Many tissues and cell types, starting early in embryogenesis, convert
retinol (vitamin A) into an active form, all-trans-retinoic acid. This
article will discuss a current model of retinol and retinoic acid met
abolism that integrates the various reactions which maintain retinoic
acid homeostasis, and will also integrate the enzymology with the func
tions of cellular retinoid binding proteins. These conserved high-affi
nity binding proteins enjoy widespread expression throughout all verte
brates and throughout most vertebrate tissues. The binding proteins li
mit access to retinol and retinoic acid to select enzymes and serve as
substrates and affecters of retinoid metabolism.