Molecular Basis for Vitamin A Uptake and Storage in Vertebrates

Chełstowska, Sylwia; Widjaja‐Adhi, Made Airanthi K.; Silvaroli, J.A.; Golczak, Marcin

doi:10.3390/nu8110676

Cited by 56 publications

(51 citation statements)

References 144 publications

(197 reference statements)

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“…The initial steps are the cleavage of carotenoids by the two known human carotenoid-oxygenases BCO1 and 2 (132,133) . The resulting apo-carotenals (named retinal in the case of apo-15′-carotenal), can then further be reduced to alcohols and esterified to store retinoids as retinyl esters, a reaction mediated by LRAT and diacylglycerol O-acyltransferase 1/2 (DGAT1/2) (134)(135)(136)(137) . Retinyl-esters can further be de-esterified by esterases (REHs) to alcohols and especially retinol to serve as precursors for later bioactivation (138,139) .…”

Section: Liver Metabolism and Blood Transport Of β-Carotene And Its Mmentioning

confidence: 99%

β-Carotene in the human body: metabolic bioactivation pathways – from digestion to tissue distribution and excretion

et al. 2019

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5Paprika Bioanalytics BT, Debrecen, Hungary β-Carotene intake and tissue/blood concentrations have been associated with reduced incidence of several chronic diseases. Further bioactive carotenoid-metabolites can modulate the expression of specific genes mainly via the nuclear hormone receptors: retinoic acid receptor-and retinoid X receptor-mediated signalling. To better understand the metabolic conversion of β-carotene, inter-individual differences regarding β-carotene bioavailability and bioactivity are key steps that determine its further metabolism and bioactivation and mediated signalling. Major carotenoid metabolites, the retinoids, can be stored as esters or further oxidised and excreted via phase 2 metabolism pathways. In this review, we aim to highlight the major critical control points that determine the fate of β-carotene in the human body, with a special emphasis on β-carotene oxygenase 1. The hypothesis that higher dietary β-carotene intake and serum level results in higher β-carotene-mediated signalling is partly questioned. Alternative autoregulatory mechanisms in β-carotene / retinoid-mediated signalling are highlighted to better predict and optimise nutritional strategies involving βcarotene-related health beneficial mediated effects.

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Section: Liver Metabolism and Blood Transport Of β-Carotene And Its Mmentioning

confidence: 99%

β-Carotene in the human body: metabolic bioactivation pathways – from digestion to tissue distribution and excretion

et al. 2019

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“…There is one system, in particular, involved in retinoid biosynthesis and signalling, that is a strong contender for consideration in the context of schizophrenia because of its well-known role in neural development via control of neuronal differentiation. Retinoids are metabolites of vitamin A (all-trans retinol)commonly referred to as retinol, a fat soluble vitamin derived from foods in active form or as provitamin precursors such as a beta-carotene [11]. All-trans retinoic acid (at-RA) is the most biologically active retinoid and exerts a number of vital genomic and non-genomic effects [12,13].…”

Section: Introductionmentioning

confidence: 99%

The role of the retinoids in schizophrenia: genomic and clinical perspectives

Cairns

2019

Mol Psychiatry

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Signalling by retinoid compounds is vital for embryonic development, with particular importance for neurogenesis in the human brain. Retinoids, metabolites of vitamin A, exert influence over the expression of thousands of transcripts genome wide, and thus, act as master regulators of many important biological processes. A significant body of evidence in the literature now supports dysregulation of the retinoid system as being involved in the aetiology of schizophrenia. This includes mechanistic insights from large-scale genomic, transcriptomic and, proteomic studies, which implicate disruption of disparate aspects of retinoid biology such as transport, metabolism, and signalling. As a result, retinoids may present a valuable clinical opportunity in schizophrenia via novel pharmacotherapies and dietary intervention. Further work, however, is required to expand on the largely observational data collected thus far and confirm causality. This review will highlight the fundamentals of retinoid biology and examine the evidence for retinoid dysregulation in schizophrenia.

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“…Biologically active forms of vitamin A (retinol, retinal and retinoic acid) have essential roles in normal vision, immune function, cell differentiation and reproduction, with actions exerted through nuclear receptors (RARα, β and γ) which, like VDR, heterodimerise with RXR and alter gene transcription. Recent reviews describe vitamin A uptake, transport and storage in general (Chelstowska et al 2016) and by the placenta (Spiegler et al 2012).…”

Section: Vitamin Amentioning

confidence: 99%

Effects of micronutrients on placental function: evidence from clinical studies to animal models

Baker¹,

Hayes²,

Jones³

2018

Reproduction

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Micronutrient deficiencies are common in pregnant women due to low dietary intake and increased requirements for fetal development. Low maternal micronutrient status is associated with a range of pregnancy pathologies involving placental dysfunction, including fetal growth restriction (FGR), small-for-gestational age (SGA), pre-eclampsia and preterm birth. However, clinical trials commonly fail to convincingly demonstrate beneficial effects of supplementation of individual micronutrients, attributed to heterogeneity and insufficient power, potential interactions and lack of mechanistic knowledge of effects on the placenta. We aimed to provide current evidence of relationships between selected micronutrients (vitamin D, vitamin A, iron, folate, vitamin B12) and adverse pregnancy outcomes, combined with understanding of actions on the placenta. Following a systematic literature search, we reviewed data from clinical, and studies of micronutrient deficiency and supplementation. Key findings are potential effects of micronutrient deficiencies on placental development and function, leading to impaired fetal growth. Studies in human trophoblast cells and rodent models provide insights into underpinning mechanisms. Interestingly, there is emerging evidence that deficiencies in all micronutrients examined induce a pro-inflammatory state in the placenta, drawing parallels with the inflammation detected in FGR, pre-eclampsia, stillbirth and preterm birth. Beneficial effects of supplementation are apparent and in animal models and for combined micronutrients in clinical studies. However, greater understanding of the roles of these micronutrients, and insight into their involvement in placental dysfunction, combined with more robust clinical studies, is needed to fully ascertain the potential benefits of supplementation in pregnancy.

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Molecular Basis for Vitamin A Uptake and Storage in Vertebrates

Cited by 56 publications

References 144 publications

β-Carotene in the human body: metabolic bioactivation pathways – from digestion to tissue distribution and excretion

β-Carotene in the human body: metabolic bioactivation pathways – from digestion to tissue distribution and excretion

The role of the retinoids in schizophrenia: genomic and clinical perspectives

Effects of micronutrients on placental function: evidence from clinical studies to animal models

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