The relationship of vitamin A status to retinol (ROH) utilization rate (disposal rate, DR) and other kinetic parameters was studied in rats with low (LO), marginal (MAR) or high (HI) mean liver vitamin A levels (2.2, 43 and 985 micrograms, respectively) and low or normal plasma ROH concentrations (6.8, 46 and 42 micrograms/dL). Kinetic parameters were calculated by input-output analysis of plasma [3H]ROH turnover monitored for 35 (LO and MAR) or 115 d (HI) after injection of [3H]ROH in its plasma transport complex. There was a highly significant negative correlation between fraction of dose in plasma 5 d after injection of [3H]ROH and the natural log of liver total vitamin A. The total time an average ROH molecule spent in plasma (residence time), as well as the time spent during each pass (transit time), was significantly lower in HI (0.77 d and 1.9 h) than in LO (0.98 d and 2.7 h) and MAR (0.92 d and 2.8 h) rats; however, the total time in the system (mean sojourn time) increased markedly with vitamin A status (5, 18 and 77 d). The number of times an average ROH molecule recycled through plasma before irreversible loss (7-9 times) was similar in all groups. Most of the ROH molecules (approximately 90%) that left the plasma were recycled, not irreversibly metabolized, in all groups. Among groups, ROH DR increased significantly from 1.2 (LO) to 8.0 (MAR) to 11.8 micrograms/d (HI). For LO versus MAR and LO versus HI, differences in DR were positively related to differences in the plasma ROH pool size. These results suggest that low plasma ROH concentrations are associated not only with low liver vitamin A levels, but also with a decreased ROH DR. This decreased DR may or may not reflect a compromised functioning of ROH-dependent systems.
In view of evidence that nutritional status of iron and vitamin A may affect the other nutrient's metabolism, we used model-based compartmental analysis to examine effects of iron deficiency on whole-body vitamin A dynamics in rats. Weanling male Sprague-Dawley rats were fed the AIN93G diet with 2.5 nmol retinyl palmitate/g and either 45 [control (CN)] or 4 microg/g Fe [iron-deficient (ID)] for 8 wk. ID rats consumed food ad libitum; CN rats were food-restricted so that their body weights were the same as ID rats. Two rats/group were killed; liver vitamin A was determined and used for vitamin A balance calculations. [(3)H]Retinol-labeled plasma was administered intravenously to remaining rats, and 27 serial blood samples were collected for 7 wk. At killing, plasma vitamin A was 0.52+/-0.12 (ID, n = 5) vs. 1.34+/-0.12 micromol/L (CN, n = 6; P<0.001), and liver vitamin A was 809+/-94 (ID) vs. 112+/-24 nmol (CN, P<0.001). Plasma tracer data were fit to a three- or four-compartment model using the Simulation, Analysis and Modeling computer program and kinetic parameters were calculated. Vitamin A transfer rate between the retinyl ester storage pool [14+/-3 (ID) vs. 24+/-4 nmol/d (CN), P<0.05] and plasma was lower in ID rats. Vitamin A remained longer in the body [44+/-11 (ID) vs. 22+/-3 d (CN), P<0.05]. Adjusted mean disposal rate was lower in ID (10.0) than CN rats (19.9 nmol/d), as was estimated vitamin A absorption efficiency [58% (ID) vs. 76% (CN)]. Our results suggest that iron deficiency inhibits mobilization of vitamin A stores and may decrease the absorption and irreversible utilization of vitamin A.
To investigate the influence of vitamin A intake on the contribution of chylomicrons vs. holo retinol-binding protein to milk vitamin A, female rats were fed diets containing either 10 (n = 6) or 50 micromol vitamin A/kg body (n = 4) during pregnancy and through d 13 of lactation. [3H]Vitamin A was incorporated into each diet beginning on d 6 of lactation. Vitamin A concentrations on d 13 were significantly higher in dam liver (x 3), pup liver (x 2.6), milk (x 2.5) and mammary tissue (x 1.3) in rats consuming the higher level of vitamin A. In both groups, vitamin A specific activities in plasma and milk reached apparent plateaus by 2.33 d after addition of [3H]vitamin A to the diets. Vitamin A specific activity in milk was higher than in plasma at all times in both groups. The estimated minimum contribution of chylomicrons to milk vitamin A was 32 +/- 3% in rats fed the lower level of vitamin A vs. 52 +/- 10% at the higher level (P = 0.014). We concluded that dietary vitamin A, like triglycerides, may be directed to mammary tissue during lactation for preferential secretion into milk; thus, increasing vitamin A intakes will increase the contribution of dietary vitamin A to milk. In contrast to milk, mammary tissue vitamin A turns over very slowly.
To study effects of vitamin A status on retinol dynamics, male rats were fed purified diets varying in vitamin A concentration. Group 1 rats had marginal liver vitamin A levels (approximately 500 nmol) and were in a slight positive vitamin A balance; Group 2 had similar liver levels but were in a slight negative balance; Group 3 had lower liver levels (approximately 370 nmol) and were in a slight negative balance; Group 4 had depleted liver reserves (<10 nmol) and were in vitamin A balance. [3H]Retinol-labeled plasma was injected intravenously, and serial plasma samples were collected for 41 d while rats (six per group) consumed approximately 50 nmol retinol/d (Group 1) or -25 nmol/d (Groups 2-4). Plasma retinol was normal in Groups 1-3 (1.9-2.0 micromol/L) and lower in Group 4 (0.96 micromol/L). Plasma tracer data were fit to a three-compartment model. The central plasma retinol compartment (transit time, 1.5-1.7 h) exchanged with a fast turning-over extravascular vitamin A pool (transit time, 3-4.5 h; -40 nmol) and with a larger, slow turning-over extravascular pool (transit time, 5.5-10 d) that was the site of irreversible utilization of vitamin A. Irreversible utilization was 36 nmol/d (Group 1), 29 nmol/d (Groups 2 and 3) and 20 nmol/d (Group 4). The data indicate that in rats with low or marginal vitamin A status, vitamin A intake, vitamin A reserves and plasma retinol concentration all influence vitamin A utilization and other aspects of retinol dynamics.
Background: Retinol isotope dilution (RID) is used to determine vitamin A total body stores (TBS) after an oral dose of a vitamin A stable isotope. The generally accepted prediction equation proposed by Olson’s group in 1989 (Furr et al. Am J Clin Nutr 1989;49:713–6) includes factors related to dose absorption and retention, isotope equilibration in plasma compared with stores, catabolism during the mixing period, and the optimal time for measuring plasma isotope enrichment.Objectives: The objectives were 1) to develop a modified RID equation and identify an earlier sampling time for predicting TBS and 2) to improve prediction in individuals as well as groups.Methods: To develop a modified RID equation, we used results of model-based compartmental analysis [the Simulation, Analysis and Modeling software (WinSAAM version 3.0.8; http://www.WinSAAM.org)] of plasma [13C10]retinol kinetic data from 32 previously studied, healthy young adults of European ancestry who had moderate vitamin A intakes and who ingested 2.95 μmol [13C10]retinyl acetate.Results: We examined the time dependence of factors in the prediction equation related to absorption/retention (Fa) and isotope equilibration (S) and determined that 4 or 5 d postdosing was the optimal sampling time. TBS calculated by the equation TBS = Fa x S x (1/SAp), where SAp is plasma retinol specific activity (fraction of dose/μmol), were highly correlated with model-predicted TBS (r = 0.95 and 0.96 for 4 and 5 d, respectively; P < 0.001); predictions for individuals were also highly correlated (Rs = 0.94 and 0.94; P < 0.001).Conclusion: The equation TBS ≈ 0.5 × (1/SAp) accurately predicted vitamin A TBS in this group of 32 healthy young adults and its individual members with the use of data from 1 blood sample taken 4 d after isotope administration.
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