Two different metabolic alterations in
vitamin A status are known to cause changes in the amount of circulating
retinol-binding protein (RBP) and
cellular retinol-binding protein (CRBP) in experimental animals; namely
vitamin A deficiency, characterized by depleted
retinol-liver stores and
hypervitaminosis A, characterized by hepatic accumulation of
retinyl esters. We have induced
vitamin A deficiency and
hypervitaminosis A in two groups of rats with the aim of determining whether the expression of the genes coding for these two
proteins might be directly regulated by
retinol. Using human RBP and CRBP cDNAs as probes, we measured the rate of transcription of the two genes in liver nuclei from control and treated rats by run-on transcription assays, and the steady-state level of the mRNAs by Northern blot analysis of total liver
RNA. The distribution profile of RBP and CRBP mRNAs on fractionated liver polysomes was also examined. We have found a threefold decrease in the hepatic level of CRBP
mRNA in
vitamin-A-deficient animals, while the RBP
mRNA is not affected by this nutritional deprivation. The decreases does not correspond to a lower transcription rate of the gene and therefore it is likely to result from lower stability of the CRBP
mRNA. In
hypervitaminosis A, we do not observe any differences in both the steady-state level of the mRNAs and in the rate of transcription of the two genes. The results are discussed in terms of
retinol-dependent stabilization of the
mRNA coding for CRBP.