Metabolism of Retinol During Mammalian Placental and Embryonic Development

Retinol (vitamin A) is a fat‐soluble nutrient indispensable for a harmonious mammalian gestation. The absence or excess of retinol and its active derivatives [i.e., the retinoic acids (RAs)] can lead to abnormal development of embryonic and extraembryonic (placental) structures. The embryo is unable to synthesize the retinol and is strongly dependent on the maternal delivery of retinol itself or precursors: retinyl esters or carotenoids. Before reaching the embryonic tissue, the retinol or the precursors have to pass through the placental structures. During this placental step, a simple diffusion of retinol can occur between maternal and fetal compartments; but retinol can also be used in situ after its activation into RA 1 or stored as retinyl esters. Using retinol‐binding protein knockout model, an alternative way of embryonic retinol supply was described using retinyl esters incorporated into maternal chylomicrons. In the embryo, the principal metabolic event occurring for retinol is its conversion into RAs, the active molecules implicated on the molecular control of embryonic morphogenesis and organogenesis. All these placental and embryonic events of retinol transport and metabolism are highly regulated. Nevertheless, some genetic and/or environmental abnormalities in the transport and/or metabolism of retinol can be related to developmental pathologies during mammalian development.