Retinol dietary needs

Pharmacokinetics Rapidly absorbed from the GI tract if bile salts, pancreatic lipase, protein, and dietary fat are present. Transported in blood to the liver, where it s metabolized stored in parenchymal hepatic cells, then transported in plasma as retinol, as needed. Excreted primarily in bile and, to a lesser extent, in urine. 

Because it is the precursor for the retinaldehyde prosthetic group of rhodopsin (Wald, 1968), retinol is needed to maintain the visual process. Additionally, retinal neurones may require retinoids for their normal functioning. Therefore, retinoids must be supplied to the eye from the circulation, transported between its layers, and stored in its tissues as a reserve against dietary deprivation. 

Dietary vitamin A is stored in the liver and secreted into the bloodstream when needed. The circulating retinol is taken up by target cells and oxidized in part to retinoic acid, which induces the synthesis of proteins through the direct control of gene expression. This type of action—gene activation—establishes vitamin A (in the form of its metabolite, retinoic acid) as a hormone, similar to the steroid hormones and the thyroid hormone. 

Generally, vitamin A serves three classes of functions (1) support of the differentiation of epithelial cells, (2) support of the viability of the reproductive system (fetal growth and vitality of the testes), and (3) utilization in the visual cycle. Dietary retinoic acid can support only the first function. Animals raised on diets containing retinoic acid as the only source of vitamin lose their ability to see in dim light and become sterile. In males, sperm production ceases. In females, fetuses are resorbed. Retinoic acid cannot be stored in the liver, as it lacks the hydroxyl group needed for attachment of the fatty acid. Retinyl esters, retinol, and retinal are interconvertible. Retinal can be oxidized to form retinoic acid. All three functions of vitamin A can be supported by dietary retinyl esters, retinol, or retinal. Although these forms can be converted to retinoic acid, retinoic acid apparently cannot be reduced to form retinal. These relationships are summarized in Figure 9.44. 

The compartmental model was also able to predict the efficiency of conversion of /3-carotene to vitamin A in our subject. The model predicted that 1 (ig dietary /3-carotene yielded 0.054 /ug retinol (the same as 0.101 /unol retinol/pimol /3-carotene). The 0.054-/i4g value is considerably lower than the 0.167 fig retinol//ug /3-carotene which is widely accepted. However, the 0.167-/iig value was established in growing rats with low reserves of retinol who were adapted to maximizing the retinol yield (Brubacher and Weiser, 1985). If our subject had been in marginal or deficient vitamin A status, the predicted yield would probably have exceeded 0.054 fig retinol//ig /3-carotene. Further studies are needed to determine the influence of vitamin A status on conversion of /3-carotene to vitamin A and the ability of dietary carotene to maintain tissue retinoid. 

The effects of protein-energy malnutrition (PEM), and its treatment, on the plasma retinol transport system have been investigated in a large number of studies during the past decade. Patients with PEM have decreased plasma concentrations of RBP, TTR, and vitamin A. Two major factors can contribute to these low plasma concentrations. First, patients with PEM manifest a defective hepatic production of RBP because of a lack of substrate (calories, amino acids from dietary protein) needed for RBP synthesis. Thus, PEM per se is associated with impaired production of RBP and TTR and defective vitamin A mobilization from the liver. Second, however, PEM is often accompanied by inadequate... 

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