Vitamin D-A group of fat-soluble compounds resembing steroids.

Sources of vitamin D

Vitamin D can come from the diet, or from endogenous production in the body. Ergocalciferol (vitamin D₂ is obtained from plants. Cholecalciferol (vitamin D₃ is obtained from animal tissues. These two derivatives of vitamin D are sources of preformed vitamin D activity.

Endogenous vitamin D is derived from intermediates in cholesterol synthesis. 7-dehydrocholesterol is an intermediate in the synthesis of cholesterol and is converted to cholecalciferol in the dermis and epidermis when exposed to sunlight. Preformed vitamin D is only required in the diet if a person cannot be exposed to sunlight for any reason.

Vitamins D₂ and D₃ are not active. They must be converted to the active form inside the body. Vitamin D₃ is hydroxylated at the 25-position by a hydroxylase present in the liver. The result is 25-hydroxycholecalciferol (25-OH-D₃ and is the major plasma form and storage form of vitamin D.

25-OH-D₃ is hydroxylated again, this time at the 1- position by 25-hydroxycholecalciferol 1-hydroxyolase, an enzyme found in the kidney. After hydroxylation, the result is 1,25-dihydroxycholecalciferol (1,25-diOH-D₃). 1,25-diOH-D₃ is the most useful form of vitamin D and its synthesis is strictly monitored by the concentrations of serum phosphate and calcium.

Activity of the renal enzyme 25-Hydroxycholecalciferol 1-hydroxylase is directly increased by low serum phosphate and/or indirectly by low serum calcium. Low level of serum calcium and phosphate stimulate the release of parathyroid hormone (PTH). In summary, low levels of calcium stimulate the production of 1,25-diOH-D₃. Why do low levels of calcium and phosphate cause a rise in active vitamin D? The answer is quite simple if we look at the function of vitamin D. The active form of vitamin D (1,25-diOH-D₃) is to maintain normal serum levels of calcium. 1,25-diOH-D₃ achieves this by stimulating the intestine to increase the uptake in calcium, stimulating the bone to release calcium from its supply (resorption), and by lowering the loss of calcium through the kidney.

Sources of vitamin D

Sources of vitamin D include eggs, liver, butter, fatty fish and milk (only if fortified with vitamin D).

RDA of vitamin D

5 micrograms/day of cholecalciferol or 200 IU/day of vitamin D is recommended for adults.

Deficiency of vitamin D

Vitamin deficiency causes bone demineralization. Calcium and phosphates are is regarded as minerals. Therefore, removal of this mineral from the bone is referred to as demineralization. Demineralization of the bone is known as rickets in children and osteomalacia in adults. In rickets, continued formation of collagen (the protein framework of bone) occurs, but bone mineralization (for compression strength, like a sidewalk or walkway) is incomplete. This is because calcium is not absorbed properly without vitamin D, therefore, the child becomes calcium deficient. The result in the child is soft, pliable bones. These bones can bend over time due to compressional forces, such as when walking. This bending of the femur, tibia and fibula can result in the child developing "bowed" legs. In the adult, osteomalacia increases the risk of bone fractures.

Toxicity of vitamin D

Vitamin D, being fat-soluble, is stored in the body in appreciable amounts and is slowly metabolized. Chronic excessive doses can cause anorexia, nausea, vomiting, thirst and stupor. Excess vitamin D administration also causes hypercalcaemia (higher than normal calcium in the blood). This can lead to calcium deposit in the organs, and blood vessels.