cholecalciferol Vitamin D also known as calciferol, ergosterol, ergocalciferol, "sunshine vitamin", anti-rickets vitamin. Vitamin D is a type of fat-soluble vitamin. There are many types, but vitamin D2 (ergocalciferol) and vitamin D3 (cholecalciferol) are more important.
It is colorless needle crystal or white crystalline powder, odorless and tasteless. Melting point 87 ~ 88 ℃ (decomposition). Easily soluble in ethanol, acetone, chloroform, slightly soluble in vegetable oil, insoluble in water. It is obtained by 7-dehydrocholesterol ring-opening by ultraviolet light irradiation, and then purified by chromatography and esterification. This product can promote the absorption of calcium and phosphorus in the intestine, maintain the balance of calcium and phosphorus in the blood, and promote the storage of calcium and phosphorus in the bones. For rickets, osteomalacia, hypothyroidism. Generally non-toxic, long-term use of large doses can cause hypercalcemia, ectopic calcification of soft tissue and loss of appetite, vomiting, diarrhea, polyuria, etc.
Vitamin D3, the most important form of the vitamin D family, mainly regulates calcium and phosphorus metabolism in the body. Vitamin D is a fat-soluble vitamin that belongs to cholesterol, mainly in liver, milk and egg yolk, and is most abundant in cod liver oil. There are two forms of vitamin D, namely vitamin D2 or calciferol or ergocalciferol; and vitamin D3 or cholecalciferol. Vitamin D2 is converted from a plant alcohol, ergosterol (24-methyl-22-dehydro-7-deoxycholesterol). Under the action of ultraviolet light, ergosterol breaks its intramolecular B ring and converts it into vitamin D2. Vitamin D3 is converted from 7-dehydrocholesterol in the skin by ultraviolet radiation. Vitamin D3 is the natural form of vitamin D, but not its biologically active form.
After vitamin D enters the blood circulation, it is mainly stored in the liver. In the liver, vitamin D3 is catalyzed by D3-25-hydroxylase (requires the presence of NADPH, O2 and Mg2+) to generate 25-dihydroxyvitamin D3 (25-OH-D3). The biological effect of this substance is 3 to 5 times greater than that of vitamin D3, but it has no physiological function at physiological doses, and it needs further metabolism. 25-OH-D3 enters the blood from the liver, binds to a specific globulin in the plasma, and is transported to the kidney. 1,25-hydroxyvitamin D3 [1,25-(OH)2-D3] is produced by the action of ferritase, iron-sulfur protein, and cytochrome P-450. 1,25-(OH)2-D3 is the most effective form of vitamin D3, and its biological effect is about 8 to 10 times that of vitamin D3. 1,25-(OH)2-D3 cannot be produced in kidney-enucleated animals, so the kidney is the only place for 25-OH-D3 to undergo hydroxylation at the 1α position. Since 1,25-(OH)2-D3 is generated in the kidney and enters the blood circulation, and then exerts physiological effects in distant organs (such as the small intestine and stomach), 1,25-(OH)2-D3 can also be converted into seen as a hormone.
Under certain conditions, 25-OH-D3 can be converted into 24,25-(OH)2-D3 by the action of 24-hydroxylase. 24-hydroxylase can also convert 1,25-(OH)2-D3 Hydroxylated to generate 1,24,25-(OH)3-D3. The physiological role of these 24-hydroxylated vitamin D3 is unclear, and they may be metabolic intermediates of inactivation of the vitamin D3 molecule. The final metabolite of vitamin D3 is excreted in bile. Mammalian and bird vitamin D2 is metabolized to 25-OH-D2. 25-OH-D2 was also found to become 1,25-(OH)2-D2 in rats and chickens. This substance has the same biological effect as its vitamin D3 counterpart in rats. In chickens, its activity is only 1/10 that of its vitamin D3 counterpart.
The main physiological functions of vitamin D are: regulating calcium and phosphorus metabolism, and promoting calcium and phosphorus absorption. When lacking, children can cause rickets, systemic metabolic disorders, and dysplasia; adults can cause osteomalacia, especially in pregnant and lactating women. It can effectively utilize calcium and phosphorus to make strong bones and teeth; take vitamin A and vitamin C at the same time to prevent colds; help in the treatment of conjunctivitis; help absorb vitamin A.
Symptoms of vitamin D deficiency in the body are osteomalacia and osteomalacia. The role of vitamin D is to increase blood calcium and phosphorus levels. Deficiency of vitamin D will lead to insufficient supply of calcium and phosphorus. Disorders causing bone mineralization. Its main functions are: ①Promote the absorption of calcium and phosphorus in the small intestine. It mainly stimulates the active transport of calcium on the surface of the microvilli of the small intestinal mucosa. It is generally believed that 1,25-(OH)2-D3 binds to receptor proteins in the cytosol of intestinal epithelial cells, and then this complex interacts with the nucleus to cause message transcription, forming a "calcium transporter" in cells . This transporter acts on the surface of microvilli to promote calcium absorption. In addition, vitamin D3 stimulates the production of a calcium-binding protein on the surface of the microvilli. The rate of Ca2+ uptake by intestinal epithelial cells is proportional to the number of calcium binding proteins. 1,25-(OH)2-D3 also promotes the absorption of phosphorus in the small intestine. ②1,25-(OH)2-D3 can promote the reabsorption of phosphorus and calcium in renal tubules. Vitamin D-sensitive calcium-binding proteins have been demonstrated in both chicken and rat kidneys. ③1,25-(OH)2-D3 plays an important role in bone calcium mobilization and bone salt deposition. It decalcifies the formed bone, an action that requires the presence of parathyroid hormone under physiological conditions. Since the ribonucleic acid synthesis inhibitor, actinomycin D, can completely eliminate the role of vitamin D in mobilizing bone calcium, it can be considered that the role of vitamin D requires transcription to generate certain proteins that mobilize calcium.
Regulation of 1,25-(OH)2-D3 Production The production of 1,25-(OH)2-D3, the active form of vitamin D, can be regulated by some negative feedback. For example, 25-OH-D3 inhibits the action of 25-hydroxylase and inhibits 25-hydroxylation of D3; 1,25-(OH)2-D3 inhibits 1α-hydroxylase and inhibits 1,25-(OH) ) 2-D3 generation. On the other hand, the metabolic process of vitamin D3 can also be modulated. For example, when 1,25-(OH)2-D3 inhibits 1α-hydroxylase, 24-hydroxylase can be induced to produce 1,24,25-(OH)2-D3. In addition, vitamin D3 and overall adaptation are regulated by the following factors: ① Parathyroid hormone is regarded as a vitamin D-stimulating hormone, which is the main factor regulating the production of 1,25-(OH)2-D3. ②In terms of diet, the production of 1,25-(OH)2-D3 was increased in animals deficient in vitamin D. A low calcium diet or hypocalcemia stimulates the production of 1,25-(OH)2-D3 by stimulating the level of 25-OH-D3-1-hydroxylase. Conversely, a high-calcium diet reduced the production of 1,25-(OH)2-D3 and increased the production of 24,25-(OH)2-D3. ③ Since 1,25-(OH)2-D3 can be regarded as a hormone that utilizes phosphorus, it can also stimulate and inhibit the production and inhibition of 1,25-(OH)2-D3 when phosphorus is deficient or the body's need for phosphorus increases. , the formation of 25-(OH)2-D3. Phosphorus levels in renal tubular epithelial cells are determinants of regulation of 1,25-(OH)2-D3 production. High phosphorus levels in renal tubular epithelial cells stimulate 24-hydroxylase; low phosphorus levels stimulate 1-hydroxylase to generate 1,25-(OH)2-D3.
Foods rich in vitamin D: cod liver oil, sardines, herring, salmon, tuna, milk, dairy products; people living in urban areas, especially those in areas with heavy smoke pollution should get more vitamin D; night workers, Nuns, or people who don't get enough sunlight because of clothing or lifestyle, should pay special attention to increasing their intake of vitamin D in their diet; if you are taking antispasmodic drugs, you must increase your intake of vitamin D