VitaminDStoffwechselprodukts

Vitamin D metabolism refers to the processing of vitamin D and its metabolites in the body, including synthesis, transport, activation, and degradation. It plays a central role in calcium and phosphate homeostasis and bone mineralization, and is linked to broader physiological processes such as immune function.

Vitamin D exists in two main forms: vitamin D3 (cholecalciferol) produced in the skin upon ultraviolet B exposure and vitamin D2 (ergocalciferol) from certain plant sources and fortified foods. Both can be obtained from diet or supplements and are converted by the body into active forms.

Activation occurs in two hydroxylation steps. First, liver enzymes convert cholecalciferol or ergocalciferol to 25-hydroxyvitamin D [25(OH)D], the main circulating form used to assess status. Then the kidney converts 25(OH)D to the biologically active 1,25-dihydroxyvitamin D [1,25(OH)2D], primarily via the enzyme 1α-hydroxylase (CYP27B1).

Regulation is driven by calcium and phosphate balance and parathyroid hormone (PTH). Low calcium or low vitamin D increases PTH, stimulating renal CYP27B1 to raise 1,25(OH)2D levels. FGF23 and calcium-phosphate status provide additional control; excess 1,25(OH)2D is degraded by CYP24A1.

Functions include enhancing intestinal absorption of calcium and phosphate, supporting bone mineralization, and modulating immune and cellular processes. The circulating 25(OH)D level is the standard measure of status, with various guidelines distinguishing sufficiency, insufficiency, and deficiency thresholds.

Deficiency can lead to rickets in children and osteomalacia in adults. Excessive supplementation can cause hypercalcemia and related complications, though vitamin D toxicity is uncommon at typical intakes. Public health guidance emphasizes safe sun exposure, diet, and appropriate supplementation when needed.

Clinical interest in vitamin D metabolism continues to address its role in diverse health outcomes, the impact of genetic factors on enzymes such as CYP27B1 and CYP24A1, and the optimization of screening strategies.