Function of Vitamin A in Vertebrate Embryonic Development
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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.
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Vitamin A deficiency affects the heart, central nervous system and associated structures, circulatory, urogenital, and respiratory systems, as well as the skull, skeleton, and eyes, and can cause serious malformations, including early embryonic death.
“The primary organs and systems affected by vitamin A deficiency (VAD) include the heart, central nervous system and its associated structures, the circulatory, urogenital, and respiratory systems, as well as the skull, skeleton, and eyes. Vitamin A is essential for the early formation of the primitive heart and circulatory system and for the proper development of the rhombencephalon; deficiency”
From Maternal Overnutrition and Fetal Programming: Long-Term Metabolic, Cognitive, and Epigenetic Consequences (2026) · cites this paper as [131]
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- Authors
- Zile, M. H.
- Affiliations
- Michigan State University (US)
- Corresponding author
- Zile, Maija H.
- Venue
- The Journal of Nutrition
- Publisher
- Elsevier BV
- Published
- 2001-03
- Volume
- 131
- Issue
- 3
- Pages
- 705-708
- ISSN
- 0022-3166 (ISSN-L)
- OpenAlex
- W2105106545
- Cited by
- 263
- References
- 43
- Citations by year
- 2026: 4 · 2025: 5 · 2024: 5 · 2023: 4 · 2022: 6 · 2021: 5 · 2020: 15 · 2019: 13 · 2018: 2 · 2017: 10 · 2016: 8 · 2015: 6 · 2014: 15 · 2013: 10 · 2012: 13
- FWCI
- 1.40
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Journal of Nutrition (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinoids in leukemia and cellular processes
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinal Development and Disorders
- Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Birth, Development, and Health
- Keywords
- vitamin A, embryonic development, retinoic acid receptor, retinoid X receptor alpha, vitamin A metabolism, vitamin A deficiency, avian embryo, rodent embryo, heart development, central nervous system development, skeletal development, congenital malformations, prenatal nutrition
- MeSH terms
- Animals, Embryonic and Fetal Development, Humans, Quail, Tretinoin, Vitamin A, Vitamin A Deficiency, Receptors, Retinoic Acid, Mice, Knockout, Models, Animal, Mice, Rats
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