Plasma Concentrations

In normal plasma in the fasting state, more than 95% of retinol is bound to RBP. Retinyl esters also are present during the absorption of vitamin A-rich meals, but they are bound to plasma lipoproteins.

Although there is a significant relationship between plasma retinol and liver vitamin A storage (considered a 'gold standard' for assessing vitamin A status), the relationship is by no means linear. In fact, plasma retinol is nearly constant over a rather wide range of liver vitamin A concentrations, all consistent with vitamin A adequacy. The constancy of plasma retinol reflects its close homeostatic regulation. Plasma retinol levels in normal adults show only minor day-to-day variations, staying close to and 1.7 mmoll-1 in males and females, respectively. The molar concentration of RBP (1.9-2.4 mmolT1) is slightly higher and thus RBP is normally 80-90% saturated. A small proportion of circulating RBP is apo-RBP (RBP without retinol). Owing to its reduced affinity for TTR, apo-RBP is readily filtered in the kidneys and catabolized.

When liver vitamin A reserves fall below about 20-30 mg retinol g liver, the secretion of holo-RBP is compromised due to inadequate retinol. Plasma reti-nol levels begin to fall and, if liver vitamin A continues to decline, plasma levels will fall into the deficient range and will be inadequate to supply retinol to tissues. Essentially all of the vitamin A in liver can be mobilized when it is needed to meet the needs of peripheral tissues. But ultimately, vitamin A intake must increase to bring plasma retinol levels back to the normal range.

Conversely, when vitamin A is consumed in excess of needs, its concentration in liver can increase markedly. When the concentration rises above about 300 mgg-1, as occurs in hypervitamino-sis A (see later section), the levels of plasma retinol and RBP remain almost normal but total vitamin A increases due to retinyl esters bound to plasma lipoproteins.

Plasma Vitamin A Kinetics

Both RBP and TTR have a relatively short half-life (~0.5 and 2-3 days, respectively) and, therefore, they must be synthesized continuously to maintain normal plasma levels. Plasma retinol, RBP, and TTR are reduced in states of impaired protein synthesis, which may be due to an inadequate intake of protein or energy or to impairments in metabolism. Plasma RBP and TTR are sometimes used as clinical indicators of visceral protein synthesis. During infection and/or inflammation, plasma retinol, RBP, and TTR fall transiently, even though liver vitamin A reserves are adequate, due to altered protein synthesis during the acute-phase response. Because multiple nutritional and metabolic disturbances can lead to a similar decrease in plasma retinol, RBP, and TTR, laboratory values must be interpreted with caution.

Studies using computer-based compartmental modeling to analyze plasma retinol kinetics have shown that each molecule of retinol circulates through the plasma compartment several times before it is irreversibly degraded (see 'Tissue Reti-noid Metabolism'). In a young man who consumed 105 mmol of retinyl palmitate in a test meal, 50 mmol of retinol passed through his plasma per day, while only 4 mmolday-1 was degraded. Unlike retinol, RBP is not recycled, implying that RBP is synthesized in extrahepatic tissues for the release and continued recycling of retinol. Some extrahepatic tissues, such as kidney and adipose, contain RBP mRNA at a level ~5-10% of that in liver. The kidneys evidently play a very significant role in the recycling and conservation of retinol after the glo-merular filtration of holo-RBP. Cell culture studies have shown that holo-RBP can bind to renal epithelial cells and cross the epithelium by transcytosis, suggesting a mechanism for the recovery of retinol lost by filtration.

Overall, the body is efficient at conserving retinol, but relatively inefficient in degrading and eliminating excess retinoids. These differences seem to explain the propensity for retinyl esters to accumulate in tissues when vitamin A is consumed in amounts that substantially exceed requirements.


Carotenoids circulate in plasma in association with low-density and high-density lipoproteins. The level of ^-carotene reflects its recent intake, but it also is higher when plasma lipoprotein levels are elevated. Beta-carotene is stored at relatively low concentrations in liver and fatty tissues. A prolonged slow rate of postabsorptive conversion to retinol has been observed in volunteers in isotope kinetic studies.

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