Vitamin E intestinal absorption: Regulation of membrane transport across the enterocyte

Reboul, Emmanuelle

doi:10.1002/iub.1955

Cited by 38 publications

(24 citation statements)

References 94 publications

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“…SR-BI post-transcriptional regulation also seems be dependent on bile secretion, with bile salts leading to a rise of intestinal SR-BI expression in rodents [86]. Finally, NPC1L1 expression was increased by estrogen [87] and cholecystokinin [88] in mouse intestines, while its expression was decreased by peptide YY in Caco-2 cells [89] (see [90] for review).…”

Section: Regulation Of Carotenoid Transporter Expressions In the Ementioning

confidence: 99%

Mechanisms of Carotenoid Intestinal Absorption: Where Do We Stand?

Reboul

2019

Nutrients

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146

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A growing literature is dedicated to the understanding of carotenoid beneficial health effects. However, the absorption process of this broad family of molecules is still poorly understood. These highly lipophilic plant metabolites are usually weakly absorbed. It was long believed that β-carotene absorption (the principal provitamin A carotenoid in the human diet), and thus all other carotenoid absorption, was driven by passive diffusion through the brush border of the enterocytes. The identification of transporters able to facilitate carotenoid uptake by the enterocytes has challenged established statements. After a brief overview of carotenoid metabolism in the human upper gastrointestinal tract, a focus will be put on the identified proteins participating in the transport and the metabolism of carotenoids in intestinal cells and the regulation of these processes. Further progress in the understanding of the molecular mechanisms regulating carotenoid intestinal absorption is still required to optimize their bioavailability and, thus, their health effects.

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Section: Regulation Of Carotenoid Transporter Expressions In the Ementioning

confidence: 99%

Mechanisms of Carotenoid Intestinal Absorption: Where Do We Stand?

Reboul

2019

Nutrients

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146

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“…However, after vitamin E intake, postprandial responses are very variable in humans. Some recent advances show that the absorption of αand γ-tocopherol is in reality more complex and involves at least partially different receptors and transporters, in particular Scavenger Receptor Class B Type 1 (SR-B1), CD36 molecule, and NPC1-like intracellular cholesterol Transporter 1 (NPC1L1) (Reboul 2017(Reboul , 2019b. No studies determine precisely the quantification of α-tocopherol in humans.…”

Section: Absorptionmentioning

confidence: 99%

“…Absorption, distribution, and metabolism of vitamin E. Adapted from(Galli et al 2017;Reboul 2019b;Schmölz 2016). ABCA1, ATP-binding cassette transporter; α-TTP, α-tocopherol transfer protein; CETP, cholesteryl ester transfer protein; 13'-COOH, 13'-carboxychromanol; HDL, high density lipoproteins; NPC1L1, Niemann-Pick C1-like intracellular cholesterol Transporter 1; 13'-OH, 13'-hydroxychromanol; PLTP, phospholipid transfer protein; SR-B1: Scavenger Receptor Class B Type 1; LDL, low density lipoproteins; LDLR, LDL receptor; LRP, LDL receptor-related proteins; VLDL, very low density lipoproteins.…”

mentioning

confidence: 99%

Plant Kingdom as Source of Vitamins

Hennebelle¹

2020

Handbook of Dietary Phytochemicals

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A vitamin is an organic substance necessary, in small quantities, for the correct functioning of the metabolism of a living organism. It is an essential nutrient because this substance cannot be synthesized in sufficient quantity by this organism and thus must be provided through the food intake. Each organism has specific needs: a molecule can be a vitamin for one species and not be it for another. It is the case for example of Vitamin C. Some vitamins are water-soluble compounds, including all vitamin Bs (B1, B2, B3, B5, B6, B7, B9, B12) and vitamin C. Others are fat-soluble compounds and encompass vitamins A, D, E, and K. In this chapter, we have chosen to provide an overview of recent literature data only about vitamins provided exclusively or significantly by plant food, in particular vitamins A (as provitaminic carotenoids), B1, B9, C, E, and K1. Vitamins provided by animal food, such as vitamin D or vitamin B12, will be not discussed in this chapter.

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“…The mechanisms of vitamin E intestinal absorption are only partially understood. Data obtained in recent years, show that its intestinal absorption is mediated, at least in part, by cholesterol membrane transporters including the scavenger receptor class B type I (SR-BI), cluster differentiation 36 molecule (CD36), Nieman-Pick-C1/like 1 (NPC1L1), and ATP-binding cassettes A1 and G1 (ABCA1 and ABCG1) [25].…”

Section: Vitamin E Metabolism and Subcellular Distributionmentioning

confidence: 99%

Vitamin E Supplementation and Mitochondria in Experimental and Functional Hyperthyroidism: A Mini-Review

et al. 2019

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Mitochondria are both the main sites of production and the main target of reactive oxygen species (ROS). This can lead to mitochondrial dysfunction with harmful consequences for the cells and the whole organism, resulting in metabolic and neurodegenerative disorders such as type 2 diabetes, obesity, dementia, and aging. To protect themselves from ROS, mitochondria are equipped with an efficient antioxidant system, which includes low-molecular-mass molecules and enzymes able to scavenge ROS or repair the oxidative damage. In the mitochondrial membranes, a major role is played by the lipid-soluble antioxidant vitamin E, which reacts with the peroxyl radicals faster than the molecules of polyunsaturated fatty acids, and in doing so, protects membranes from excessive oxidative damage. In the present review, we summarize the available data concerning the capacity of vitamin E supplementation to protect mitochondria from oxidative damage in hyperthyroidism, a condition that leads to increased mitochondrial ROS production and oxidative damage. Vitamin E supplementation to hyperthyroid animals limits the thyroid hormone-induced increases in mitochondrial ROS and oxidative damage. Moreover, it prevents the reduction of the high functionality components of the mitochondrial population induced by hyperthyroidism, thus preserving cell function.

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Vitamin E intestinal absorption: Regulation of membrane transport across the enterocyte

Cited by 38 publications

References 94 publications

Mechanisms of Carotenoid Intestinal Absorption: Where Do We Stand?

Mechanisms of Carotenoid Intestinal Absorption: Where Do We Stand?

Plant Kingdom as Source of Vitamins

Vitamin E Supplementation and Mitochondria in Experimental and Functional Hyperthyroidism: A Mini-Review

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