ABCG1 is involved in vitamin E efflux

Olivier, Maryline; Bott, Raoul; Frisdal, Éric; Nowicki, Marion; Plengpanich, Wanee; Desmarchelier, Charles; Roi, Stéphanie; Quinn, Carmel M.; Gelissen, Ingrid C.; Jessup, Wendy; Eck, Miranda Van; Guérin, Maryse; Goff, Wilfried Le; Reboul, Emmanuelle

doi:10.1016/j.bbalip.2014.10.003

Cited by 28 publications

(28 citation statements)

References 48 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Thus, the association observed between genetic variants in this gene and α-tocopherol bioavailability suggests that this protein is able to transport α-tocopherol as well. This was confirmed recently by a study in ABCG1-deficient mice [60]. Although there has only been one study dedicated to identifying the genetic variants involved in α-tocopherol bioavailability, and although we acknowledge that the results obtained should be confirmed in other groups of subjects, we confidently conclude that it is likely that several SNPs in different genes have an effect of VE bioavailability.…”

Section: Genetic Variations Associated With the Variability In Vitsupporting

confidence: 82%

Genetic Variations Involved in Vitamin E Status

Borel

Desmarchelier

2016

IJMS

Self Cite

View full text Add to dashboard Cite

Vitamin E (VE) is the generic term for four tocopherols and four tocotrienols that exhibit the biological activity of α-tocopherol. VE status, which is usually estimated by measuring fasting blood VE concentration, is affected by numerous factors, such as dietary VE intake, VE absorption efficiency, and VE catabolism. Several of these factors are in turn modulated by genetic variations in genes encoding proteins involved in these factors. To identify these genetic variations, two strategies have been used: genome-wide association studies and candidate gene association studies. Each of these strategies has its advantages and its drawbacks, nevertheless they have allowed us to identify a list of single nucleotide polymorphisms associated with fasting blood VE concentration and α-tocopherol bioavailability. However, much work remains to be done to identify, and to replicate in different populations, all the single nucleotide polymorphisms involved, to assess the possible involvement of other kind of genetic variations, e.g., copy number variants and epigenetic modifications, in order to establish a reliable list of genetic variations that will allow us to predict the VE status of an individual by knowing their genotype in these genetic variations. Yet, the potential usefulness of this area of research is exciting with regard to personalized nutrition and for future clinical trials dedicated to assessing the biological effects of the various isoforms of VE.

show abstract

Section: Genetic Variations Associated With the Variability In Vitsupporting

confidence: 82%

Genetic Variations Involved in Vitamin E Status

Borel

Desmarchelier

2016

IJMS

Self Cite

View full text Add to dashboard Cite

show abstract

“…These CD36 polymorphisms as well as gene variants resulting from alternative splicing may affect the ability of CD36 to modulate signal transduction and gene expression and thus affect the responsiveness to vitamin E (5,34,60,131,224,239,281), which may ultimately translate into an altered risk for diseases such as atherosclerosis (130) and metabolic syndrome (173). Similar to CD36, polymorphisms in SR-BI (19), ABCA1, and ATP-binding cassette transporter G1 (ABCG1) may influence vitamin E levels in plasma and tissues (66,75,158,170,179,180).…”

Section: Gene Polymorphisms As Determinants Of Regulatory Effects Of mentioning

confidence: 98%

Vitamin E: A Role in Signal Transduction

Zingg

2015

Annu. Rev. Nutr.

109

View full text Add to dashboard Cite

Vitamin E modulates the activity of several signal transduction enzymes with consequent alterations of gene expression. At the molecular level, vitamin E may directly bind to these enzymes and compete with their substrates, or it may change their activity by redox regulation. The translocation of several of these enzymes to the plasma membrane is regulated by vitamin E, suggesting the modulation of protein-membrane interactions as a common mechanism for vitamin E action. Enzyme-membrane interactions can be affected by vitamin E by interference with binding to specific membrane lipids or by altering cellular structures such as membrane microdomains (lipid rafts). Moreover, competition by vitamin E for common binding sites within lipid transport proteins may alter the traffic of lipid mediators and thus affect their signaling and enzymatic conversion. In this review, the main effects of vitamin E on enzymes involved in signal transduction are summarized and possible molecular mechanisms leading to enzyme modulation are evaluated.

show abstract

“…Whether this secretion occurs in the lymph or in the portal vein remains to be determined. Recently, it has been suggested that the basolateral membrane protein ATP-binding cassette sub-family G member 1 (ABCG1) could also be involved in VE basolateral efflux to HDL (75,76) and a SNP in its encoding gene has been shown to be associated with the postprandial chylomicron VE concentration following consumption of a VE-rich meal (22). The qualitative or quantitative contribution of non-apolipoprotein Bdependent routes to VE absorption efficiency are not known and further investigations are warranted.…”

Section: Vitamin E Secretion From the Basolateral Side Of The Enterocmentioning

confidence: 99%

“…ABCG1 is a candidate protein in the basolateral efflux of VE to HDL in enterocytes (75,76). Solute carrier family 10 member 2 encodes for ASBT, which functions as an apical membrane enterocyte transporter responsible for the uptake of luminal bile acids in the ileum To date, there has only been one study dedicated to identify genetic variants involved in VE bioavailability.…”

Section: Genetic Factorsmentioning

confidence: 99%

“…More precisely, -and γ-tocopherol have both been shown to indirectly decrease liver X receptor  (LXR) activity in an in vitro enterocyte cell model (132), which can in turn inhibit the expression of ABCA1 and ABCG1 (132,133). ABCA1 is involved in enterocyte VE basolateral efflux to apolipoprotein A1-containing HDL while ABCG1 is a candidate for enterocyte VE basolateral efflux to HDL (76,134). Additionally, pregnane X receptor (PXR), whose expression can be modulated by most VE vitamers (135), has been shown to decrease SR-B1 and ABCA1 expression in an in vitro model of hepatocytes (136).…”

Section: Vitamin E (Nutrient) Status Of the Hostmentioning

confidence: 99%

See 1 more Smart Citation