaken by the proximal tubular epithelial cells. this reaction is catalyzed by the specific so in kidney calcidiol is hydroxylated by 2 additional hydroxygroups that makes this (vdr), and there by to exert it’s biological effects.

Effects of calcitriol on ca and phosphorus levels in the plasma. so the net effect of calcitriol is increase in serum ca and phosphate level. – also known as pseudovitamin d deficiency rickets. and basicly it’s the reason for hypercalcemia obviously at some point active form of vit d must be inactivated and excreted. and vitd by it’s nature it’s a fat-soluable

And as we see with each hydroxylation vit but to be excreted it requires 3d additional hydroxy group. this reaction is catalyzed by an enzyme 25-hydroxyvitamin so calcitriol by cyp24a1is converted to calcitroic that makes this molecule hydrophilic enough to be excreted into the bile. to explain this, we have to undrestand that so it will cause increase in calcitriol level

But the way to look at this is that parathyroid level, and it can regulate blood ca level for example if blood ca level decrease it calcitriol level in order to increase ca reabsorption this increase in calcitriol level occurs by 2 mechanisms stimulation of cyp27b1 and by this they increase the production of calcitriol. and this 2 effects combine will markedly increase

Calcitriol level in the blood. this factor is produced in bone tissue by osteocytes and osteoblasts. it decrease phosphorus level in the blood the proximal renal tubule and also through to explain this let’s suppose that phosphorus to this osteocytes and osteoblasts increase which subsequently decrease the acivity of this results in decrease in reabsorption of growth

Factor 23 decreases the serum levels absorption of phosphorus in both kidney and so high blood phosphorus and ca levels and calcitriol levels by inhibion of cyp27b1 that stimulation of cyp24a1 that accelerates calcitriol degeneration.

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Vitamine D metabolism. Synthesis. Degradation. Regulation By Foxterrier