The elucidation of how vitamin A exerts its pleiotropic effects has become a molecular biology–driven endeavor for many nutritionists since the discovery and realization that the biological effects of vitamin A, except for its role in vision, are mediated by its active form, all-trans-retinoic acid via specific nuclear receptors that are members of the steroid superfamily of ligand-activated transcription factors (4
,8 9 10) , i.e., the retinoic acid receptors (RAR) 
, ß and 
that are activated by retinoic acid (RA), and the retinoid X receptors (RXR) , ß and that are obligatory partners for the RAR. The RAR-RXR heterodimers are the functional units in transducing the retinoid signal at the gene level. The pleiotropic effects of vitamin A are explained by the discovery that many of the RA target genes are genes involved in diverse biological processes (4 ,8 9 10) . Redundancy of retinoid receptors, evidenced in studies with receptor gene knockouts (4) , attests to the paramount importance of vitamin A in development. During the course of normal embryonic development, distinct developmental events are regulated by the presence of the vitamin A active form, RA. The function of vitamin A is inseparable from its metabolism because the biogeneration of RA in the embryo is the first developmental step in the initiation of RA-regulated signaling pathways and must be linked to regulated metabolic systems for the inactivation of unused RA. All of the physiologically important vitamin A metabolites and enzyme systems that regulate vitamin A metabolism have been demonstrated in embryos (3 4 5 6 7 8 ,11 12 13 14 15) .
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