Regulation of the α‐tocopherol transfer protein in mice: Lack of response to dietary vitamin E or oxidative stress

Bella, Deborah; Schock, Bettina; Lim, Yunsook; Leonard, Scott W.; Berry, C. G.; Cross, Carroll E.; Traber, Maret G.

doi:10.1007/s11745-006-5077-7

Cited by 24 publications

(25 citation statements)

References 44 publications

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“…The most abundant isoforms are a-tocopherol and g-tocopherol, which differ by one methyl group ( Figure 1A). There are approximately 10-fold higher tissue concentrations of a-tocopherol than g-tocopherol due to preferential transfer of a-tocopherol in the liver by a-tocopherol transfer protein and due to a higher rate of production of g-tocopherol metabolites for excretion (10,11). The plasma levels of tocopherols correlate with lung tissue levels of tocopherols in humans and mice (7,8,12).…”

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confidence: 99%

Two Faces of Vitamin E in the Lung

Cook‐Mills

Abdala-Valencia

Hartert

2013

Am J Respir Crit Care Med

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Asthma and allergic lung disease occur as complex environmental and genetic interactions. Clinical studies of asthma indicate a number of protective dietary factors, such as vitamin E, on asthma risk. However, these studies have had seemingly conflicting outcomes. In this perspective, we discuss opposing regulatory effects of tocopherol isoforms of vitamin E, mechanisms for tocopherol isoform regulation of allergic lung inflammation, association of vitamin E isoforms with outcomes in clinical studies, and how the variation in global prevalence of asthma may be explained, at least in part, by vitamin E isoforms.Keywords: asthma; a-tocopherol; g-tocopherol; human; mouse Asthma and allergic lung disease occur as complex environmental and genetic interactions (1). The World Health Organization has reported that the prevalence of asthma from 1950 to the present has increased in many countries, including countries with high rates of asthma, intermediate rates of asthma, or low rates of asthma (2-4). The marked differences in rates of asthma within countries, in migrating populations, and over relatively short periods of time support an important role of the local environment, such as diet, in asthma inception. Prospective epidemiological studies, observational cross-sectional studies, and some randomized prevention trials have demonstrated the impact of a number of protective dietary factors, such as vitamin E, on asthma risk. However, these studies have had seemingly conflicting outcomes. We need to determine why there are low rates of allergic disease in developing countries and better understand the differences in diet and lifestyle that may really underpin allergic disease. One environmental change over the past 40 years has been an increase in the g-tocopherol isoform of vitamin E in the diet and in infant formulas (5, 6). We recently demonstrated that g-tocopherol increases allergic lung inflammation in mice (6)(7)(8). In this perspective, we discuss why we have yet to uncover the complex and potentially protective effects of isoforms of vitamin E on asthma in humans and in animal models of lung inflammation. We also review mechanisms for tocopherol isoform regulation of allergic lung inflammation in animals and discuss how the variation in global prevalence of asthma may be explained, at least in part, by country-specific plasma g-tocopherol differences.Vitamin E consists of natural isoforms and synthetic racemic isoforms. The eight natural isomers are d-a-, d-b-, d-g-, d-d-tocopherol and d-a-, d-b-, d-g-, d-d-tocotrienol. Plants synthesize the natural isoforms from tyrosine and chlorophyll (9). Then, these tocols are consumed in the diet from plant lipids. Mammals do not interconvert the tocopherol isoforms. The most abundant isoforms are a-tocopherol and g-tocopherol, which differ by one methyl group ( Figure 1A). There are approximately 10-fold higher tissue concentrations of a-tocopherol than g-tocopherol due to preferential transfer of a-tocopherol in the liver by a-tocopherol transfer protein and due to ...

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confidence: 99%

Two Faces of Vitamin E in the Lung

Cook‐Mills

Abdala-Valencia

Hartert

2013

Am J Respir Crit Care Med

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“…Moreover, a-TTP expression is reduced in the liver of methioninecholine deficiency (MCD) rats, which are known as a model of non-alcoholic fatty liver disease, and presents increased lipid peroxidation of the liver and hepatic dysfunction (33). Bella et al reported that exposure to environmental tobacco smoke does not alter hepatic expression (34). We have previously reported that hepatic a-TTP expression and plasma a-tocopherol levels were elevated in rat models with type 2 diabetes showing lipid peroxidation (5).…”

Section: Discussionmentioning

confidence: 83%

α-Tocopherol Status and Altered Expression of α-Tocopherol-Related Proteins in Streptozotocin-Induced Type 1 Diabetes in Rat Models

Takitani

Inoue

Koh

et al. 2014

Journal of Nutritional Science and Vitaminology, J Nutr Sci Vit

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Vitamin E is a fat-soluble antioxidant that comprises 4 tocopherols (a-, b-, g-, and d-) and 4 tocotrienols (a-, b-, g-, and d-). Of all these vitamin E subtypes, a-tocopherol is the most well-known for its antioxidant activity (1). Lipid-soluble vitamin E has a critical role as an antioxidant protecting the lipids of the plasma membranes and lipoproteins from peroxidation. Dietary vitamin E, including tocopherols and tocotrienols, which are components of bile salt micelles, is absorbed in the intestine. Vitamin E, along with lipids, is incorporated into nascent chylomicrons within the enterocyte, and these chylomicrons are then secreted into the lymphatics and blood vessels (2). After transporting dietary lipids to other locations in the body, chylomicrons are returned to and taken up by the liver. In the liver, a-tocopherol selectively binds to a-tocopherol transfer protein (a-TTP) and is incorporated into very low-density lipoproteins (VLDL). a-TTP is a hepatic cytosolic protein, which facilitates the transport of a-tocopherol to the plasma membrane for the secretion of a-tocopherol into VLDL (1). a-TTP has a critical role in maintaining circulatory a-tocopherol levels. a-TTP gene disrupted mice reveal markedly reduced plasma a-tocopherol levels; moreover, the mutation of the human a-TTP gene is responsible for ataxia with vitamin E deficiency (1, 2). The ATPbinding cassette transporter-1 (ABCA-1), which transports cholesterol and phospholipids, facilitates the secretion of a-tocopherol in the plasma membrane. VLDL, including a-tocopherol, in circulation is lipolysed into low-density lipoprotein (LDL) by lipoprotein lipase, and this LDL is taken up into the peripheral tissues via the action of the LDL receptor. The mechanism of a-tocopherol metabolism has been recently determined (2). The catabolism of tocopherols and tocotrienols is mediated by cytochrome P450 4F2 (CYP4F2), and the resulting metabolite, carboxyethyl hydroxychroman (CEHC), is excreted in urine as glucuronic conjugates.Diabetes is a metabolic disorder pertaining to glucose uptake due to a lack of insulin production by pancreatic b-cells (type 1 diabetes), or it manifests as peripheral insulin resistance, including adipose tissue and muscles (type 2 diabetes). The production of reactive oxygen species (ROS) is the major pathogenesis of diabetes and its complications. Hyperglycemia leads to an increased release of ROS in peripheral tissues (3). In experimental studies, vitamin E supplementation improved the Summary Vitamin E plays a critical role as an antioxidant in several pathological conditions, including diabetes, cancer, cardiovascular diseases, and neurodegenerative disorders. Diabetes is a metabolic disorder of glucose due to the lack of adequate insulin production (type 1) or peripheral insulin resistance (type 2). Oxidative stress plays a major role in the pathogenesis of diabetes and its complications. The purpose of the present study was to determine a-tocopherol status and the expression of a-tocopherol-related proteins, including ...

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“…However, in the present study, hepatic α-TTP protein levels in both groups of rats fed the OFO diet were unchanged, although lipid peroxidation increased. Unchanged hepatic α-TTP protein levels are also observed in rats exposed to tobacco smoke [35], despite a lower α-tocopherol concentrationin lung and higher lipid peroxidation in the rat liver. The downregulation of α-TTP levels seen in galactosamineinduced liver injury [34] is an acute response (24-48 h), and, since the OFO diet was fed for a long time, α-TTP levels may have changed during the acute injury and restored subsequently.…”

Section: Discussionmentioning

confidence: 94%

Effects of Oxidized Frying Oil on Proteins Related to α-Tocopherol Metabolism in Rat Liver

Huang

Kang

et al. 2009

J. Clin. Biochem. Nutr.

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Summary An oxidized frying oil (OFO) diet has been reported to induce an increase in lipid peroxidation and a reduction in vitamin E status in animal tissues. This study was performed to investigate how vitamin E metabolism is influenced by OFO. Male Wistar rats were divided into three groups, a control group (CO) and two OFO-fed groups (OF and OFE). The diet of the OFE group was supplemented with an extra 50 mg/kg of α-tocopherol acetate and thus contained twice as much vitamin E as that of the OF group. After six weeks on these diets, liver α-tocopherol levels in the OF group were the significantly lowest among the three groups. Excretion of the α-tocopherol metabolite, α-carboxyethyl hydroxychroman (α-CEHC) in the urine was significantly lower in the OF group than in the other two groups. There were no significant differences in protein levels of α-tocopherol transfer protein (α-TTP) and multidrug resistance protein among the three groups. Protein levels of cytochrome P450 monooxygenase (CYP) 3A, CYP4A, and catalase were markedly increased in both groups on the OFO diet. This suggests that an OFO diet may interfere with medicine metabolism and needs further investigation.

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Regulation of the α‐tocopherol transfer protein in mice: Lack of response to dietary vitamin E or oxidative stress

Cited by 24 publications

References 44 publications

Two Faces of Vitamin E in the Lung

Two Faces of Vitamin E in the Lung

α-Tocopherol Status and Altered Expression of α-Tocopherol-Related Proteins in Streptozotocin-Induced Type 1 Diabetes in Rat Models

Effects of Oxidized Frying Oil on Proteins Related to α-Tocopherol Metabolism in Rat Liver

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Regulation of the α‐tocopherol transfer protein in mice: Lack of response to dietary vitamin E or oxidative stress

Cited by 24 publications

References 44 publications

Two Faces of Vitamin E in the Lung

Two Faces of Vitamin E in the Lung

&alpha;-Tocopherol Status and Altered Expression of &alpha;-Tocopherol-Related Proteins in Streptozotocin-Induced Type 1 Diabetes in Rat Models

Effects of Oxidized Frying Oil on Proteins Related to α-Tocopherol Metabolism in Rat Liver

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α-Tocopherol Status and Altered Expression of α-Tocopherol-Related Proteins in Streptozotocin-Induced Type 1 Diabetes in Rat Models