TitleFunction of vitamin A in vertebrate embryonic development
Publication TypeJournal Article
Year of Publication2001
AuthorsZile, MH
JournalThe Journal of Nutrition
Volume131
Issue3
Pagination705 - 708
Date Published2001/03//
KeywordsAnimals, Embryonic and Fetal Development, Humans, Mice, Mice, Knockout, Models, Animal, Quail, Rats, Receptors, Retinoic Acid, Tretinoin, Vit A, Vitamin A, Vitamin A Deficiency
Abstract

Advances in molecular biology and retinoic acid receptor research have significantly contributed to the understanding of the role of vitamin A during vertebrate development. Examination of the function of this vitamin during very early developmental stages using the completely vitamin A-depleted avian embryo has revealed that the vitamin A requirement begins at the time of formation of the primitive heart, circulation and specification of hindbrain. The lack of vitamin A at this critical time results in gross abnormalities and early embryonic death. In rodent models, vitamin A deficiency can be targeted to later gestational windows and documents the need for vitamin A for more advanced stages of development. Major target tissues of vitamin A deficiency include the heart, central nervous system and structures derived from it, the circulatory, urogenital and respiratory systems, and the development of skull, skeleton and limbs. These abnormalities are also evident in mice mutants from retinoid receptor knockouts; they have revealed both morphological and molecular aspects of vitamin A function during development. Retinoic acid receptors (RAR) in partnership with retinoid X receptor (RXR)alpha appear to be the important retinoid receptor transcription factors regulating vitamin A function at the gene level during development via the physiologic ligand all-trans-retinoic acid. Homeostasis of retinoic acid is maintained by developmentally regulated vitamin A metabolism enzyme systems. Inadequate vitamin A nutrition during early pregnancy may account for some pediatric congenital abnormalities.

Short TitleJ. Nutr.