Vitamin A Alltransretinol Homeostasis

Insight into the sources, metabolism, and homeostasis of vitamin A will facilitate our ability to decipher whether vitamin A status in humans correlates inversely with cancer risk and supports its potential as a cancer chemopreventive agent. Vitamin A is the compound all-trans-retinol. All-trans-retinol, however, does not have biological activity in its own right. Rather, it serves as the substrate for producing metabolites that fulfill the functions of vitamin A. These metabolites include, but may not be limited to, the cofactor in rhodopsin, 11-ds-retinal, and the humoral transducer of systemic vitamin A action, all-trans-retinoic acid (RA).1-5 The term vitamin A, therefore, pertains to a specific compound, all-trans-retinol. The term also denotes the spectrum of biological activity, as in "vitamin A activity," produced indirectly by retinol.6 The term retinoids refers to all compounds, both naturally occurring and synthetic, which have vitamin A activity.7 Although vitamin A intake seems adequate in most of the population of North America and Europe, this appears to be an evolutionarily aberrant situation. Indeed, the usual situation, as evidenced by recurrent problems in countries outside of North America and Europe, seems to be limited vitamin A intake, resulting from generally poor, often nutritionally monotonous diets.8 In North America and Europe preformed vitamin A accounts for 60 to 80% of vitamin A

fruits & vegetables carotenoids (provitamin A)

preformed vitamin A

fruits & vegetables carotenoids (provitamin A)

preformed vitamin A

Most Tissues

RA effects on differentiation status and apoptosis

FIGURE 3.1 A schematic depicting the sources of vitamin A and its uptake and storage in the liver as retinyl esters. Vitamin A is converted into RA in liver and delivered to extrahepatic tissues, and vitamin A itself is delivered to extrahepatic tissues and converted in situ into RA.

Most Tissues

RA effects on differentiation status and apoptosis

FIGURE 3.1 A schematic depicting the sources of vitamin A and its uptake and storage in the liver as retinyl esters. Vitamin A is converted into RA in liver and delivered to extrahepatic tissues, and vitamin A itself is delivered to extrahepatic tissues and converted in situ into RA.

requirements, whereas in south Asia and Africa, carotenoids serve as the major vitamin A precursors. This confounds the issue whether dietary intake of vitamin A or carotenoids, or both, correlate with risk of various diseases. Common dietary sources of vitamin A include liver, dairy products, and fish, such as herring, sardines, and tuna. Common dietary sources of provitamin A carotenoids include carrots, yellow squash, corn, dark-green leafy vegetables, and red palm oil. Only ~50 of the 600 carotenoids found in nature have provitamin A activity, however. As a result, color is not a reliable indicator of the vitamin A value of vegetables. Regardless of the source, all-trans-retinol accounts for the quantitatively major circulating retinoid in serum. But unless it is very low or in excess, serum retinol does not reflect vitamin A status, because with adequate vitamin A stores in liver, the liver homeostatically controls plasma retinol levels. In addition, other factors can affect plasma vitamin A within the genetically and liver-stores determined range, such as infection and inadequate intake of other nutrients (e.g., zinc and protein) (Figure 3.1).

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