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Open AccessJournal Article

Transport and metabolism of vitamin A

TLDR
Findings on vitamin A transport from intestines to target-cell and metabolism of this fat-soluble vitamin are reviewed and possible roles of cellular retinoid-binding proteins in the process of Vitamin A transport and metabolism are reviewed.
Abstract
The present paper is a review of up-to-date findings on vitamin A transport from intestines to target-cell and metabolism of this fat-soluble vitamin. The hypotheses of possible enzymes participation in the process of etherification/hydrolysis and oxidation/reduction of vitamin A are discussed. Furthermore, possible roles of cellular retinoid-binding proteins in the process of vitamin A transport and metabolism are reviewed.

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Dietary Carotenoids and Vitamins A, C, and E and Risk of Breast Cancer

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International Union of Pharmacology. LX. Retinoic Acid Receptors

TL;DR: This review summarizes the considerable amount of knowledge generated on retinoids, members of the nuclear hormone receptor superfamily, which regulate a wide variety of essential biological processes, such as vertebrate embryonic morphogenesis and organogenesis, cell growth arrest, differentiation and apoptosis, and homeostasis, as well as their disorders.
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Vitamins A and E: metabolism, roles and transfer to offspring.

TL;DR: An overview of their biological functions, metabolism and dynamics of transfer to offspring in mammals, including the biochemical aspects of their intestinal absorption, blood transport, tissue uptake, storage and catabolism is presented.
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Modulation of T Cell and Innate Immune Responses by Retinoic Acid

TL;DR: Retinoic acid plays a role in immune homeostasis in the steady-state but activates pathogenic T cells in conditions of inflammation.
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The vitamin A-redox hypothesis: a biochemical basis for honest signaling via carotenoid pigmentation.

TL;DR: The vitamin A–redox hypothesis is presented as a testable alternative hypothesis to the resource trade-off hypothesis for the maintenance of honesty of carotenoid pigmentation.
References
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Cellular Retinol-Binding Protein-1 Expression and Modulation during In Vivo and In Vitro Myofibroblastic Differentiation of Rat Hepatic Stellate Cells and Portal Fibroblasts

TL;DR: In normal liver, CRBP-1 expression was different among fibroblastic cells, a finding that adds to the concept of heterogeneity of liver fibrogenic cells, and data suggest a correlation between CRBP -1 expression and myofibro Blastic differentiation.

Thematic Review Series: Fat-Soluble Vitamins: Vitamin A Carotenoid metabolism in mammals, including man: formation, occurrence, and function of apocarotenoids

TL;DR: Eroglu et al. as discussed by the authors reviewed the role of apocarotenoids in the formation, occurrence, and function of carotenoid metabolites in mammals, including man.
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Smooth Muscle Cell Differentiation: Model Systems, Regulatory Mechanisms, and Vascular Diseases.

TL;DR: The goal of this review is to provide a brief overview of the recent advancements in the understanding of SMC differentiation and the development of in vitroSMC differentiation models, with a particular emphasis on examination of molecular mechanisms involved in the regulation of SMCs differentiation and phenotypic modulation.
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Isoforms of Retinol binding protein 4 (RBP4) are increased in chronic diseases of the kidney but not of the liver

TL;DR: The occurrence of RBP4 isoforms is not influenced by liver function but seems to be strongly related to kidneys function and may therefore be important in investigating kidney function and related disorders.
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A novel signaling by vitamin A/retinol promotes self renewal of mouse embryonic stem cells by activating PI3K/Akt signaling pathway via insulin-like growth factor-1 receptor.

TL;DR: This study demonstrates for the first time that retinol directly activates phosphoinositide three (PI3) kinase signaling pathway through IGF‐1 receptor/insulin receptor substrate one (IRS‐1) by engaging Akt/PKB‐mTORC1 mammalian target of rapamycin‐2 (mammalian target ofRapamycin complex 2), indicating a growth factor‐like function of vitamin A.
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