The function of vitamin A in cellular growth and differentiation, and its roles during pregnancy and lactation.
Recent advances in the molecular biology of the retinoids have provided a mechanistic explanation for the observations, first made several decades ago, that vitamin A profoundly influences the differentiation of tissues throughout the body. A central concept has recently emerged, namely that retinoids seldom exist "free" in solution but, rather, are nearly always associated with specific retinoid-binding proteins. In plasma, these include RBP and the chylomicron whereas, in cells two distinct classes of retinoid-binding proteins exist: the cellular (cytoplasmic) proteins (CRBPs and CRABPs) and the nuclear receptors proteins (RARs and RXRs). Whereas the cellular retinoid-binding proteins serve as buffers and as chaperones during metabolism (Ross, 1993b), the nuclear receptors are now recognized to be the direct mediators of retinoid actions on the genome. Both the cytoplasmic and nuclear classes of retinoid-binding proteins are expressed early in development and are proposed to control the concentration of retinoic acid and the transcription of retinoid-responsive genes, respectively. Given the profound effects of retinoic deficiency or excess on the developing fetus, it is not surprising that mechanisms have evolved to control the placental transfer of vitamin A. Transfer is nearly uniform over a rather wide range of maternal dietary vitamin A intake. The importance of RBP in transporting retinol to tissues is suggested by the observations that the visceral yolk sac and the liver of the fetus transcribe and translate RBP. In comparison to pregnancy, vitamin A transport during lactation is much more responsive to variations in maternal vitamin A intake. The young of mothers with good vitamin A nutriture may thus accumulate significant retinol reserves during the suckling period. Conversely, young nursed by mothers with poor vitamin A status and low intake during lactation may fail to develop adequate stores and be vulnerable to vitamin A deficiency if the post-weaning diet is also poor in vitamin A. In populations with low vitamin A status, the lactation period provides an excellent window of opportunity for supplementing mothers and, indirectly, their offspring, with vitamin A to replenish the mother's vitamin A reserves and assure that the infant's growth and development are not limited by an inadequate quantity of this essential nutrient.
Ross
A C
AC
Department of Biochemistry, Medical College of Pennsylvania, Philadelphia 19129.
Gardner
E M
EM
D002454:Cell Differentiation / Q000502:physiology*; D002455:Cell Division / Q000502:physiology*; D005260:Female; D005333:Fetus / Q000502:physiology; D005786:Gene Expression Regulation; D006801:Humans; D007774:Lactation / Q000502:physiology*; D008431:Maternal-Fetal Exchange; D011247:Pregnancy / Q000502:physiology*; D018168:Receptors, Retinoic Acid / Q000502:physiology; D014212:Tretinoin / Q000378:metabolism / Q000494:pharmacology; D014801:Vitamin A / Q000502:physiology*
D018168:Receptors, Retinoic Acid; D014801:Vitamin A; D014212:Tretinoin