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. [ABSTRACT FROM AUTHOR]