All-trans beta-carotene is absorbed preferentially to 9-cis beta-carotene, but the latter accumulates in the tissues of domestic ferrets (Mustela putorius puro).

The algae Dunaliella bardawil and Dunaliella salina naturally contain large concentrations of all-trans and 9-cis beta-carotene (betaC). The purpose of this study was to compare the relative serum and tissue accumulation of all-trans and 9-cis betaC in ferrets fed different ratios of all-trans/9-cis betaC derived from two commercial sources, D. bardawil or D. salina (Betatene). Male ferrets (7 wk old) were fed carotene-free, pelleted diets for 27 d. Beginning on d 18, groups of ferrets (n = 6 or 7) received daily, one of six oral supplements varying in ratios of 9-cis and all-trans betaC mixed with approximately 1.0mL of Ensure. Four supplements containing 5.2-8.3 micromol total betaC were prepared from a 20% Betatene preparation, D. bardawil, a high-cis Betatene preparation, and Betatene further enriched in 9-cis betaC with all-trans betaC/9-cis betaC ratios of 2.2, 1.5, 0.6 and 0.4, respectively. Two control supplements, high and low betaC, were prepared from commercial betaC beadlets. The high control supplement had an all-trans/9-cis ratio of 19.0, whereas 9-cis betaC was not detected in the low supplement. On d 27, serum and tissues were obtained for HPLC analysis of betaC and its isomers. Analysis of livers showed that all-trans betaC was the primary isomer present, but 9-cis and other isomers were also detected in all groups. The hepatic all-trans/9-cis ratios were 5.9, 4.9, 2.5, 1.4, 52.2 and47.5, respectively, for the groups listed above. Lower amounts of all-trans and 9-cis betaC were found in kidneys compared with the liver, but ratios of all-trans/9-cis were not different among groups. Only trace amounts of 9-cis betaC were found in serum. These results demonstrate that the algae D. bardawil and D. salina provide a bioavailable source of betaC isomers, but, as in humans, absorption of 9-cis betaC is poor and any 9-cis betaC absorbed is apparently cleared by the liver.

Tissue stores of beta-carotene are not conserved for later use as a source of vitamin A during compromised vitamin A status in mongolian gerbils (Meriones unguiculatus).

Vitamin A (VA) deficiency remains a serious problem in the world today. Current approaches to preventing or treating VA deficiency, including dietary intervention with provitamin A compounds, rely on the body converting ingested beta-carotene (betaC) to VA. However, it is not known whether betaC that is already in the tissues can be used as a source of VA to prevent deficiency. The objectives of these studies were to determine whether tissue betaC stores are converted to VA when the Mongolian gerbils have low VA status and whether previously fed betaC is retained in the tissues for later conversion to VA. In the first study, gerbils were prefed diets with betaC (20.3 +/- 6.2 nmol/g diet) (+betaC) or without betaC (-betaC), and with VA [2.4 +/- 1.5 nmol/g diet (+betaC diet) or 12.0 +/- 4.2 nmol/g diet (-betaC diet)] for 7 d, and then depleted of both betaC and VA for up to 84 d. On d 0 after the prefeeding period, hepatic betaC stores were 13.3 +/- 9.1 nmol. These stores were significantly lower after 28d of consuming the -VA/-betaC diet (2.16 +/- 1.7 nmol), even though the hepatic VA concentrations did not change. In the second study, the gerbils were prefed a -VA/+betaC diet (74.3 +/- 19. 7 nmol betaC/g diet) for 7 d, and then fed a betaC-free diet either with (7.1 +/- 1.4 nmol/g) or without VA for up to 34 d. Hepatic betaC stores after the 7-d prefeeding period were 38.1 +/- 20.6 nmol, and were significantly higher than after 7d of consuming either a +VA/-betaC (12.4 +/- 10.8 mmol) or -VA/-betaC diet (11.4 +/- 8.0 nmol). The results from both studies suggest that a substantial amount of hepatic betaC is rapidly lost when betaC is eliminated from the diet and therefore is not conserved to meet later VA needs. The presence of VA in the diet (Study 2) did not affect the rate of betaC loss from the serum and tissues. Moreover, no evidence was found that the stored betaC was utilized for VA. The data suggest that there may be two pools of hepatic betaC, one that is lost rapidly and another that is lost more slowly over time, but losses are not affected by VA status.