Liver α-Tocopherol Transfer Protein and Its mRNA Are Differentially Altered by Dietary Vitamin E Deficiency and Protein Insufficiency in Rats

Shaw, Huey-Mei; Huang, Ching-jang

doi:10.1093/jn/128.12.2348

Cited by 54 publications

(35 citation statements)

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“…Although the levels of dietary vitamin E in our study were not identical to those used by Shaw and Huang (17), the direction and magnitude of changes in hepatic TTP levels were similar between the two studies. The authors (17) observed that TTP levels were ca. 25% higher in mice fed vitamin E-containing diets (for both their control and High E diets) compared with those fed a vitamin E-deficient diet, whereas no changes were observed in TTP mRNA levels (17).…”

Section: Discussionmentioning

confidence: 99%

“…In rats that were fed vitamin E-deficient diets, TTP mRNA was higher, but protein levels were unchanged compared with controls. In contrast, Shaw and Huang (17) showed that in vitamin E-deficient rats, hepatic TTP was lower compared with rats fed control diets (50 mg all-rac-α-tocopheryl acetate/kg diet) but control and vitamin E-supplemented (5,000 mg all-rac-α-tocopheryl acetate/kg diet) rats had similar TTP concentrations. No changes in TTP mRNA were observed.…”

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confidence: 91%

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

Bella

Schock

Lim

et al. 2006

Lipids

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The alpha-tocopherol transfer protein (TTP) plays an important role in the regulation of plasma alpha-tocopherol concentrations. We hypothesized that hepatic TTP levels would be modulated by dietary vitamin E supplementation and/or by oxidative stress. Mice were fed either a High E (1150 mg RRR-alpha-tocopheryl acetate/kg diet) or a Low E (11.5 mg/kg diet) diet for 2 wk. High E increased plasma and liver alpha-tocopherol concentrations approximately 8- and 40-fold, respectively, compared with Low E-fed mice, whereas hepatic TTP increased approximately 20%. Hepatic TTP concentrations were unaffected by fasting (24 h) in mice fed either diet. To induce oxidative stress, chow-fed mice were exposed for 3 d to environmental tobacco smoke (ETS) for 6 h/d (total suspended particulate, 57.4 +/- 1.8 mg/m3). ETS exposure, while resulting in pulmonary and systemic oxidative stress, had no effect on hepatic alpha-tocopherol concentrations or hepatic TTP. Overall, changes in hepatic TTP concentrations were minimal in response to dietary vitamin E levels or ETS-related oxidative stress. Thus, hepatic TTP concentrations may be at sufficient levels such that they are unaffected by either modulations of dietary vitamin E or by the conditions of environmentally related oxidative stress used in the present studies.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 91%

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

Bella

Schock

Lim

et al. 2006

Lipids

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“…In 1991 Angelo Azzi's group first described such properties by demonstrating that VE inhibits protein kinase C activity in smooth muscle cells (9). Subsequently, modulation by alpha-tocopherol of the expression of various genes has been discovered, including the CD36 scavenger receptor in smooth muscle cells (10), hepatic alpha-tocopherol transfer protein (11), liver collagen alpha-1 (12), as well as collagenase (13) and alpha-tropomyosin (14).…”

Section: Introductionmentioning

confidence: 99%

Differential gene expression in skeletal muscle of rats with Vitamin E deficiency

Nier

Weinberg

Rimbach

et al. 2006

IUBMB Life (International Union of Biochemistry and Molecular B

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SummaryVitamin E (VE) deficiency is accompanied by myopathy in various animal species including man. Although gene expression profiles related to degenerative and regenerative processes in different kinds of myopathies have been studied, no global expression profile for skeletal muscle subject to VE deficiency has previously been reported. In the present study, Affymetrix GeneChip 1 technology was used to obtain such a profile. Two groups of male rats were fed with either a diet deficient in VE or a control diet. Differential gene expression was monitored at five timepoints over 430 days, with all animals individually profiled. Out of *7000 genes represented on the Genechip, 56 were found to be upregulated in response to VE deficiency in at least four consecutive time-points from as early as 91 days of deficiency. Up-regulated genes included muscle structure and extra cellular matrix genes, as well as anti-oxidative, anti-inflammatory and anti-fibrotic genes. Our data show that molecular transcription might provide a very early marker to detect oncoming degenerative conditions in VE deficiency. They provide further insight into possible molecular mechanisms underlying VE deficiency in skeletal muscle, and reveal the activation of an intensive protection program that can explain the long maintenance of muscle structure during deficiency.

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“…Second, the nutritional status of STZ rats may affect circulatory a-tocopherol levels and hepatic a-TTP expression. Hepatic mRNA a-TTP expression is reduced by protein insufficiency (47). Third, we cannot rule out the possibility that the toxicity of STZ affects the hepatic gene expression.…”

Section: Discussionmentioning

confidence: 94%

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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Liver α-Tocopherol Transfer Protein and Its mRNA Are Differentially Altered by Dietary Vitamin E Deficiency and Protein Insufficiency in Rats

Cited by 54 publications

References 34 publications

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

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

Differential gene expression in skeletal muscle of rats with Vitamin E deficiency

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

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Liver α-Tocopherol Transfer Protein and Its mRNA Are Differentially Altered by Dietary Vitamin E Deficiency and Protein Insufficiency in Rats

Cited by 54 publications

References 34 publications

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

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

Differential gene expression in skeletal muscle of rats with Vitamin E deficiency

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

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