Vitamin E – The Next 100 Years

Khadangi F, Azzi A

IUBMB Life. 2018 Dec 14. doi: 10.1002/iub.1990. [Epub ahead of print]

Abstract

α-Tocopherol is the only tocopherol that has been shown to prevent the human deficiency disease Ataxia with Isolated Vitamin E Deficiency (AVED), and thus it is the only one that, for humans, can be called vitamin EVitamin E in addition to preventing AVED has documented immune boosting properties and an activity against nonalcoholic hepatosteatosis and low-grade inflammation. Epidemiological studies indicating that vitamin E could prevent cardiovascular events, neurodegenerative disease, macular degeneration, and cancer were in general not confirmed by clinical intervention studies. Vitamin E and some of its metabolites modulate cell signaling and gene transcription. Future research is needed to achieve a better understanding of the molecular events leading to gene regulation by vitamin E, especially in its phosphorylated form. Isolation and characterization of the vitamin E kinase and vitamin E phosphate phosphatase will help in the understanding of cell regulation processes modulated by vitamin E. A clarification of the pathogenesis of AVED remains an important goal to be achieved.

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Vitamin E intake and risk of stroke: a meta-analysis

Cheng P, Wang L, Ning S, Liu Z, Lin H, Chen S, Zhu J

Br J Nutr. 2018 Nov;120(10):1181-1188. doi: 10.1017/S0007114518002647.

Abstract

Findings from observational studies on the associations between vitamin E intake and stroke risk remain controversial, and the dose-response relationship between vitamin E intake and risk of stroke remains to be determined. We conducted a meta-analysis of prospective studies aiming to clarify the relationships between vitamin E intake and risk of stroke. Relevant studies were identified by searching online databases through to June 2018. We computed summary relative risks (RR) with corresponding 95 % CI. Among 3156 articles retrieved from online databases and relevant bibliographies, nine studies involving 3284 events and 220 371 participants were included in the final analyses. High dietary vitamin E intake was inversely associated with the risk of overall stroke (RR=0·83, 95 % CI 0·73, 0·94), and with the risk of stroke for individuals who were followed-up for <10 (RR=0·84, 95 % CI 0·72, 0·91). There was a non-linear association between dietary vitamin E intake and stroke risk (P=0·0249). Omission of any single study did not alter the summary result. In conclusion, this meta-analysis suggests that there is a significant inverse relationship between dietary vitamin E intake and stroke risk. This meta-analysis provides evidence that a higher dietary vitamin E intake is associated with a lower stroke risk.

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The Effect of Magnesium and Vitamin E Co-Supplementation on Glycemic Control and Markers of Cardio-Metabolic Risk in Women with Polycystic Ovary Syndrome: A Randomized, Double-Blind, Placebo-Controlled Trial

Jamilian M, Sabzevar NK, Asemi Z

Horm Metab Res. 2018 Oct 4. doi: 10.1055/a-0749-6431. [Epub ahead of print]

Abstract

Data on the effects of magnesium and vitamin E co-supplementation on glycemic control and markers of cardio-metabolic risk of patients with polycystic ovary syndrome (PCOS) were collected. This investigation was conducted to evaluate the effects of magnesium and vitamin E co-supplementation on glycemic control and markers of cardio-metabolic risk in women with PCOS. This randomized, double-blind, placebo-controlled trial was carried out on 60 women with PCOS, aged 18-40 years old. Participants were randomly divided into two groups to receive 250 mg/day magnesium plus 400 mg/day vitamin E supplements or placebo (n=30 each group) for 12 weeks. Fasting blood samples were taken at baseline and after the 12-week intervention to quantify related variables. After the 12-week intervention, compared with the placebo, magnesium and vitamin E co-supplementation led to a significant reduction in serum insulin levels (-1.1±3.0 vs. +1.6±3.7 μIU/ml, p=0.003) and homeostatic model of assessment for insulin resistance (-0.2±0.7 vs. +0.4±0.9, p=0.002), and a significant increase in the quantitative insulin sensitivity check index (+0.01±0.01 vs. -0.009±0.02, p=0.003). Furthermore, magnesium plus vitamin E supplementation significantly decreased serum triglycerides (-15.0±24.4 vs. +6.7±22.2 mg/dl, p=0.001) and VLDL-cholesterol concentrations (-3.0±4.9 vs. +0.6±2.4 mg/dl, P=0.01) compared with the placebo. A trend toward a greater decrease in total cholesterol levels was observed in magnesium plus vitamin Egroup compared to placebo group (-7.0±32.6 vs. +8.1±26.6 mg/dl, p=0.05). In conclusion, magnesium and vitamin E co-supplementation for 12 weeks to PCOS women had beneficial effects on parameters of insulin metabolism and few markers of cardio-metabolic risk.

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Nonalcoholic steatohepatitis, obesity, and cardiac dysfunction

Mathews SE, Kumar RB, Shukla AP

Curr Opin Endocrinol Diabetes Obes. 2018 Oct;25(5):315-320. doi: 10.1097/MED.0000000000000432.

Abstract

PURPOSE OF REVIEW:

Obesity and nonalcoholic steatohepatitis (NASH) are epidemiologically and pathophysiologically linked disorders. Here, we summarize the effect of obesity on NASH and how it has a cascading effect on cardiovascular dysfunction. We also review the current and emerging treatment options for NASH.

RECENT FINDINGS:

The link between NASH and cardiac dysfunction has been further delineated in recent studies demonstrating endothelial dysfunction, diastolic dysfunction, and increased coronary artery calcification in patients with known NASH. Standard treatment of obesity with lifestyle interventions including diet, exercise, and behavioral modification has been shown to improve NASH as well as reduce cardiovascular dysfunction. In addition to FDA-approved drugs like vitamin E and pioglitazone, several agents including NGM282, obeticholic acid, elafibranor, and liraglutide are currently being investigated for their therapeutic potential in NASH. Recent studies show that bariatric surgery results in significant improvement or resolution of NASH.

SUMMARY:

Obesity is a major factor in the development of nonalcoholic fatty liver disease (NAFLD) and its progression to steatohepatitis. Patients with NAFLD have a significant increase in cardiovascular disease risk. For biopsy-proven NASH, vitamin E and pioglitazone are the recommended medical treatments in addition to lifestyle modification.

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Antiglycation study of HMG-R inhibitors and tocotrienol against glycated BSA and LDL: A comparative study.

Nabi R, Alvi SS, Khan RH, Ahmad S, Ahmad S, Khan MS

Int J Biol Macromol. 2018 Sep;116:983-992. doi: 10.1016/j.ijbiomac.2018.05.115. Epub 2018 May 18.

Abstract

Non-enzymatic glycation mediated advanced glycation end products (AGEs) generation results in the pathogenesis of diabetic complications and atherosclerotic cardiovascular disease (ASCVD) which is greatly influenced by 3-hydroxy-3-methyl-glutaryl Co-A reductase (HMG-R) activity. HMG-R inhibitors, statins, are well known for reducing mortality and morbidity of ASCVD in patients with diabetes due to their pleiotropic effects independent of cholesterol lowering. Due to distinct chemical structures, various statins may play important role in the inhibition of AGEs mediated pathologies. Herein, we evaluated the anti-glycating potential of atorvastatin (AT), rosuvastatin (RT), pitavastatin (PT), fluvastatin (FT), simvastatin (ST) alone as well in combination with ezetimibe (EZ) and tocotrienol (TT) against d-ribose mediated BSA and LDL glycation by various physicochemical approaches. Our data suggested that AT, TT, RT, EZ, EZ-AT, and EZ-RT were able to substantially inhibit the AGEs formation via modulation of hyperchromicity, fluorogenic AGEs, % contribution of α-helix and β-sheets to protein secondary structure, amide-I band stretching, carbonyl and HMF content in Gly-BSA as well as Gly-LDL. On the basis of above findings, we concluded that HMG-R inhibitors and TT, alone or in combination with EZ, may be established as terrific therapeutic agents for the patients suffering from AGEs induced diabetic cum ASCVD complications.

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Low intake of vitamin E accelerates cellular aging in patients with established cardiovascular disease: The CORDIOPREV study

Corina A, Rangel-Zúñiga OA, Jiménez-Lucena R, Alcalá-Díaz JF, Quintana-Navarro G, Yubero-Serrano EM, López-Moreno J, Delgado-Lista J, Tinahones F, Ordovás JM, López-Miranda J, Pérez-Martínez P

J Gerontol A Biol Sci Med Sci. 2018 Aug 27. doi: 10.1093/gerona/gly195. [Epub ahead of print]

Abstract

Leukocyte telomere length (LTL) shortening is a biomarker of cellular aging that can be decelerated by diet. We aimed to investigate the effect of dietary intake of vitamin E on biomarkers of cellular senescence in patients with established cardiovascular disease. To this end, DNA from 1002 participants of the CORDIOPREV study (NCT00924937) was isolated and LTL wa s measured by real-time PCR. Dietary information was collected using a 146-item food frequency questionnaire, and several oxidative stress and damage biomarkers were determined. We found that patients with an inadequate intake of vitamin E according to the European Food Safety Authority, U.S. Food and Nutrition Board, and Spanish dietary recommendation had shorter LTL than those with an adequate intake (p=0.004, p=0.015 and p=0.005, respectively). Moreover, we observed a positive correlation between olive oil, fish consumption and LTL (r2=0.083, p=0.010; r2=0.090, p=0.006, respectively). Subjects who consumed more than 30 mL olive oil/day had longer LTL than subjects with lower consumption (p=0.013). Furthermore, we observed higher glutathione peroxidase activity in subjects consuming less vitamin E (p=0.031). Our findings support the importance of an adequate consumption of the antioxidant vitamin E, and the value of the diet as a modulating tool of the senescence process.Read More

Vitamin E hydroquinone is an endogenous regulator of ferroptosis via redox control of 15-lipoxygenase

Hinman A, Holst CR, Latham JC, Bruegger JJ, Ulas G, McCusker KP, Amagata A, Davis D, Hoff KG, Kahn-Kirby AH, Kim V, Kosaka Y, Lee E, Malone SA, Mei JJ, Richards SJ, Rivera V, Miller G, Trimmer JK, Shrader WD

PLoS One. 2018 Aug 15;13(8):e0201369. doi: 10.1371/journal.pone.0201369. eCollection 2018.

Abstract

Ferroptosis is a form of programmed cell death associated with inflammation, neurodegeneration, and ischemia. Vitamin E (alpha-tocopherol) has been reported to prevent ferroptosis, but the mechanism by which this occurs is controversial. To elucidate the biochemical mechanism of vitamin E activity, we systematically investigated the effects of its major vitamers and metabolites on lipid oxidation and ferroptosis in a striatal cell model. We found that a specific endogenous metabolite of vitamin E, alpha-tocopherol hydroquinone, was a dramatically more potent inhibitor of ferroptosis than its parent compound, and inhibits 15-lipoxygenase via reduction of the enzyme’s non-heme iron from its active Fe3+ state to an inactive Fe2+ state. Furthermore, a non-metabolizable isosteric analog of vitamin E which retains antioxidant activity neither inhibited 15-lipoxygenase nor prevented ferroptosis. These results call into question the prevailing model that vitamin E acts predominantly as a non-specific lipophilic antioxidant. We propose that, similar to the other lipophilic vitamins A, D and K, vitamin E is instead a pro-vitamin, with its quinone/hydroquinone metabolites responsible for its anti-ferroptotic cytoprotective activity.

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Combination of vitamin E and L-carnitine is superior in protection against Isoproterenol-induced cardiac affection: a histopathological evidence

Huwait EA

Folia Morphol (Warsz). 2018 Aug 14. doi: 10.5603/FM.a2018.0070. [Epub ahead of print]

Abstract

BACKGROUND:

L-carnitine and Vitamin E have antioxidant properties. This study aimed to assess the effectiveness of L-carnitine, Vitamin Eand the combination of them in protection against isoproterenol (ISO)-induced biochemical and histopathological changes in rat heart.

MATERIAL AND METHODS:

Fifty male Wistar rats assigned to 5 groups; control, ISO-treated group (100 mg/kg), ISO+vitamin E-treated group (100 IU/kg), ISO+L-carnitine (100 mg/kg) and ISO+vitamin E+L-carnitine treated group. At the end of the experiment, serum cardiac enzyme as well as the cardiac level Malondialdehyde (MDA), antioxidant enzymes and inflammatory cytokines IL-6, TNF-alpha were assessed. Histopathological changes in the left ventricle wall was assessed using the light and electron microscopy.

RESULTS:

Treating rats with vitamin E and L-carnitine could alleviate ISO-induced changes as it significantly reduced the serum level cardiac enzymes, MDA and IL-6, TNF-alpha and improved the antioxidants enzymes (SOD, GSPxase and GSRase). Histopathological, they improved cardiac fibers atrophy, hemorrhages between cardiac fibers, lost striations, and disturbed sarcomere structure. The combined effect of vitamin E and L-carnitine was more superior compared to the other groups.

CONCLUSION:

Combined administration of vitamin E, L-carnitine ameliorated the biochemical and histopathological cardiac affection induced by ISO. The effect seemed to be mediated through the antioxidant and anti-inflammatory effect of vitamin E, L-carnitine. Administration of these two element is recommended for patient at risk for myocardial infarction.

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Vitamin E, Deficiency

Kemnic TR, Coleman M

StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2018-. 2018 Jul 24.

Excerpt

Vitamin E is all the following eight compounds alpha, beta, gamma, and delta-tocopherol and alpha, beta, gamma, and delta-tocotrienol. Alpha-tocopherol is the only compound of the eight that are known to meet human dietary needs. All of the vitamin E forms are absorbed in the small intestine, and then the liver metabolizes only alpha-tocopherol. The liver then removes and excretes the remaining vitamin E forms. Vitamin E deficiency is extremely rare in humans as it is unlikely caused by a diet consisting of low vitamin E. Rather, it tends to be caused by irregularities in dietary fat absorption or metabolism. Vitamin E is a lipid-soluble nutrient. Vitamin E may have a role in reducing atherosclerosis and lowering rates of ischemic heart disease. Premature infants have low vitamin E reserves due to vitamin E only able to cross the placenta in small amounts.

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Identifying Potential Therapeutics for Osteoporosis by Exploiting the Relationship between Mevalonate Pathway and Bone Metabolism

Wan Hasan WN, Chin KY, Jolly JJ, Abd Ghafar N, Soelaiman IN.

Endocr Metab Immune Disord Drug Targets. 2018 Apr 23. doi: 10.2174/1871530318666180423122409. [Epub ahead of print]

Abstract

BACKGROUND:

Osteoporosis is a silent skeletal disease characterized by low bone mass and destruction of skeletal microarchitecture, leading to an increased fracture risk. This occurs due to an imbalance in bone remodelling, whereby the rate of bone resorption is greater than bone formation. Mevalonate pathway, previously known to involve in cholesterol synthesis, is an important regulatory pathway for bone remodelling.

OBJECTIVE:

This review aimed to provide an overview of the relationship between mevalonate pathway and bone metabolism, as well as agents which act through this pathway to achieve their therapeutic potential.

DISCUSSION:

Mevalonate pathway produces farnesyl pyrophosphate and geranylgeranyl pyrophosphate essential in protein prenylation. An increase in protein prenylation favours bone resorption over bone formation. Non-nitrogen containing bisphosphonates inhibit farnesyl diphosphate synthase which produces farnesyl pyrophosphate. They are used as the first line therapy for osteoporosis. Statins, a well-known class of cholesterol-lowering agents, inhibit 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) reductase, the rate-determining enzyme in the mevalonate pathway. It was shown to increase bone mineral density and prevent fracture in humans. Tocotrienol is a group of vitamin E commonly found in palm oil, rice bran and annatto bean. It causes degradation of HMG-CoA reductase. Many studies demonstrated that tocotrienol prevented bone loss in animal studies but its efficacy has not been tested in humans.

CONCLUSION:

mevalonate pathway can be exploited to develop effective antiosteoporosis agents.

KEYWORDS:

bone; bone metabolism; mevalonate pathway; tocotrienol; vitamin E.

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