The visual cycle (part 1)

Vitamin A Metabolism:

Vitamin A Metabolism (click on drawing to enlarge)

An adequate concentration of vitamin A in its storage depot, the liver depends on the balance between the input and the output. In this example, using the  “wash basin model” to analyse a biological process, note that the concentration of the metabolite (vitamin A) is influenced more by its input than its output. Future examples in the blog e.g. hydration, acid/base balance, will show that both input and output can be major determinants

Vitamins cannot be synthesized in animals and are supplied in the diet i.e. exogenous input. Vitamin A is one of the fat soluble vitamin group i.e. vitamins A, D, E, and K, and so an adequate supply depends on efficient fat absorption in the intestine. Vitamin A is a term referring to a group of compounds: retinol, retinal, and carotenoids including β carotene, which is a precursor of retinol. Vitamin A is stored in fat depots e.g. liver and a vitamin A deficient diet must continue for a long time before a deficiency will occur. Deficiency of vitamin A is rare in the developed world because of adequate diets and vitamin supplementation. It occurs when there is an inadequate input due to a poor diet e.g. malnutrition or malabsorption of fat. Fat absorption requires synergistic action of bile from the liver and lipase enzyme from the pancreas. Bile acts as a soap emulsifying the lipids into small fat globules which have a larger surface area (analogous to small animals losing more heat because of their relatively larger surface area) allowing easier attachment and digestion by lipase. The released fatty acids are absorbed by intestinal cells, and then pass via the lymphatic system of the intestine into the blood stream for transport to the liver. Thus vitamin A deficiency occurs in patients with liver, pancreatic, or intestinal diseases. However an excess input of vitamin A e.g. an overdose of multivitamins can produce serious side effects e.g. brain swelling. Excess β carotene ingestion occurs in people on fad diets. I remember many years ago an acquaintance turned yellow. He thought he had liver disease, but it was “carotinemia” due to his passion for pumpkin!  Interestingly enough, although it is a precursor of retinol, the side effect of “carotinemia” is limited to the transient yellow discoloration of the skin. The output of vitamin A is mainly via its metabolism in various organs. But it is also excreted exogenously via the kidneys, and excess levels can occur in renal failure.

The vitamin A is stored as retinol in the liver and then transported to tissues e.g. the retina as required. Retinol is not water-soluble, and it is transported in blood plasma bound to a protein, the “retinol binding protein” (RBP). Tissue cells can take up the retinol via a cellular retinol binding protein. The retinol plays an essential role in cell differentiation, gene expression, and fetal development. But our particular interest in this vitamin is because of its role in the visual cycle and night vision. It is interesting to note that the ancient Egyptians knew that feeding liver would cure night blindness.

It is clear that vitamin A metabolism is very complex. Details are given in these two references (a) and (b) . But for our purposes  just remember that the concentration in our cells depends on a balance between its input and output. Its significance for our discussion is that it is an essential component in night vision. The visual cycle, which will be discussed in the next post, will now be easier to understand (hopefully!).

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