Document Detail


n-3 fatty acids prevent whereas trans-fatty acids induce vascular inflammation and sudden cardiac death.
MedLine Citation:
PMID:  19822033     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
n-3 PUFA have well-recognised cardio-beneficial effects. In contrast, premature coronary deaths are associated with consumption of high levels of trans-fatty acids (TFA). The present study determined the effects of n-3 PUFA and TFA on sudden cardiac death and vascular inflammation. A rat coronary ligation model was used to study the effect of fatty acids on sudden cardiac death, whereas a mouse femoral artery ligation model was used to study compensatory vascular remodelling. Human aortic endothelial cells (HAEC) were utilised for the in vitro studies to investigate expression of inflammatory molecules. Feeding animals an n-3 PUFA-enriched diet caused a sevenfold increase in plasma n-3 PUFA compared with that of the TFA-fed group, whereas a TFA-enriched diet caused a 2.5-fold increase in plasma TFA compared with the n-3 PUFA group. Animals on a TFA diet had a lower survival rate due to sudden cardiac death and exhibited variable degrees of aortic atherosclerotic lesions. Animals on a TFA diet had diminished hindlimb collateral growth, whereas animals on the n-3 PUFA diet exhibited extensive collateral growth about ligated regions. HAEC treated with TFA (trans-18 : 2) showed significantly increased expression of intracellular adhesion molecule-1 and nitrosylation of cellular proteins than those treated with DHA (n-3 PUFA, 22 : 6). The in vivo study demonstrates that, in contrast to TFA, n-3 PUFA improve animal survival after myocardial infarction, prevent development of atherosclerotic lesions and stimulate compensatory vascular remodelling. The in vitro study demonstrates that TFA induce, while n-3 PUFA prevent, vascular inflammation.
Authors:
Rafat A Siddiqui; Kevin A Harvey; Nargiz Ruzmetov; Steven J Miller; Gary P Zaloga
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The British journal of nutrition     Volume:  102     ISSN:  1475-2662     ISO Abbreviation:  Br. J. Nutr.     Publication Date:  2009 Dec 
Date Detail:
Created Date:  2009-12-16     Completed Date:  2010-01-20     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0372547     Medline TA:  Br J Nutr     Country:  England    
Other Details:
Languages:  eng     Pagination:  1811-9     Citation Subset:  IM    
Affiliation:
Cellular Biochemistry and Lipid Biology Laboratories, Methodist Research Institute, Indianapolis, IN, USA. rsiddiqu@clarian.org
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MeSH Terms
Descriptor/Qualifier:
Animals
Aorta
Atherosclerosis / chemically induced,  pathology
Cell Line
Coronary Vessels
Death, Sudden, Cardiac / etiology*,  prevention & control*
Diet
Disease Models, Animal
Endothelial Cells / chemistry,  drug effects
Fatty Acids / blood
Fatty Acids, Omega-3 / administration & dosage*
Femoral Artery
Humans
Intercellular Adhesion Molecule-1 / analysis
Ligation
Male
Mice
Mice, Inbred C57BL
Myocardial Infarction / drug therapy
Oxidative Stress / drug effects
Rats
Rats, Wistar
Trans Fatty Acids / administration & dosage*
Vasculitis / etiology*,  prevention & control*
Chemical
Reg. No./Substance:
0/Fatty Acids; 0/Fatty Acids, Omega-3; 0/Trans Fatty Acids; 126547-89-5/Intercellular Adhesion Molecule-1

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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