Retinyl ester turnover

When some of the model parameters lack sufficient statistical certainty, the investigator may search the scientific literature for relevant information and use it to set constraints on the numerical values of some parameters of the model. Several statistical constraints were added in constructing the model shown in Fig. 3. The FTC of retinyl ester from the chylomicron retinyl ester to the fast turnover liver retinyl ester compartment was constrained to be inside the range of two statistical deviations of 60 36/day (mean ... 

Fast turnover liver 0-carotene Fast turnover liver retinyl ester 0.091 0.088 0.405... 

Fast turnover liver retinyl ester Slow turnover liver retinyl ester 2.60 0.22 13.2... 

Fast turnover liver retinyl ester Retinol-binding protein retinol 2.74 0.11 13.9... 

Retinol-binding protein retinol Fast turnover liver retinyl ester 2.99 0.21 26.4... 

Chylomicron retinyl ester Fast turnover liver retinyl ester 122.7 0.077 0.297... 

Note FTC is the fractional transfer coefficient its units are per day. FSD is fractional standard deviation of FTC. Flow (rates) are /onol/day. Ineveisble loss of -carotene (fecal) = 240 - FTC from GIT to GIT delay compartment. FTC from chylomicron retinyl ester to fast turnover liver retinyl ester = 60 36. Values apply to model in Figure 3. Reprinted with permission from Novotny et al. (1995). 

FIG. 7. Compartmental model predicted masses and concentrations of retinol and retinyl ester in plasma, liver, and extrahepatic tissue of a healthy adult who ingested a single 73-/imol dose of /S-carotene-dn orally. The Fast turnover liver retinoid (bottom left) and Slow turnover liver retinoid (bottom right) each include the protio and deuterated species. 

Zinc deficiency accompanied by a depression in plasma retinol has been noted in several studies. Some investigators have reported an increased liver vitamin A in several species of zinc-deficient animals (Stevenson and Earle, 1956 Saraswat and Arora, 1972 J. C. Smith et aL, 1973, 1976 Brown et aL, 1976 Jacobs et al., 1978 Carney et aL, 1976). There are also reports in humans in an association between lowered zinc, retinol, and RBP (Jacobs et a/., 1978 Solomons and Russell, 1980). J. C. Smith et al, (1973) suggested that hepatic mobilization of vitamin A was impaired by zinc deficiency and their follow-up studies demonstrated a depression in liver and plasma RBP in the zinc-deficient rat compared to pair-fed controls (Brown et al., 1976 Smith et al., 1974). The depression was hypothesized to be the result of a depressed synthesis rather than an increased turnover of RBP. That preformed RBP is present in zinc-deficient rats was demonstrated by Carney et al. (1976) using labeled vitamin A. Zinc-deficient rats, whether or not they were also vitamin A-deficient, were able to mobilize over a short time span a small oral dose of vitamin A as well as could their pair-fed controls. Those animals deficient only in zinc excreted metabolites of the labeled vitamin in a similar quantitative manner as the pair-fed controls for 6 days postdosing. These data suggest that the release of retinol from retinyl ester stores, as well as a depressed RBP synthetic rate, contributed to low plasma levels of vitamin A in zinc deficiency. 

---