Document Detail


Pretreatment with n-6 PUFA protects against subsequent high fat diet induced atherosclerosis--potential role of oxidative stress-induced antioxidant defense.
MedLine Citation:
PMID:  22035574     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVES: Recent evidence suggests that oxidative stress can promote antioxidant defense and thus be athero-protective. n-6 polyunsaturated fatty acids (n-6 PUFA) are more prone to oxidation, compared to monounsaturated fatty acids (MUFA) and yet have proven anti-atherosclerotic effects. In this study, we tested whether early exposure to a diet rich in n-6 PUFA, compared to a MUFA rich diet would reduce lesion burden, even with subsequent exposure to a high fat, high cholesterol diet (HF). Further, we tested to determine whether oxidative mechanisms are involved in such protection.
METHODS AND RESULTS: Twenty four, 4 week old, male, LDL receptor knockout (LDL-R(-/-)) mice were divided into two groups and fed either a n-6 PUFA rich or a MUFA rich diet for a period of 12 weeks. At this point, 4 mice from each group were euthanized and the remaining 8 mice from each group were fed a HF diet for four weeks. Atherosclerotic lesions, plasma lipids, autoantibodies to lipid peroxide modified proteins, isoprostanes and aortic catalase levels were measured. The n-6 PUFA diet reduced aortic lesions and plasma lipids compared to the MUFA diet and this reduction in lesions continued even after the mice were switched over to the HF diet, despite the fact that the plasma lipids were similar in both groups after the HF diet. n-6 PUFA fed mice had highest plasma isoprostane levels, indicating oxidative stress, but also had higher levels of aortic catalase. On the other hand, MUFA fed mice had comparatively lower levels of isoprostanes and their aortic catalase levels remained low. Finally, aortic lesions were negatively correlated with isoprostanes and catalase.
CONCLUSION: An initial exposure to a n-6 PUFA rich diet compared to a MUFA rich diet reduces atherosclerotic lesions and this protection probably involves oxidative stress induced by PUFA.
Authors:
M Penumetcha; M Song; N Merchant; S Parthasarathy
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2011-10-12
Journal Detail:
Title:  Atherosclerosis     Volume:  220     ISSN:  1879-1484     ISO Abbreviation:  Atherosclerosis     Publication Date:  2012 Jan 
Date Detail:
Created Date:  2011-12-26     Completed Date:  2012-04-20     Revised Date:  2013-06-27    
Medline Journal Info:
Nlm Unique ID:  0242543     Medline TA:  Atherosclerosis     Country:  Ireland    
Other Details:
Languages:  eng     Pagination:  53-8     Citation Subset:  IM    
Copyright Information:
Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.
Affiliation:
Department of Gynecology and Obstetrics and Fellowships in Research and Science Teaching (FIRST), Emory University School of Medicine, Atlanta, GA 30322, USA. mpenumetcha@gsu.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Antioxidants / metabolism*
Aorta / drug effects,  metabolism
Aortic Diseases / blood,  etiology,  genetics,  prevention & control*
Atherosclerosis / blood,  etiology,  genetics,  prevention & control*
Autoantibodies / blood
Biological Markers / blood
Catalase / metabolism
Diet, High-Fat*
Dinoprost / analogs & derivatives,  blood
Disease Models, Animal
Fatty Acids, Monounsaturated / pharmacology
Fatty Acids, Omega-6 / pharmacology*
Lipid Peroxidation / immunology
Lipids / blood
Male
Mice
Mice, Knockout
Oxidative Stress / drug effects*
Receptors, LDL / deficiency,  genetics
Time Factors
Grant Support
ID/Acronym/Agency:
HL-069038/HL/NHLBI NIH HHS; R01 DK056353-01A1/DK/NIDDK NIH HHS; R01 DK56353-01A1/DK/NIDDK NIH HHS; R01 HL069038-01/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Antioxidants; 0/Autoantibodies; 0/Biological Markers; 0/Fatty Acids, Monounsaturated; 0/Fatty Acids, Omega-6; 0/Lipids; 0/Receptors, LDL; 27415-26-5/8-epi-prostaglandin F2alpha; 551-11-1/Dinoprost; EC 1.11.1.6/Catalase
Comments/Corrections

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