Abstract:
:Since the late 1980s, there has been an explosion of information on the molecular mechanisms and functions of vitamin A. This review focuses on the essential role of vitamin A in female reproduction and embryonic development and the metabolism of vitamin A (retinol) that results in these functions. Evidence strongly supports that in situ-generated all-trans retinoic acid (atRA) is the functional form of vitamin A in female reproduction and embryonic development. This is supported by the ability to reverse most reproductive and developmental blocks found in vitamin A deficiency with atRA, the block in embryonic development that occurs in retinaldehyde dehydrogenase type 2 null mutant mice, and the essential roles of the retinoic acid receptors, at least in embryogenesis. Early studies of embryos from marginally vitamin A-deficient (VAD) pregnant rats revealed a collection of defects called the vitamin A-deficiency syndrome. The manipulation of all-trans retinoic acid (atRA) levels in the diet of VAD female rats undergoing a reproduction cycle has proved to be an important new tool in deciphering the points of atRA function in early embryos and has provided a means to generate large numbers of embryos at later stages of development with the vitamin A-deficiency syndrome. The essentiality of the retinoid receptors in mediating the activity of atRA is exemplified by the many compound null mutant embryos that now recapitulate both the original vitamin A-deficiency syndrome and exhibit a host of new defects, many of which can also be observed in the VAD-atRA-supported rat embryo model and in retinaldehyde dehydrogenase type 2 (RALDH2) mutant mice. A major task for the future is to elucidate the atRA-dependent pathways that are normally operational in vitamin A-sufficient animals and that are perturbed in deficiency, thus leading to the characteristic VAD phenotypes described above.
journal_name
Annu Rev Nutrjournal_title
Annual review of nutritionauthors
Clagett-Dame M,DeLuca HFdoi
10.1146/annurev.nutr.22.010402.102745Esubject
Has Abstractpub_date
2002-01-01 00:00:00pages
347-81eissn
0199-9885issn
1545-4312pii
22/1/347journal_volume
22pub_type
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journal_title:Annual review of nutrition
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journal_title:Annual review of nutrition
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journal_title:Annual review of nutrition
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更新日期:2007-01-01 00:00:00
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journal_title:Annual review of nutrition
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更新日期:2004-01-01 00:00:00
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journal_title:Annual review of nutrition
pub_type: 杂志文章,评审
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更新日期:1982-01-01 00:00:00
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journal_title:Annual review of nutrition
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更新日期:1990-01-01 00:00:00
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