Metabolism and synthesis of active forms
The pathway of vitamin D in the body begins in the skin, where cholecalciferol (vitamin D₃) is formed from 7-dehydrocholesterol under the influence of ultraviolet radiation. Next, the first hydroxylation occurs in the liver: the enzyme 25-hydroxylase adds a group to the 25th carbon atom. This produces 25-hydroxycholecalciferol (25(OH)D), which circulates in the blood as the main transport form.
The final stage takes place in the proximal renal tubules. Here, under the influence of parathyroid hormone, 1-alpha-hydroxylation occurs with the participation of NADPH. As a result, the final active metabolite—1,25-dihydroxycholecalciferol (calcitriol)—is synthesized, acting similarly to a steroid hormone.
Physiological effects in target organs
The active forms of vitamin D regulate metabolism by influencing three key systems:
- Intestine: stimulates the absorption of calcium and phosphorus ions by activating the synthesis of calbindin, a specialized calcium-binding protein.
- Kidneys: enhance the reabsorption of calcium and phosphates in the tubules.
- Bone tissue: promote mineralization, stimulate the synthesis of glycosaminoglycans to bind calcium, influence the activity of osteoblasts and osteoclasts, and ensure skeletal growth and proper ossification.
Laboratory assessment of status
To assess vitamin D status, the concentration of the stable circulating metabolite, calcidiol (25(OH)D), is measured. Other active forms are not suitable for routine analysis due to rapid degradation.
| 25(OH)D level | Supply status |
|---|---|
| ≥ 20 ng/mL (> 50 nmol/L) | Adequate supply |
| 12–20 ng/mL (30–50 nmol/L) | Insufficiency |
| < 12 ng/mL (< 30 nmol/L) | Deficiency |
| > 100 ng/mL (> 250 nmol/L) | Risk of toxic effects |
Metabolic disorders in deficiency
Vitamin D deficiency leads to a disruption of calcium and phosphorus balance, a clear example of which is rickets. In grade I severity, the level of 25(OH)D decreases, and the body initiates compensation through an increase in parathyroid hormone and alkaline phosphatase. In grade II, blood phosphorus levels drop consistently, and hypophosphatemia develops. In grade III, complete failure of compensation occurs: calcium levels drop, and maximum values of parathyroid hormone and alkaline phosphatase are recorded.
The skin catches the sun, the liver adds the first hydroxyl (25), and the kidneys provide the final touch (1,25) to conquer rickets!
Class and exam questions
Why is 25(OH)D specifically measured to assess vitamin D status?
Specifically, 25-hydroxycholecalciferol is the primary transport and circulating form of the vitamin in the blood with the most stable concentration. Active metabolites degrade rapidly and are not suitable for standard analysis.
How do the kidneys participate in the activation of vitamin D?
In the mitochondria of renal tubular cells, 1-alpha-hydroxylation takes place involving NADPH. This process is stimulated by parathyroid hormone and leads to the formation of active calcitriol.
Which laboratory parameters change in severe rickets?
There is a profound deficiency of 25(OH)D, a marked drop in blood phosphorus and calcium levels, as well as a maximum increase in parathyroid hormone and alkaline phosphatase levels.
What else to study on this topic
- The role of parathyroid hormone and calcitonin in the regulation of calcium and phosphorus metabolism
- Mechanisms of secondary hyperparathyroidism in vitamin D deficiency
- Features of the use of active vitamin D metabolites in renal failure
- Extraskeletal effects of calcitriol via intracellular VDR receptors
- Risk factors and comprehensive treatment of D-deficiency rickets in children
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