Vitamin A
Dietary vitamin A (i.e., retinyl esters) is hydrolyzed in the gastrointestinal tract into retinol and is absorbed in this form across the mucosal cell membrane into the cell. where it recombines with a fatty acid, usually palmitate or stearate. The retinvl ester then travels in the chylomicrons by way of the lympha tic system and blood stream to the liver, where it is stored.
Liver stores of vitamin A (retinyl esters) are hydroby enzymes to free retinol, which is transported by a retinol-binding protein (RBP) complex to the tissues of the wherever a metabolic requirement exists. The liver s can maintain the blood at relatively constant vitamin A levels even when the diet is deficient. For this reson, vitamin A deficiencies may not develop for long periods of time, depending on the reserve stores in the and the ability of the body to mobilize these reserves of vitamin A.
RBP is a relatively small protein synthesized in the and released in response to the need for vitamin A transport. In plasma it forms a complex with another larger known as prealbumin (PA), which also sports plasma thyroxine. This larger complex is believed to protect retinol from oxidative destruction and to ce the removal and catabolism of retinol and RBP by kidneys. In vitamin A deficiency RBP accumulates in liver and is rapidly released upon administration of A.
Protein deficiency can interfere with vitamin A mobilization from the liver reserves. With inadequate protein (and energy) intake the concentration of several plasma ells synthesized in the liver decreases; RBP and P A are among the first ones affected. Because of their rapid response to changes in protein-energy status, the plasma concentration of RBP and PA has been recommended as a of detecting subclinical malnutrition and of moitoring the effectiveness of dietary treatment.
Plasma levels of vitamin A, RBP, and PA are also low in liver disease and in children with protein-energy malnutrition. When such children are treated with a diet adequate in protein and energy, their plasma vitamin A, RBP, and PA levels increase, suggesting that low plasma levels of vitamin A were due to protein deficiency rather than lack of vitamin A. However, in most severely malnourished children the liver reserves of vitamin A are minimal, and, unless vitamin A is provided with protein and energy, an acute vitamin A deficiency may develop as their vitamin A requirement is suddenly increased with the restoration of rapid growth.
It is estimated that the liver may contain as much as 95% of the vitamin A of the entire body, with small amounts in adipose tissue, lungs, and kidneys. Infants and young animals probably have low reserves of vitamin A at birth but, if they are well-fed, they store it rapidly. The liver gradually acquires, over a period of years, an increasing reserve of vitamin A, which normally reaches its peak in adult life. The function of this reserve is chiefly to take care of temporary shortages or increased requirements. Obviously, an intake above the minimum requirement must be maintained most ofthe time ifsuch a reserve is to be built up. Reserve stores of vitamin A are evident even in young animals.
Carotene
In the presence of fat and bile acids carotene is absorbed into the intestinal wall, where some is converted to vitamin A. The carotene that is not converted is absorbed into the lymph and carried. Approximately one-third ofthe carotene in food is available to the body. Moreover, the amount of available carotene that is then converted to vitamin A varies considerably, but, in general, only about half is used this way. As a result, in the human the utilization efficiency of carotene is 1/6; in other terms, 1 mcg of B-carotene would have the same biologic activity as 0.167 mcg of vitamin A alcohol, retinol. Other carotenoids have about 1/2 the biologic activity of B-carotene (1 mcg other carotenoids = 0.0833 mcg retinol).
Inadequate protein intakes decrease the absorption, transport, and metabolism of carotenes.
