Relevant bibliographies by topics / Intestinal vitamin C transporters

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Academic literature on the topic 'Intestinal vitamin C transporters'

Author: Grafiati
Published: 4 June 2021
Last updated: 16 February 2022

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Journal articles on the topic "Intestinal vitamin C transporters"

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Subramanian, Veedamali S., Padmanabhan Srinivasan, Alexis J. Wildman, Jonathan S. Marchant, and Hamid M. Said. "Molecular mechanism(s) involved in differential expression of vitamin C transporters along the intestinal tract." American Journal of Physiology-Gastrointestinal and Liver Physiology 312, no. 4 (April 1, 2017): G340—G347. http://dx.doi.org/10.1152/ajpgi.00369.2016.

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Mammalian cells utilize two transporters for the uptake of ascorbic acid (AA), Na+-dependent vitamin C transporter SVCT-1 and SVCT-2. In the intestine, these transporters are involved in AA absorption and are expressed at the apical and basolateral membrane domains of the polarized epithelia, respectively. Little is known about the differential expression of these two transporters along the anterior-posterior axis of the intestinal tract and the molecular mechanism(s) that dictate this pattern of expression. We used mouse and human intestinal cDNAs to address these issues. The results showed a significantly lower rate of carrier-mediated AA uptake by mouse colon than jejunum. This was associated with a significantly lower level of expression of SVCT-1 and SVCT-2 at the protein, mRNA, and heterogeneous nuclear RNA (hnRNA) levels in the colon than the jejunum, implying the involvement of transcriptional mechanism(s). Similarly, expression levels of SVCT-1 and SVCT-2 mRNA and hnRNA were significantly lower in human colon. We also examined the levels of expression of hepatocyte nuclear factor 1α and specificity protein 1, which drive transcription of the Slc23a1 and Slc23a2 promoters, respectively, and found them to be markedly lower in the colon. Furthermore, significantly lower levels of the activating markers for histone (H3) modifications [H3 trimethylation of lysine 4 (H3K4me3) and H3 triacetylation of lysine 9 (H3K9ac)] were observed in the Slc23a1 and Slc23a2 promoters in the colon. These findings show, for the first time, that SVCT-1 and SVCT-2 are differentially expressed along the intestinal tract and that this pattern of expression is, at least in part, mediated via transcriptional/epigenetic mechanisms. NEW & NOTEWORTHY Our findings show, for the first time, that transporters of the water-soluble vitamin ascorbic acid (i.e., the vitamin C transporters SVCT-1 and SVCT-2) are differentially expressed along the length of the intestinal tract and that the pattern of expression is mediated, at least in part, by transcriptional and epigenetic mechanism(s) affecting both Slc23a1 and Slc23a2 genes.
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MacDonald, Lauren, Alfred E. Thumser, and Paul Sharp. "Decreased expression of the vitamin C transporter SVCT1 by ascorbic acid in a human intestinal epithelial cell line." British Journal of Nutrition 87, no. 2 (February 2002): 97–100. http://dx.doi.org/10.1079/bjn2001492.

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Vitamin C (ascorbic acid) is an essential nutrient that is involved in a number of cellular processes. However, unlike most mammals, man is unable to synthesize vitamin C and it must therefore be acquired from the diet. Absorption of vitamin C is achieved by two transporters, SVCT1 and SVCT2, recently cloned from rat and human kidney. SVCT1 is thought to be the predominant transporter in the intestine. Vitamin C supplements are increasingly common, thus contributing to an increased dietary load, and therefore the aim of the present study was to investigate the effect of high doses of ascorbic acid on SVCT1 expression. Using the Caco-2 TC7 cell model of small intestinal enterocytes, we measured the effects of ascorbic acid (4·5 mg/ml culture medium) on L-[14C]ascorbic acid uptake and SVCT1 expression (determined by reverse transcription-polymerase chain reaction). Ascorbic acid uptake was decreased significantly in Caco-2 TC7 cells exposed to ascorbate for 24 h (-50 %, P<0·0005). Expression of SVCT1 was also significantly reduced by exposure to elevated levels of ascorbate for 24 h (-77 %, P<0·005). Taken together these results suggest that high-dose supplements might not be the most efficient way of increasing the body pool of vitamin C.
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Teafatiller, Trevor, Christopher W. Heskett, Anshu Agrawal, Jonathan S. Marchant, Janet E. Baulch, Munjal M. Acharya, and Veedamali S. Subramanian. "Upregulation of Vitamin C Transporter Functional Expression in 5xFAD Mouse Intestine." Nutrients 13, no. 2 (February 14, 2021): 617. http://dx.doi.org/10.3390/nu13020617.

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The process of obtaining ascorbic acid (AA) via intestinal absorption and blood circulation is carrier-mediated utilizing the AA transporters SVCT1 and SVCT2, which are expressed in the intestine and brain (SVCT2 in abundance). AA concentration is decreased in Alzheimer’s disease (AD), but information regarding the status of intestinal AA uptake in the AD is still lacking. We aimed here to understand how AA homeostasis is modulated in a transgenic mouse model (5xFAD) of AD. AA levels in serum from 5xFAD mice were markedly lower than controls. Expression of oxidative stress response genes (glutathione peroxidase 1 (GPX1) and superoxide dismutase 1 (SOD1)) were significantly increased in AD mice jejunum, and this increase was mitigated by AA supplementation. Uptake of AA in the jejunum was upregulated. This increased AA transport was caused by a marked increase in SVCT1 and SVCT2 protein, mRNA, and heterogeneous nuclear RNA (hnRNA) expression. A significant increase in the expression of HNF1α and specific protein 1 (Sp1), which drive SLC23A1 and SLC23A2 promoter activity, respectively, was observed. Expression of hSVCT interacting proteins GRHPR and CLSTN3 were also increased. SVCT2 protein and mRNA expression in the hippocampus of 5xFAD mice was not altered. Together, these investigations reveal adaptive up-regulation of intestinal AA uptake in the 5xFAD mouse model.
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Song, Jian, Oran Kwon, Shenglin Chen, Rushad Daruwala, Peter Eck, Jae B. Park, and Mark Levine. "Flavonoid Inhibition of Sodium-dependent Vitamin C Transporter 1 (SVCT1) and Glucose Transporter Isoform 2 (GLUT2), Intestinal Transporters for Vitamin C and Glucose." Journal of Biological Chemistry 277, no. 18 (February 7, 2002): 15252–60. http://dx.doi.org/10.1074/jbc.m110496200.

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Szarka, András, and Tamás Lőrincz. "Cellular and intracellular transport of vitamin C. The physiologic aspects." Orvosi Hetilap 154, no. 42 (October 2013): 1651–56. http://dx.doi.org/10.1556/oh.2013.29712.

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Vitamin C requirement is satisfied by natural sources and vitamin C supplements in the ordinary human diet. The two major forms of vitamin C in the diet are L-ascorbic acid and L-dehydroascorbic acid. Both ascorbate and dehydroascorbate are absorbed along the entire length of the human intestine. The reduced form, L-ascorbic acid is imported by an active mechanism, requiring two sodium-dependent vitamin C transporters (SVCT1 and SVCT2). The transport of the oxidized form, dehydroascorbate is mediated by glucose transporters GLUT1, GLUT3 and possibly GLUT4. Initial rate of uptake of both ascorbate and dehydroascorbate is saturable with increasing external substrate concentration. Vitamin C plasma concentrations are tightly controlled when the vitamin is taken orally. It has two simple reasons, on the one hand, the capacity of the transporters is limited, on the other hand the two Na+-dependent transporters can be down-regulated by an elevated level of ascorbate. Orv. Hetil., 154 (42), 1651–1656.
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Subramenium, Ganapathy A., Subrata Sabui, Jonathan S. Marchant, Hamid M. Said, and Veedamali S. Subramanian. "EnterotoxigenicEscherichia coliheat labile enterotoxin inhibits intestinal ascorbic acid uptake via a cAMP-dependent NF-κB-mediated pathway." American Journal of Physiology-Gastrointestinal and Liver Physiology 316, no. 1 (January 1, 2019): G55—G63. http://dx.doi.org/10.1152/ajpgi.00259.2018.

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Vitamin C is an antioxidant and acts as a cofactor for many enzymatic reactions. Humans obtain vitamin C from dietary sources via intestinal absorption, a process that involves the sodium-dependent vitamin C transporters-1 and -2 (SVCT1 and SVCT2). Enterotoxigenic Escherichia coli (ETEC) infection impacts intestinal absorption/secretory functions, but nothing is known about its effect on ascorbic acid (AA) uptake. Here we demonstrate that infection of Caco-2 cells with ETEC led to a significant inhibition in intestinal AA uptake. This inhibition was associated with a marked reduction in hSVCT1 and hSVCT2 protein, mRNA, and heterogeneous nuclear RNA (hnRNA) expression levels as well as significant inhibition in the activity of both the SLC23A1 and SLC23A2 promoters. Similarly, exposure of mice to ETEC led to a significant inhibition in intestinal AA uptake and reduction in mSVCT1 and mSVCT2 protein, mRNA, and hnRNA expression levels. Inhibition was caused by the action of heat labile enterotoxin (LT), since infecting Caco-2 cells with LT-deficient ETEC (ΔLT) failed to impact AA uptake. Because LT activates adenylate cyclase, we also examined the effect of dibutyryl-cAMP in AA uptake by Caco-2 cells and observed a significant inhibition. Furthermore, treating the cells with celastrol, a specific NF-κB inhibitor, significantly blocked the inhibition of AA uptake caused by ETEC infection. Together, these data demonstrate that ETEC infection impairs intestinal AA uptake through a cAMP-dependent NF-κB-mediated pathway that regulates both SLC23A1 and SLC23A2 transcription.NEW & NOTEWORTHY Our findings demonstrate that heat-labile enterotoxin produced by enterotoxigenic Escherichia coli inhibits AA uptake in intestinal epithelial cells and mouse intestine. This effect is mediated through transcriptional repression of SLC23A1 (SVCT1) and SLC23A2 (SVCT2) via a cAMP-dependent NF-κB signaling pathway.
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Subramanian, Veedamali S., Subrata Sabui, Ganapathy A. Subramenium, Jonathan S. Marchant, and Hamid M. Said. "Tumor necrosis factor alpha reduces intestinal vitamin C uptake: a role for NF-κB-mediated signaling." American Journal of Physiology-Gastrointestinal and Liver Physiology 315, no. 2 (August 1, 2018): G241—G248. http://dx.doi.org/10.1152/ajpgi.00071.2018.

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Sodium-dependent vitamin C transporter-1 (SVCT-1) is the major transporter mediating intestinal vitamin C uptake. Intestinal inflammation and prolonged infection are associated with increased serum and intestinal mucosa levels of tumor necrosis factor-α (TNF-α), which also exerts profound effects on the intestinal absorption process. Elevated levels of TNF-α have been linked to the pathogenesis of inflammatory bowel disease (IBD) and malabsorption of nutrients, and patients with this condition have low levels of vitamin C. To date, little is known about the effect of TNF-α on intestinal absorption of vitamin C. We studied the impact of TNF-α on ascorbic acid (AA) transport using a variety of intestinal preparations. The expression level of human SVCT-1 mRNA is significantly lower in patients with IBD. TNF-α treated Caco-2 cells and mice showed a significant inhibition of intestinal14C-AA uptake. This inhibition was associated with significant decreases in SVCT-1 protein, mRNA, and heterogeneous nuclear RNA levels in TNF-α treated Caco-2 cells, mouse jejunum, and enteroids. Also, TNF-α caused a significant inhibition in the SLC23A1 promoter activity. Furthermore, treatment of Caco-2 cells with celastrol (NF-κB inhibitor) blocked the inhibitory effect caused by TNF-α on AA uptake, SVCT-1 protein, and mRNA expression, as well as the activity of SLC23A1 promoter. Treatment of TNF-α also led to a significant decrease in the expression of hepatocyte nuclear factor-1-α, which drives the basal activity of SLC23A1 promoter, and this effect was reversed by celastrol. Together, these findings show that TNF-α inhibits intestinal AA uptake, and this effect is mediated, at least in part, at the level of transcription of the SLC23A1 gene via the NF-κB pathway.NEW & NOTEWORTHY Our findings show that tumor necrosis factor-α inhibits intestinal ascorbic acid uptake in both in vitro and in vivo systems, and this inhibitory effect is mediated, at least in part, at the level of transcription of the SLC23A1 (sodium-dependent vitamin C transporter-1) gene via the NF-κB pathway.
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Masuda, Masashi, Hironori Yamamoto, Yuichiro Takei, Otoki Nakahashi, Yuichiro Adachi, Kohta Ohnishi, Hirokazu Ohminami, et al. "All-trans retinoic acid reduces the transcriptional regulation of intestinal sodium-dependent phosphate co-transporter gene (Npt2b)." Biochemical Journal 477, no. 4 (February 28, 2020): 817–31. http://dx.doi.org/10.1042/bcj20190716.

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Inorganic phosphate (Pi) homeostasis is regulated by intestinal absorption via type II sodium-dependent co-transporter (Npt2b) and by renal reabsorption via Npt2a and Npt2c. Although we previously reported that vitamin A-deficient (VAD) rats had increased urine Pi excretion through the decreased renal expression of Npt2a and Npt2c, the effect of vitamin A on the intestinal Npt2b expression remains unclear. In this study, we investigated the effects of treatment with all-trans retinoic acid (ATRA), a metabolite of vitamin A, on the Pi absorption and the Npt2b expression in the intestine of VAD rats, as well as and the underlying molecular mechanisms. In VAD rats, the intestinal Pi uptake activity and the expression of Npt2b were increased, but were reduced by the administration of ATRA. The transcriptional activity of reporter plasmid containing the promoter region of the rat Npt2b gene was reduced by ATRA in NIH3T3 cells overexpressing retinoic acid receptor (RAR) and retinoid X receptor (RXR). On the other hand, CCAAT/enhancer-binding proteins (C/EBP) induced transcriptional activity of the Npt2b gene. Knockdown of the C/EBP gene and a mutation analysis of the C/EBP responsible element in the Npt2b gene promoter indicated that C/EBP plays a pivotal role in the regulation of Npt2b gene transcriptional activity by ATRA. EMSA revealed that the RAR/RXR complex inhibits binding of C/EBP to Npt2b gene promoter. Together, these results suggest that ATRA may reduce the intestinal Pi uptake by preventing C/EBP activation of the intestinal Npt2b gene.
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Subramanian, Veedamali S., Padmanabhan Srinivasan, Alexis Wildman, Jonathan Marchant, and Hamid M. Said. "Differential-Expression of Vitamin C Transporters (SVCT-1 and SVCT-2) Along the Intestinal Tract: A Molecular Approach." Gastroenterology 152, no. 5 (April 2017): S272. http://dx.doi.org/10.1016/s0016-5085(17)31207-6.

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Subramanian, Veedamali S., Trevor Teafatiller, Hamid Moradi, and Jonathan S. Marchant. "Histone deacetylase inhibitors regulate vitamin C transporter functional expression in intestinal epithelial cells." Journal of Nutritional Biochemistry 98 (December 2021): 108838. http://dx.doi.org/10.1016/j.jnutbio.2021.108838.

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Dissertations / Theses on the topic "Intestinal vitamin C transporters"

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Amir, Shaghaghi Mandana. "Genetic and functional studies of two intestinal vitamin C transporters, SLC23A1 and GLUT14, associated with inflammatory bowel disease." American Journal of Clinical Nutrition, 2013. http://hdl.handle.net/1993/31001.

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It had long been known that individuals with inflammatory bowel disease (IBD), comprising Crohn’s disease (CD) and ulcerative colitis (UC), have locally reduced vitamin C levels in the intestinal mucosa, which equates to an overall loss of the antioxidant capacity and increase risk of oxidative tissue damage. The aim of the present work was to expand on this concept, through investigating the role of genetic variations in intestinal vitamin C transporters in vulnerability to IBD and further characterizing their functions. The studies focused on a known intestinal transporter for ascorbic acid, SLC23A1, and a novel intestinal transporter of dehydroascorbic acid, SLC2A14 (GLUT14). To investigate any association between the SLC23A1 and SLC2A14 with IBD, genomic DNA of 311 Caucasian individuals with IBD, participated in the Manitoba IBD Cohort Study, and 142 healthy controls were genotyped for tagging single nucleotide polymorphism (SNP) of each gene, using TaqMan Assays. New splice variants of SLC23A1 and SLC2A14 were determined by In silico analyses, followed by sub-cloning of the splice variants to verify their subcellular locations. Substrates and functions were determined, using the Xenopus laevis oocyte system for each transporter. The presence of the SLC23A1 variant rs10063949 G allele elevated the risk for CD by 150% (Odds ratios (OR) = 2.54, 95% CI 1.83-3.53). An allele dosage effect was confirmed; compared to rs10063949-AA homozygotes the 10063949-AG heterozygotes have a 150% elevated risk and the 10063949-GG homozygotes have a 370% elevated CD risk (OR=2.54, 95% CI 1.38-4.66; OR=4.72, 95% CI 2.53-8.81, p<0.001; respectively). No relation was observed between genetic variants in SLC23A1 and UC. Through database search, a novel 5’exon was discovered for SLC23A1 locus which is located 1078 nucleotides upstream of the canonical first exon. The two first exons are not mutually exclusive since they splice together to create a novel SLC23A1 protein isoform, we named it isoform 1A, with a N-terminus that is elongated by 36 amino acid. The novel SLC23A1 isoform located at the plasma membrane, but mediates only 7% of the ascorbic acid transport exhibited by the shorter isoform. The presence of the SLC2A14 SNP rs2889504 A allele elevated the risk for UC by 260% and CD by 468% (OR: 3.60, 95% CI: 1.95-6.64; OR: 4.68, 95% CI: 2.78-8.50, respectively). The rs10846086-G allele elevated the risk of UC and CD approximately 3-fold (OR: 2.91, 95% CI: 1.49-5.68; OR: 3.00, 95% CI: 1.55-5.78, respectively). The variant rs12815313-T increased the risk for CD by 112% (OR: 2.12, 95% CI: 1.33-3.36). All the genetic variations in SLC2A14 gene, associated with IBD, were independent from each other, strengthening the evidence that functional SNPs in the SLC2A14 locus contribute to IBD. It was identified that the two major GLUT14 isoforms locate to the plasmalemma membrane and mediate cellular uptake of dehydroascorbic acid. Significant expression in extra-testicular tissues was confirmed for SLC2A14, notably in intestinal segments, explaining the association with IBD. Re-analysis of genomic showed a dramatically expanded locus of SLC2A14, containing twenty exons which covered 103,477 nucleotides from the first Transcriptional Start Site (TSS) to the termination of the longest transcript. All together, the presented evidence indicate that functional SNPs in the SLC2A14 gene and SLC23A1 could contribute to vitamin C imbalance in mucosal cells which contributes to an elevated risks of IBD. Furthermore, novel information about genetic and functional characteristics of SLC23A1 and GLUT14 transporters was identified.
February 2016
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Velho, Albertina Menezes. "Topology of human sodium dependent vitamin C transporters." Thesis, University of Kent, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.405985.

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Ceddia, Ryan P. "Sodium dependent vitamin C transporters in the sheep corpus luteum sequence analysis /." Connect to this title online, 2005. http://hdl.handle.net/1811/351.

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Thesis (Honors)--Ohio State University, 2005.
Title from first page of PDF file. Document formattted into pages: contains, 28 p.; also includes graphics. Includes bibliographical references (p. 22-28). Available online via Ohio State University's Knowledge Bank.
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Paice, Shannon. "Investigations of sodium dependent vitamin c transporters in the ovine corpus luteum." Connect to resource, 2008. http://hdl.handle.net/1811/35995.

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Vakil, Priyal R. "Expression and Clinicopathological Implications of the Vitamin C Transporters SVCT-1 and SVCT-2 in Colon Cancer." Thesis, University of the Sciences in Philadelphia, 2019. http://pqdtopen.proquest.com/#viewpdf?dispub=13860024.

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Most of the colon cancer patient tumors progress to metastases, despite undergoing surgical resection or adjuvant chemotherapy. Predicting which patients will progress to metastases has been extremely challenging. There is an urgent need to identify early novel prognostic biomarkers that can early on predict the patient outcome. Vitamin C has been shown to have a pro-oxidant effect on cancer that enhances tumor growth and survival. Vitamin C is transported into mammalian cells via two isoforms of sodium-dependent vitamin C transporters (SVCTs), SVCT1 and SVCT2. The expression and clinical implications of SVCTs in tumor tissues could help us investigate its prognostic value in predicting patient outcome. In this report, we performed immunohistochemistry to determine SVCT1 and SVCT2 expression on primary tumors of 178 colon cancer patients. Colon cancer cells selectively expressed SVCT2 but not SVCT1. Moreover, poorly differentiated and metastatic tumors correlated with higher SVCT2 expression. Furthermore, increased SVCT2 expression was associated with shorter progression-free survival in patients with no or little lymph node invasion. We confirmed that SVCT2 could be an early stage prognostic biomarker that can predict colon cancer disease progression and survival.

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Varma, Saaket. "Human sodium dependent vitamin C transporters, hSVCT1 and hSVCT2 role of TM1 in their activity and the identification of trafficking motifs /." 2008. http://proquest.umi.com/pqdweb?did=1594496301&sid=20&Fmt=2&clientId=39334&RQT=309&VName=PQD.

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Thesis (Ph.D.)--State University of New York at Buffalo, 2008.
Title from PDF title page (viewed on Feb. 12, 2009) Available through UMI ProQuest Digital Dissertations. Thesis adviser: Kuo, Shiu-Ming Includes bibliographical references.
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Cahill, Leah Elizabeth. "Genetic Determinants of Serum Ascorbic Acid Concentrations." Thesis, 2010. http://hdl.handle.net/1807/26134.

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Background: The adequacy of serum ascorbic acid (vitamin C) concentrations in young Canadian adults is unknown. Individuals have varied serum ascorbic acid response to dietary vitamin C, possibly due to genetic variation. Objective: To investigate the prevalence of serum ascorbic acid deficiency in young Canadians and to determine whether common genotypes modify the association between dietary vitamin C and serum ascorbic acid. Methods: Subjects were 1277 men and women aged 20-29 years from the Toronto Nutrigenomics and Health study. Vitamin C intakes were estimated by a 196-item FFQ. Fasting blood was collected to measure serum ascorbic acid by HPLC and to genotype for common polymorphisms in genes that code for glutathione S-transferase (GST) (GSTM1, GSTT1 and GSTP1), haptoglobin (Hp), and vitamin C transporters (SLC23A1 and SLC23A2). Results: 53% of subjects had adequate, 33% had suboptimal and 14% had deficient serum ascorbic acid. Subjects with deficiency had higher mean C-reactive protein, waist circumference, BMI and blood pressure than subjects with adequate serum ascorbic acid. The odds ratio (95% confidence interval) for serum ascorbic acid deficiency was 3.43 (2.14, 5.50) for subjects who did not meet the vitamin C recommendation compared to those who did. The corresponding odds ratios were 2.17 (1.10, 4.28) and 12.28 (4.26, 33.42) for individuals with the GSTT1 functional and null genotypes respectively (interaction p=0.01), and 2.29 (0.96, 5.45) and 4.03 (2.01, 8.09) for the GSTM1 functional and null genotypes (interaction p=0.04). These odds ratios were 4.77 (2.36, 9.65) for the Hp2-2 genotype, but 1.69 (0.80, 3.63) for carriers of the Hp1 allele (interaction p=0.02). Serum ascorbic acid concentrations (mean +/- SE) differed among SLC23A1 rs4257763 genotypes (GG: 24.4 +/- 1.3, GA: 26.8 +/- 1.1, AA: 29.7 +/- 1.4, p=0.002). Conclusions: Serum ascorbic acid deficiency is prevalent and associated with markers of chronic disease. Individuals with GST null or Hp2-2 genotypes had an increased risk of deficiency if they did not meet the recommendation for vitamin C, suggesting that GSTs and haptoglobin may spare ascorbic acid when dietary vitamin C is insufficient, thus protecting against serum ascorbic acid deficiency.
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Lange, Bålman Miriam. "GRAVIDA KVINNORS INTAG AV KOSTTILLSKOTT : En kvantitativ studie med fokus på järn och probiotika." Thesis, 2019. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-157637.

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Sammanfattning  Bakgrund Vitamin- och mineralbrister hos gravida kvinnor kan leda till missfall och allvarliga störningar i barnets utveckling. Moderns tarmflora överförs med stor sannolikhet till barnet under förlossningen och kan därför innebära ett viktigt steg i utvecklingen av barnets tarmflora. En tänkbar lösning för att säkra ett adekvat intag kan vara konsumtion av kosttillskott och probiotika. I dagsläget finns osäkra uppgifter om hur många gravida kvinnor som intar tillskott.  Syfte Att undersöka hur många gravida kvinnor i Västerbottens län som valde att inta kosttillskott, främst järn och probiotika, samt om det fanns en skillnad mellan olika faktorer och intag.  Metod En kvantitativ tvärsnittsstudie där gravida kvinnor (n=1473) från Northpop-studien i Västerbottens län svarade på ett frågeformulär gällande intag av kosttillskott och faktorer som ålder, utbildning, kostregim etc. De statistiska tester som användes var Chi-2-test, oberoende t-test och Mann Whitney U-test. Materialet analyserades i SPSS. Signifikansnivån sattes till p<0,05.  Resultat Majoriteten av deltagarna svarade att de intog kosttillskott. Faktorer som ökade intaget av kosttillskott hos gravida kvinnor var högre ålder (p=0,030) jämfört med lägre ålder, högre utbildningsnivå (p=0,006) jämfört med lägre utbildningsnivå och vegetarisk/vegansk kost (p=0,021) jämfört med blandkost. Femtiofem procent uppgav att de intog järntillskott. De faktorer som ökade intaget av järntillskott hos gravida kvinnor var vegetarisk/vegansk kost (p=0,001) jämfört med blandkost. Probiotika intogs av 2 procent. Ett högre intag av probiotika sågs hos personer boende i stadsområde (p=0,024) jämfört med övriga boenderegioner samt de som åt vegetarisk/vegansk kost (p=0,001) jämfört med blandkost.  Slutsats Majoriteten av deltagarna intog någon typ av kosttillskott, hälften intog järntillskott och en liten andel intog probiotika. Lågutbildade, yngre, de som äter blandkost och bor utanför stadsområde verkar vara i riskgruppen för att inte inta kosttillskott.
Abstract  Background Vitamin and mineral deficiencies in pregnant women can lead to miscarriage and serious disturbances in children’s development. The intestinal flora of the mother is most likely transmitted to the child during childbirth and may lay the foundation for the child's health. One possible solution to ensure an adequate intake may be the consumption of dietary supplements and probiotics. At present, there is insufficient data on supplement consumption among pregnant women.  Objective The purpose of the study was to examine how many pregnant women in Västerbotten County chose to consume dietary supplements, mainly iron and probiotics, and whether there was a difference between different factors and intake.  Method A quantitative cross-sectional study where pregnant women (n=1473) from the Northpop-study in Västerbotten County responded to a questionnaire regarding consumption of dietary supplements and factors such as age, education, diet etc. The material was analyzed in SPSS with Chi-2-test, independent T-Test and Mann-Whitney U-Test. Using significance level <0.05.  Results The majority of participants, 90 percent, responded that they consumed dietary supplements. The factors that increased the intake of dietary supplements in pregnant women were higher age (p=0.030), higher education (p=0.006) and vegetarian/vegan diet (p=0.021). Iron was reported to be consumed by 804 people, 55 percent. The factors that increased the intake of iron supplement in pregnant women were vegetarian/vegan diet (p=0.001). Probiotics were consumed by 25 people, 2 percent. Living in urban areas (p=0.024) and eating vegetarian/vegan diet (p=0.002) increased consumption of probiotics.  Conclusion The majority of participants chose to consume some type of dietary supplement, half of the participants consumed iron supplements and a small part consumed probiotics. It appears that pregnant women who are low educated, younger, eating an omnivorous diet and living outside urban areas are in the risk zone for not consuming dietary supplements.
Northpop
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Book chapters on the topic "Intestinal vitamin C transporters"

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Ganapathy, Vadivel, Sudha Ananth, Sylvia B. Smith, and Pamela M. Martin. "Vitamin C Transporters in the Retina." In Ocular Transporters In Ophthalmic Diseases And Drug Delivery, 437–50. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-375-2_23.

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Kannan, Ram, and Hovhannes J. Gukasyan. "Vitamin C Transport, Delivery, and Function in the Anterior Segment of the Eye." In Ocular Transporters In Ophthalmic Diseases And Drug Delivery, 47–57. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-375-2_3.

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Bürzle, Marc, and Matthias A. Hediger. "Functional and Physiological Role of Vitamin C Transporters." In Co-Transport Systems, 357–75. Elsevier, 2012. http://dx.doi.org/10.1016/b978-0-12-394316-3.00011-9.

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Conference papers on the topic "Intestinal vitamin C transporters"

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Roos-Engstrand, E., N. Larsson, J. Pourazar, I. Mudway, A. Blomberg, and AF Behndig. "Distribution of Vitamin C and Puesdo-Dehydroascorbate Transporters in Airway Leukocytes from Healthy and Asthmatic Subjects." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4949.

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You might also be interested in the extended bibliographies on the topic 'Intestinal vitamin C transporters' for particular source types:
Journal articles
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