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Vitamin D

Module 2 Assignment HUN 3231, Section #12484 Cara Rotman, N00681635 February 13, 2013

Vitamin D is found in animal tissues such as beef and dairy and in plant products that we consume. They both make a different form of vitamin D though, animal origin is called D3, cholecalciferol and the plant origin is called D2, ergosterol. You can also get vitamin D nondietary, this would have to come from sunlight, this converts to D3 in our bodies. Vitamin changes forms also as it gets metabolized in our bodies, for example in the storage and circulating form it is called calcidiol and the active hormone is called calcitriol. Without vitamin D we may have a hard time regulating calcium levels and it could hinder the transduction of some signals. Just 15 minutes of sunlight can supply you with your daily requirement of vitamin D. The UVB gets synthesized in the skin with cholesterol to make precholecalciferol, pre-vitamin D, and after two to three days is formed to make cholecalciferol via bonds rearranging. The cholecalciferol can then diffuse from the sin into the blood stream and is transported by D binding proteins, DBP. You cannot overdose from sun exposure, whatever isnt converted just gets sloughed off with dead skin. However people with more melanin may have a harder time in this conversion. Vitamin D2 only has one third the strength in our bodies as D3, so most of the reactions and metabolism will be Vitamin D3 based in the rest of my paper. Cholecalciferol digests similar to fat once ingested. Micelles passively diffuse the dietary from of cholecalciferol into the enterocyte where it is formed into the chylomicron and can then exit into the lymphatic system and circulates. Once in the blood it can travel on the chylomicron or onto a DBP. Cholecalciferol is not active though. In order to become active the body needs to signal that it is low or needs more calcitriol for it to begin the process of activation. D3 cannot be used by our body as the form of cholecalciferol so it must be metabolized to 25, OH Vitamin D3 or calcidiol via 25hydroxylase in the liver. It can stay in this form for up to three weeks and once the body signals for the Vitamin D hormone it can convert calcidiol to calcitriol via 1-hydroxylase in the kidney. However it only stays in this form for about four to six hours, once the hormone gets used its gone and your body must produce more. Once in its active form it can interact with other cells. Vitamin D plays a role in gene interaction by influencing DNA and its gene transcription. As well as expressing DNA it deals with the homeostasis of calcium. When calcium blood levels get too low it activates the parathyroid gland to release the parathyroid hormone, PTH, which turns on the enzyme 1hydroxylase which converts calcidiol to calcitriol. Once calcitriol is formed there is increased absorption from the proteins Calbindin P9K and Calbindin P28K, these actively save and reabsorb any calcium we may be losing. Once the calcium is too high PTH turns off via calcitonin which helps put the calcium back into the bones by stimulating the osteoclasts. Vitamin D also

plays a role in increasing and decrease growth of certain tissues, regulating blood pressure, and protecting against auto-immune diseases. People can become deficient in vitamin D just like any other vitamin. It is more common now too, especially in people who arent outside often or live in regions where there is not much sunlight. There are two major diseases that are a result of a vitamin D deficiency: Rickets and Osteomalacia. Rickets is defined as a failure to mineralize newly formed osteoid during modeling or remodeling before epiphyseal fusion. This occurs in children and is characterized by bowed legs or large joints. Osteomalacia is similar to osteoporosis where it is constantly pulling calcium from the bones. Calcitriol and PTH regulate the mineral metabolism and the transport of the minerals to the bones. Any defect in the pathways of these could cause a defect and ultimately one of these diseases. The vitamin can be assessed by measure blood storage levels of the calcidiol. There is no known toxicity of Vitamin D because the body is pretty good at regulating itself however it could cause negative side effects if there is too much ingested vitamin D. For example it could case calcification of soft tissues such as arteries. Vitamin D is found to be excreted in feces through bile in the metabolite form. There are many populations at risk for a deficiency in vitamin D. The elderly have poor intake of sufficient nutrients practically across the board and their skin cannot produce it as efficiently. As I mentioned earlier, those with more melanin and darker skins tones may have a harder time converting. Those people with fat malabsorption may have deficiencies since vitamin D gets metabolized like fat. And finally infants are usually low in vitamin D because there are low levels in breast milk. However to supplement these people we recommended one 50,000 IU supplement dose per week to correct and deficiency.

References 1. Jovicic S., Ignjatovic S., Majkic-Singh N. Biochemistry and Metabolism of Vitamin D. Journal of Medical Biochemistry. 2012;31(4):309-315 2. Dimitri P., Bishop N. Rickets. Pediatrics and Child Health. 2007;17(7) 279-287 3. Feldman D., Malloy P. Vitamin D Deficiency, Rickets and Osteomalacia. Encyclopedia of Endocrine Disease. 2004;666-673

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