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Effects of vitamin E on oxidative stress and atherosclerosis in an obese hyperlipidemic mouse model.
J Nutr Biochem. 2007 Feb; 18(2):127-33.JN

Abstract

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.

Authors+Show Affiliations

Department of Molecular Physiology and Biophysics, Vanderbilt University Medical Center, Nashville, TN 37232, USA. alyssa.hasty@vanderbilt.eduNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16781857

Citation

Hasty, Alyssa H., et al. "Effects of Vitamin E On Oxidative Stress and Atherosclerosis in an Obese Hyperlipidemic Mouse Model." The Journal of Nutritional Biochemistry, vol. 18, no. 2, 2007, pp. 127-33.
Hasty AH, Gruen ML, Terry ES, et al. Effects of vitamin E on oxidative stress and atherosclerosis in an obese hyperlipidemic mouse model. J Nutr Biochem. 2007;18(2):127-33.
Hasty, A. H., Gruen, M. L., Terry, E. S., Surmi, B. K., Atkinson, R. D., Gao, L., & Morrow, J. D. (2007). Effects of vitamin E on oxidative stress and atherosclerosis in an obese hyperlipidemic mouse model. The Journal of Nutritional Biochemistry, 18(2), 127-33.
Hasty AH, et al. Effects of Vitamin E On Oxidative Stress and Atherosclerosis in an Obese Hyperlipidemic Mouse Model. J Nutr Biochem. 2007;18(2):127-33. PubMed PMID: 16781857.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effects of vitamin E on oxidative stress and atherosclerosis in an obese hyperlipidemic mouse model. AU - Hasty,Alyssa H, AU - Gruen,Marnie L, AU - Terry,Erin S, AU - Surmi,Bonnie K, AU - Atkinson,Robin D, AU - Gao,Ling, AU - Morrow,Jason D, Y1 - 2006/06/16/ PY - 2006/02/08/received PY - 2006/03/30/accepted PY - 2006/6/20/pubmed PY - 2007/3/9/medline PY - 2006/6/20/entrez SP - 127 EP - 33 JF - The Journal of nutritional biochemistry JO - J Nutr Biochem VL - 18 IS - 2 N2 - 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. SN - 0955-2863 UR - https://www.unboundmedicine.com/medline/citation/16781857/Effects_of_vitamin_E_on_oxidative_stress_and_atherosclerosis_in_an_obese_hyperlipidemic_mouse_model_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0955-2863(06)00095-7 DB - PRIME DP - Unbound Medicine ER -