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Effects of vitamin E on oxidative stress and atherosclerosis in an obese hyperlipidemic mouse model.

Effects of vitamin E on oxidative stress and atherosclerosis in an obese hyperlipidemic mouse model. Research Abstract Details 

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  • Effects of vitamin E on oxidative stress and atherosclerosis in an obese hyperlipidemic mouse model. Abstract Text:

    alyssa h hastyAlyssa H Hasty,marnie l gruenMarnie L Gruen,erin s terryErin S Terry,bonnie k surmiBonnie K Surmi,robin d atkinsonRobin D Atkinson,ling gaoLing Gao,jason d morrowJason D Morrow,

    Vitamin E is a natural antioxidant that has been used in animal and human studies to determine its potential in reducing cardiovascular risk; however, a detailed study in an established obese model of atherosclerosis has yet to be performed. In our current study, we show that obesity and hyperlipidemia cause a synergistic, age-related increase in urinary isoprostane levels in mice deficient in both leptin and low-density lipoprotein receptor (ob/ob;LDLR-/-). Based upon this observation, we hypothesized that vitamin E supplementation would induce potent antiatherogenic effects in this model. Lean and obese LDLR-/- mice were provided vitamin E (2000 IU/kg) in a Western-type high-fat diet for 12 weeks. Plasma lipid parameters, such as total cholesterol (TC), triglyceride (TG) and free fatty acid, were significantly higher in obese mice compared to lean mice at baseline (P<.001). Western-type diet (WD) feeding caused an increase in TC levels in all groups (P<.001); however, TG (P<.001) and free fatty acid (P<.01) were elevated only in lean mice following WD feeding. Vitamin E supplementation neither influenced any of these parameters nor reduced urinary isoprostanes in lean or obese mice. Vitamin E supplementation in ob/ob;LDLR-/- mice resulted in a trend toward a reduction in atherosclerotic lesion area (P=.10), although no differences in lesion area were noted in lean LDLR-/- animals. These data provide evidence that vitamin E supplementation is not sufficient to reduce extreme elevations in systemic oxidative stress due to hyperlipidemia and obesity and, thus, may not be cardioprotective in this setting.

    Effects of vitamin E on oxidative stress and atherosclerosis in an obese hyperlipidemic mouse model. Publishing Authors By Initials

    ah hastyAH Hasty,ml gruenML Gruen,es terryES Terry,bk surmiBK Surmi,rd atkinsonRD Atkinson,l gaoL Gao,jd morrowJD Morrow,

    For similar heterocyclic compounds: heterocyclic compounds, 2-ring: benzopyrans: vitamin e research abstracts see: heterocyclic compounds: heterocyclic compounds, 2-ring: benzopyrans: vitamin e research

    PUBMED ID PMID:

    MEDLINE DATE:

    Effects of vitamin E on oxidative stress and atherosclerosis in an obese hyperlipidemic mouse model. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: The Journal of nutritional biochemistry

    VOLUME: 18

    Page Numbers: 127-33

    Journal Abbreviation: J. Nutr. Biochem.

    ISSN: 0955-2863

    DAY: 16

    MONTH: 06

    YEAR: 2006

    Effects of vitamin E on oxidative stress and atherosclerosis in an obese hyperlipidemic mouse model. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 9010081

    Effects of vitamin E on oxidative stress and atherosclerosis in an obese hyperlipidemic mouse model. Keywords Mesh Terms:

    KEYWORDS: Vitamin E

    MESH TERMS: administration & dosage

    Chemical & Substance for Abstract: Effects of vitamin E on oxidative stress and atherosclerosis in an obese hyperlipidemic mouse model. Information

    Substance Name: Cholesterol

    Registry Number: 57-88-5

    Grant and Affiliation Information for Effects of vitamin E on oxidative stress and atherosclerosis in an obese hyperlipidemic mouse model.

    AFFILIATION: Department of Molecular Physiology and Biophysics, Vanderbilt University Medical Center, Nashville, TN 37232, USA. alyssa.hasty@vanderbilt.edu

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NCRR

    GRANT: RR00095

    ACRONYM: RR

    MEDLINETA: J Nutr Biochem

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