Vitamin A (retinol)


Indications:

Vitamin A is essential throughout life as it is required in reproduction, embryonic and foetal development, vision, growth, differentiation and tissue maintenance [1]. The term vitamin A covers the retinoids, a group of lipid-soluble compounds which have similar physiological functions and metabolic activities: retinol, retinal (the aldehyde form), and retinoic acid. Retinol inter-converts between retinyl esters and retinal, while retinoic acid (which is not found in the diet) is an end product of retinol conversion. These substances have different actions: retinoic acid is required for the growth and differentiation of epithelial cells, whereas retinyl ester, retinol and retinal can all support cellular differentiation, reproduction and visual functions. Retinoic acid is the form of vitamin A for which a teratogenic effect on the foetus has been demonstrated and which acts as a hormone in many cells by regulating gene expression, thus controlling cell differentiation and maturation [2].

Vitamin A nutrition is quite complex and needs to be considered in terms of its relationship with other vitamins. For example, vitamin A works cooperatively at the genetic level with vitamin D. Vitamin E is required for the conversion of beta-carotene to retinol (see below), while vitamin A absorption can be reduced by excess vitamin E consumption. In turn, excess dietary vitamin A can interfere with vitamin K absorption. The conclusion is that although supplementation with vitamin A may be appropriate in cases of proven deficiency, a vitamin-rich mixed diet is the best way to maintain optimum vitamin A status.

Patient Instructions:

No vitamin A containing supplements for 24 hours prior to testing.

Included in Profiles:

Fat soluble and full vitamin profiles

Datasheet:

vita.pdf (Click to Download)

Sample Report:

rep-fat-sol-vits.pdf (Click to Download)

Sample Requirements:

Gold (SST) - protect from light.

Postal Samples Acceptable:

Yes

References:

1. Sommer A. Vitamin A Deficiency and Clinical Disease: An Historical Overview. J Nutr 2008;138:1835-1839.
2. Lammer EJ, Chen DT, Hoar RM. Retinoic acid embryopathy. N Eng J Med 1985;313:837-841.
3. Bates CJ. Vitamin A. The Lancet 1995;345:31-35.
4. Food Standards Agency. http://www.eatwell.gov.uk
5. Wald G, Brown PK. Human rhodopsin. Science 1958;127:222-249.
6. Smith FR, Goodman DS. Vitamin A transport in human vitamin A toxicity. N Eng J Med 1976;294:805-808.
7. In: Tietz Textbook of Clinical Chemistry and Molecular Diagnostics. Burtis CA, Ashwood ER, Bruns DE. Eds. Publisher Elsevier Saunders, St. Louis. 4th Edition 2006, pp 2302.
8. In: Modern Nutrition in Health and Disease. Shils ME, Shike M, Ross AC, Caballero B, Cousins R. Eds. Publisher Lippincott Williams and Wilkins, Baltimore. 10th Edition 2006, pp 369.
9. Furr HC. Analysis of Retinoids and Carotenoids: Problems Resolved and Unsolved. J Nutr 2004;134:281S- 285S

For further details please contact the laboratory at: lab@xxxxbiolab.co.uk