In many cell lines, 1,25(OH) 2D3 induced cyclin dependent kinases inhibitors (CDKIs) expression like p27kip1 and p21WAF1/CIP1 to mediate cell cycle arrest. Vitamin D is most commonly reported to repress cell cycle progression by causing cell cycle arrest at G0–G1 transition in a cell specific manner. VDR activated by vitamin D interacts with retinoid X receptor to form a heterodimeric complex, which is recruited to the vitamin D response elements (VDRE) in the target genes to activate or to repress their expression through interaction with additional co-regulators. Vitamin D mediates its function by binding to the VDR, which is a member of nuclear hormone receptors superfamily. The non-classical function of vitamin D includes the regulation of several physiological processes like cell proliferation, differentiation, and immune modulation. However, after the discovery of vitamin D receptors (VDR) in various cell types (like keratinocytes, lymphocytes, parathyroid and pituitary gland cells, pancreatic cells, etc.), many biological roles of vitamin D have been revealed in addition to its known actions in classic target tissues. For subjects with serum 25(OH)D levels between 20 and 21 ng/mL, it is generally accepted that values of serum 25(OH)D levels below 20.5 ng/mL are taken as 20 ng/mL and, therefore, considered vitamin D deficiency while serum 25(OH)D levels ≥ 20.5 ng/mL are taken as 21 ng/mL and considered to be vitamin D insufficient.įor many years, the function of vitamin D pro-hormone was considered to be limited to calcium and phosphorus homeostasis. According to the guidelines of US Endocrine Society, the serum levels of 25(OH)D below 20 ng/mL (50 nmol/L) are stated as vitamin D deficiency while 25(OH)D serum levels between 21–29 ng/mL (52.5–72.5 nmol/L) are defined as vitamin D insufficiency. The vitamin D level in serum is closely regulated through feedback loops involving the actions of calcium, phosphorous, 1,25(OH) 2D, parathyroid hormone (PTH), and fibroblast growth factor 3. Furthermore, 25(OH)D and 1,25(OH) 2D are metabolically inactivated through hydroxylation by 24-hydroxylase (CYP24A1). Vitamin D and its metabolites are transported to the target cells primarily by binding to the vitamin D binding protein (DBP). 25(OH)D is then transported to the kidneys where it is further hydroxylated by 1-α-hydroxylase (CYP27B1) to produce its biologically active form 1-α-25-dihydroxy vitamin D (1,25(OH)2D, also known as calcitriol). In the liver, vitamin D is hydroxylated by vitamin D 25-hydroxylase (CYP2R1) to produce 25-hydroxy vitamin D (25(OH)D) or calcidiol, which is the accepted biomarker for vitamin D status. Vitamin D either formed in the skin or was absorbed from the diet in the small intestine and was transported to the liver. This thermally isomerizes into more stable vitamin D3 (cholecalciferol). Absorption of UVB radiation (290–315 nm) in the skin results in the opening of ring B of 7-dehydrocholestrol, which forms a thermodynamically unstable pre-vitamin D3 (9,10-secosterol). The major source of vitamin D is UVB radiation-induced photochemical and thermal conversion of 7-dehydrocholestrol in the skin. On the other hand, vitamin D3 is obtained by photochemical reaction in the skin and through diet via intake of animal-based foods (like cod liver oil and oily fish). Vitamin D2 is synthesized by ultraviolet B (UVB) irradiation of the ergosterol found in yeast and fungi and it is present in a small number of natural foods (such as UVB-radiated mushrooms), in fortified food, and supplements. Vitamin D occurs in two major forms, which includes vitamin D2 (ergocalciferol) and vitamin D3 (cholecalciferol).
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |