Vitamin D3, a pro-hormone, is produced when Ultraviolet radiation strikes the skin and 7-dehydrocholesterol
(7-DHC), a derivative of cholesterol, is converted to pre vitamin D3.
The first is ergocalciferol (vitamin D2), derived from ergosterol after ultraviolet (UV) light exposure and the second is cholecalciferol (vitamin D3), derived from animal tissues and 7-dehydrocholesterol
, formed in human skin by the action of UV rays in sunlight (1).
The photosynthesis of vitamin D occurs in all vertebrates resulting from exposure to solar UV-B photons which penetrate the skin causing the photolysis of 7-dehydrocholesterol
Once synthesized on the skin by UV rays from 7-dehydrocholesterol
, cholecalciferol (vitamin D3) is converted to 25-hydroxy-cholecalciferol in the liver, and then to 1,25-dihydroxy-cholecalciferol in the mitochondria of renal proximal tubule cells.
Vitamin D3 is synthesized from 7-dehydrocholesterol
in the skin with sunlight.
Cholesterol biosynthetic errors elevating levels of 7-dehydrocholesterol
, lathosterol or desmosterol, should be considered in the setting of congenital malformations and impaired development.
Since cholesterol metabolism and vitamin D both share a common metabolic pathway, it is possible that prolonged use of statins would not only inhibit cholesterol biosynthesis but also reduce levels of 7-dehydrocholesterol
, a precursor molecule for vitamin D3, thereby leading to low concentration of vitamin D in the body.16 This would render such patients vulnerable to risks associated with vitamin D deficiency.
The pharmaceutical drug cholecalciferol (synthetic vitamin D3) is produced by the ultraviolet irradiation of 7-dehydrocholesterol
extracted from lanolin in sheep's wool.
Vitamin [D.sub.2] (ergocalciferol) is largely human-made and added to foods whereas vitamin [D.sub.3] (cholecalciferol) is synthesized in the skin, from 7-dehydrocholesterol
, and it can be also taken dietarily via animal-based foods.
The realization of the biological effects of vitamin D in cells is closely related to the functioning of the vitamin D-endo/para/autocrine system, which includes (1) photoconversion of 7-dehydrocholesterol
in the skin with the formation of cholecalciferol; (2) synthesis of 25OHD (calcidiol) in the liver by means of two key vitamin D 25-hydroxylases (cytochromes P450), CYP2R1 and CYP27A1; (3) conversion of 25-hydroxyvitamin D (25OHD) in the kidneys or extrarenal tissues to hormonally active form, 1[alpha],25[(OH).sub.2]D, by 25OH-1[alpha]-hydroxylase (CYP27B1); (4) calcitriol transport to target organs by vitamin D binding protein (VDBP); and (5) binding of 1[alpha],25[(OH).sub.2]D to vitamin D receptors (VDR) and regulation of gene expression .
This endogenous production is achieved by in vivo synthesis when ultraviolet B (UVB) light comes into contact with the skin and interacts with the precursor molecule 7-dehydrocholesterol
. Conversion of vitamin D to 25-hydroxyvitamin D (25-(OH)D) occurs first in the liver before being converted by the enzyme 1a-hydroxylase to the metabolically active form 1a, 25-hydroxyvitamin D (25(OH)2D), primarily in the kidneys [7, 8].
The vitamin D content of the human body is synthesized from the precursor molecule 7-dehydrocholesterol
(7-DHC) in the skin by the action of ultraviolet B (UVB) irradiation (280-320 nm) from sunlight.