Plasma retinol concentration

Dark adaption test Pupillary response test Plasma retinol concentration Relative dose response... 

The residence time for retinol in the test subject was predicted by the compartmental model to be 474 days. The residence time of 474 days is in excellent agreement with the 460 day MST that can be calculated from the data of Song et al. (1995) using the enrichment ratio method (Cobelli and Saccomani, 1992). Also, an MST of 105 to 337 days can be calculated from the half-life values (75 to 241 days) of body vitamin A reported by Sauber-lich et al. (1974) who depleted human subjects with vitamin A-deficient diets. At the same time the empirical description predicted the MST for retinol to be 26 days. While the reason for such a large discrepancy in MST (474 versus 26 days) between the compartmental model and the empirical description prediction is unclear, it is not likely to be accounted for by slight errors in estimating the final slope of the plasma retinol-d4 decay curve. Because the compartmental model embodies several features of retinol metabolism de novo production and release of retinol can occur in unobservable compartments, etc.) in addition to plasma retinol concentrations, its predicted MST is more likely to better reflect the dynamics of retinol metabolism. 

Peng Y-M, Dalton WS, Alberts DS, Xu M-J, Lim H, Meyskens FL (1989) Pharmacokinetics of N-4-hydrox-yphenyl-retinamide and the effect of its oral administration on plasma retinol concentrations in cancer patients. Int J Cancer 43 22-26... 

CONCENTRATIONS OF PLASMA RETINOL (1, NG/ML), LUTEIN (2, NG/ML), ZEAXANTHIN (3, NG/ ML), CANTHAXANTHIN (4, NG/ML) AND a-TOCOPHEROL (5, /xG/ML) IN CONTROL AND EXPERIMENTAL GREEN IGUANAS AFTER INGESTING DIETS SUPPLEMENTED WITH DIFFERENT CAROTENOIDS (80 MG/KG DIET) FOR 28 DAYS (MEAN S.D N = 5)... 

During the development of vitamin A deficiency in experimental animals, the plasma concentration of RBP falls, while the liver content rises. The administration of retinol to deficient animals results in a considerable release of holo-RBP from the liver. This is a rapid effect on the release of preformed apo-RBP in response to the availability of retinol, rather than an increase in the synthesis of the protein. There is no evidence that retinol controls the synthesis of RB P (Soprano et al., 1982). This provides the basis of the relative dose response (RDR) test for liver stores of vitamin A (Section 2.4.1.3) administration of a test dose of retinol gives a considerably greater increase in plasma retinol, bound to RBP, in deficient subjects than in those with adequate liver reserves, because of the accumulation of apo-RBP in the liver. 

Plasma Retinol Binding Protein Measurement of plasma concentrations of RBP may give some additional information. Indeed, it has been suggested that because retinol is susceptible to oxidation on storage of blood samples, measurement of RBP may be a better indication of the state of vitamin A status. In adequately nourished subjects, about 13% of immunologi-caUy reactive RBP in plasma is present as the apo-protein, whereas in vitamin A-deficient children, the proportion of apo-protein may rise to 50% to 90% of... 

The Relative Dose Response (RDR) Test The RDR test is a test of the ahUity of a dose of vitamin A to raise the plasma concentration of retinol several hours later, after chylomicrons have heen cleared from the circulation. What is being tested is the ahUity of the liver to release retinol into the circulation. In subjects who are retinol deficient, a test dose will produce a large increase in plasma retinol, because of the accumulation of apo-RBP in the liver in deficiency (Section 2.2.3). In those whose problem is due to lack of RBP, then little of the dose will be released into the circulation. An RDR greater than 20% indicates depletion of liver reserves of retinol to less than 70 /rmol per kg (Underwood, 1990). 

A concern has been raised that phytosterol doses that are effective for cholesterol reduction may impair the absorption and lower blood concentrations of fat-soluble vitamins and antioxidants. A number of studies showed that phytosterols had no effect on plasma concentrations of vitamin D, retinol, or plasma-lipid-standardized alpha-tocopherol. Moreover, the reports of the effect of phytosterols on concentrations of blood carotenoids (lutein, lycopene, and alpha-carotene) are controversial. There seems to be general agreement that phytosterol doses >1 g/d significantly decrease LDL-C standardized beta-carotene concentrations however, it remains to be determined whether a reported 15-20% reduction in beta-carotene due to phytosterol supplementation is associated with adverse health effects. Noakes et al. found that consumption of one or more carotenoid-rich vegetable or fruit servings a day was sufficient to prevent lowering of plasma carotenoid concentrations in 46 subjects with hypercholesterolemia treated with 2.3 g of either sterol or stanol esters. 

There are also changes in the binding proteins in plasma as a result of the disease process. Since serum albumin falls in association with any acute iUness, this inevitably leads to a fall in plasma zinc concentration. Similarly a reduction in retinol-binding-protein concentration as part of the APR or protein malnutrition also leads to a fall in serum retinol levels, whatever the amount of retinol stores within the liver. 

A second liver retinol (retinyl ester) compartment was added to the model for reasons analogous to those for adding a second liver /3-carotene compartment. The experimental observations show an initial rise and fall in plasma retinol-d4 concentration, then a sustained plasma retinol-d4 level for —16 days after ingesting /3-carotene-dg (Fig. 4). Prior to adding the second liver retinol compartment, the model predicted that almost all... 

Cho, Y. M., Youn, B. S., Lee, H. et al. 2006. Plasma retinol-binding protein-4 concentrations are elevated in human subjects with impaired glucose tolerance and type 2 diabetes. 

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... 

Hydrophobic compounds are transported in plasma bound to transport proteins (e.g. the plasma retinol binding protein section 11.2.2.2) or dissolved in the lipid core of plasma lipoproteins (section 5.6.2), and net intracellular accumulation to a higher concentration than in plasma depends on an intracellular binding protein that has a greater affinity for the ligand than does the plasma transport protein. 

Limits of detection for absorbance detectors (325 nm) with conventional (5 qm particle size) C18 columns and methanol water mobile phases are typically 0.35 pmol (0.1 ng) at a 5 1 signal noise ratio. Even low serum retinol concentrations as found in vitamin A deficiency (0.35 to 0.7 iM, i.e., 10 to 20 Ag/dL) require sample volumes of only 1 pL Nonetheless, fiuorescence detection can give even lower limits of detection (0.07 pmol, 20 pg in tear fluid (111) 5-pL sample sizes have been used for routine plasma assays (112). Electrochemical detection has also been used for simultaneous analysis of retinol and tocopherol (113,114). Microbore columns and smaller packing particle sizes could give improved limits of detection (115,116) but require low-dispersion fittings and detector cells. The requirements for plasma retinol quantitation are not so stringent that use of these techniques has become popular. 

The mechanisms proposed to be responsible for stress-induced reduction in RBP-ROH levels include redistribution of RBP-ROH into the extravascular space [82], reduction in liver protein synthesis due to increased zinc utilization [77] or due to reduced secretion of hepatic TTR [85], increased urinary excretion of RBP-ROH [86] and increased utilization of plasma retinol by peripheral tissues [87]. While it seems likely that several or all of these mechanisms may be contributing simultaneously, it is clear that the APR results in diminished liver RBP and TTR mRNA levels, and this may represent the primary causative effect that reduces RBP-ROH levels in the circulation. Inflammation induced in rats by turpentine oil [88] or lipopolysac-charide treatment [89, 90] results in a decrease in liver RBP mRNA levels. The decrease in RBP mRNA was accompanied by changes in the circulation parallel decreases in RBP and ROH, and a somewhat delayed decrease in TTR [89]. Interestingly, although kidney RBP and TTR protein concentrations are reduced by inflammation, in contrast to liver, kidney RBP mRNA levels were elevated, thus confirming the earlier observation that regulation of RBP expression is tissue-specific [91]. 

---