Vitamin D is a crucial fat-soluble vitamin synthesized in the skin upon exposure to ultraviolet B (UVB) radiation. It exists in two main forms: D2 (ergocalciferol) from plant sources and D3 (cholecalciferol) from animal sources and sunlight. These forms undergo hydroxylation in the liver to 25-hydroxyvitamin D [25(OH)D], the major circulating form, and further hydroxylation in the kidneys to the active form, 1,25-dihydroxyvitamin D [1,25(OH)2D]. Vitamin D enhances the intestinal absorption of these minerals, ensuring proper bone mineralization. Parathyroid hormone (PTH) is pivotal in this regulation, as low calcium levels stimulate PTH secretion, which in turn promotes the conversion of 25(OH)D to 1,25(OH)2D, increasing calcium and phosphorus levels in the blood. Vitamin D has immunomodulatory functions, influencing the innate and adaptive immune systems. It enhances the pathogen-fighting effects of monocytes and macrophages and decreases the proliferation of pro-inflammatory cytokines. Deficiency in vitamin D can lead to rickets in children, characterized by bone deformities and growth retardation, and osteomalacia in adults, causing bone pain and muscle weakness. Chronic deficiency may contribute to osteoporosis. Symptoms include fatigue, bone pain, muscle weakness, and mood changes. Conversely, vitamin D toxicity, though rare, can lead to hypercalcemia, causing nausea, vomiting, weakness, and serious complications like kidney damage. Optimal levels of vitamin D for health are generally considered to be a serum 25(OH)D concentration of 30–50 ng/mL. Maintaining these levels through appropriate sun exposure, diet, and supplementation is crucial for bone health and overall well-being.

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Physiology and Pharmacology of Vitamin D

  • Amol N. Patil

摘要

Vitamin D is a crucial fat-soluble vitamin synthesized in the skin upon exposure to ultraviolet B (UVB) radiation. It exists in two main forms: D2 (ergocalciferol) from plant sources and D3 (cholecalciferol) from animal sources and sunlight. These forms undergo hydroxylation in the liver to 25-hydroxyvitamin D [25(OH)D], the major circulating form, and further hydroxylation in the kidneys to the active form, 1,25-dihydroxyvitamin D [1,25(OH)2D]. Vitamin D enhances the intestinal absorption of these minerals, ensuring proper bone mineralization. Parathyroid hormone (PTH) is pivotal in this regulation, as low calcium levels stimulate PTH secretion, which in turn promotes the conversion of 25(OH)D to 1,25(OH)2D, increasing calcium and phosphorus levels in the blood. Vitamin D has immunomodulatory functions, influencing the innate and adaptive immune systems. It enhances the pathogen-fighting effects of monocytes and macrophages and decreases the proliferation of pro-inflammatory cytokines. Deficiency in vitamin D can lead to rickets in children, characterized by bone deformities and growth retardation, and osteomalacia in adults, causing bone pain and muscle weakness. Chronic deficiency may contribute to osteoporosis. Symptoms include fatigue, bone pain, muscle weakness, and mood changes. Conversely, vitamin D toxicity, though rare, can lead to hypercalcemia, causing nausea, vomiting, weakness, and serious complications like kidney damage. Optimal levels of vitamin D for health are generally considered to be a serum 25(OH)D concentration of 30–50 ng/mL. Maintaining these levels through appropriate sun exposure, diet, and supplementation is crucial for bone health and overall well-being.