Vitamin A

Chapter 135 Vitamin A

image Introduction

Vitamin A was the first fat-soluble vitamin to be recognized. Although identified as a necessary growth factor in 1913, it was not characterized chemically until 1930. The initial discovery of vitamin A was made almost simultaneously by two groups of research workers, McCollum and Davis at the University of Wisconsin and Osborne and Mendel at Yale University. They found that young animals fed a diet deficient in natural fats became very unhealthy, as evidenced by the inability to grow and poor immune function. These researchers also noted that the animals’ eyes would become severely inflamed and infected with the restricted diet and that this condition could be quickly relieved by the addition to the diet of either butterfat or cod liver oil. Vitamin A was once known as the “anti-infective vitamin,” and vitamin A status remains a major determinant of immune status.

image Deficiency

Vitamin A deficiency may be due to inadequate dietary intake (primary deficiency) or to some secondary factor that interferes with the absorption, storage, or transportation of vitamin A. Some factors known to induce a vitamin A deficiency are as follows:

Other Effects

Prolonged vitamin A deficiency results in the characteristic signs of follicular hyperkeratosis (buildup of cellular debris in the hair follicles, giving the skin a goose-bump appearance, which occurs most often on the back of the upper arm), night blindness, and a higher rate of infection. As the condition worsens, the mucous membranes of the respiratory tract, gastrointestinal tract, and genitourinary tract also become affected, and the classic eye disease known as xerophthalmia due to vitamin A deficiency ensues. Even a mild vitamin A deficiency is associated with a significant rise in mortality. This association is extremely significant, because vitamin A deficiency is particularly widespread in developing countries, especially in Asia, where as many as 10 million children are found to have xerophthalmia each year.3

image Metabolism

Transport, Storage, and Excretion

Upon reaching the liver, vitamin A is stored primarily in special perisinusoidal lipocytes (Ito cells); the hepatocytes contain only a minor fraction of the total vitamin A stored in the liver. Although small amounts of vitamin A are found in most tissues (Table 135-4), more than 90% of the total body vitamin A content is stored in the liver. It is stored as a lipoglycoprotein complex consisting of 96% retinyl esters and 4% unesterified retinol. The retinyl esters are hydrolyzed by a tightly bound retinyl ester hydrolase, which transfers the released all-trans retinol to intracellular retinol-binding protein (RBP). The bound retinol is then processed through the Golgi apparatus and secreted into the plasma, where it forms a reversible 1:1 molar complex with prealbumin.1,5

TABLE 135-4 Distribution of Vitamin A in Some Human Tissues (mcg/kg)

Adrenal gland 10.4 ± 7.1
Liver 149 ± 132
Testis 1.14 ± 1.23
Fat 1.46 ± 1.55
Pancreas 0.52 ± 0.28
Spleen 0.89 ± 0.88
Lung 0.91 ± 1.89
Thyroid 0.43 ± 0.33

Adequate dietary protein, iron, and zinc are necessary for proper retinol mobilization. The half-lives of RBP and prealbumin are less than 12 hours, making them particularly likely to be deficient during protein-calorie malnutrition or other situations in which protein metabolism is abnormal. A zinc, iron, or vitamin E deficiency also severely impairs vitamin A metabolism, because these nutrients function synergistically in many physiologic processes of vitamin A metabolism (absorption, transport, and mobilization in particular).6,7

Retinol is transferred into the cell after RBP binds to a cell surface receptor. The retinol is then quickly bound by cellular retinol-binding protein (CRBP) in the cell cytosol.

Retinoic acid is metabolized differently from retinol. It is absorbed through the portal system and transported in the plasma bound to albumin. It does not accumulate in the liver or other tissues in any appreciable amounts. It is metabolized quite rapidly to more polar oxygenated compounds. Intracellularly, it is bound to the cellular retinoic acid–binding protein.

Vitamin A metabolites are excreted mainly through the feces (via the bile) and the urine. During periods of deficiency there appears to be an adaptation in utilization, as evidenced by a reduction in the rate of vitamin A catabolism.1,5

Sep 12, 2016 | Posted by in MANUAL THERAPIST | Comments Off on Vitamin A
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