ω-3 Polyunsaturated Fatty Acids Prevent Pressure Overload-Induced Ventricular Dilation and Decrease in Mitochondrial Enzymes Despite no Change in Adiponectin

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dc.contributor.author O'Shea, Karen M en_US
dc.contributor.author Chess, David J en_US
dc.contributor.author Khairallah, Ramzi J en_US
dc.contributor.author Hecker, Peter A en_US
dc.contributor.author Lei, Biao en_US
dc.contributor.author Walsh, Kenneth en_US
dc.contributor.author Des Rosiers, Christine en_US
dc.contributor.author Stanley, William C en_US
dc.date.accessioned 2012-01-12T17:43:50Z
dc.date.available 2012-01-12T17:43:50Z
dc.date.copyright 2010 en_US
dc.date.issued 2010-9-6 en_US
dc.identifier.citation O'Shea, Karen M, David J Chess, Ramzi J Khairallah, Peter A Hecker, Biao Lei, Kenneth Walsh, Christine Des Rosiers, William C Stanley. "ω-3 Polyunsaturated fatty acids prevent pressure overload-induced ventricular dilation and decrease in mitochondrial enzymes despite no change in adiponectin" Lipids in Health and Disease 9:95. (2010) en_US
dc.identifier.issn 1476-511X en_US
dc.identifier.uri http://hdl.handle.net/2144/3430
dc.description.abstract BACKGROUND Pathological left ventricular (LV) hypertrophy frequently progresses to dilated heart failure with suppressed mitochondrial oxidative capacity. Dietary marine ω-3 polyunsaturated fatty acids (ω-3 PUFA) up-regulate adiponectin and prevent LV dilation in rats subjected to pressure overload. This study 1) assessed the effects of ω-3 PUFA on LV dilation and down-regulation of mitochondrial enzymes in response to pressure overload; and 2) evaluated the role of adiponectin in mediating the effects of ω-3 PUFA in heart. METHODS Wild type (WT) and adiponectin-/- mice underwent transverse aortic constriction (TAC) and were fed standard chow ± ω-3 PUFA for 6 weeks. At 6 weeks, echocardiography was performed to assess LV function, mice were terminated, and mitochondrial enzyme activities were evaluated. RESULTS TAC induced similar pathological LV hypertrophy compared to sham mice in both strains on both diets. In WT mice TAC increased LV systolic and diastolic volumes and reduced mitochondrial enzyme activities, which were attenuated by ω-3 PUFA without increasing adiponectin. In contrast, adiponectin-/- mice displayed no increase in LV end diastolic and systolic volumes or decrease in mitochondrial enzymes with TAC, and did not respond to ω-3 PUFA. CONCLUSION These findings suggest ω-3 PUFA attenuates cardiac pathology in response to pressure overload independent of an elevation in adiponectin. en_US
dc.description.sponsorship National Institutes of Health (HL074237, HL091307, HL101434) en_US
dc.language.iso en en_US
dc.publisher BioMed Central en_US
dc.rights Copyright 2010 O'Shea et al; licensee BioMed Central Ltd. en_US
dc.rights.uri http://creativecommons.org/licenses/by/2.0 en_US
dc.title ω-3 Polyunsaturated Fatty Acids Prevent Pressure Overload-Induced Ventricular Dilation and Decrease in Mitochondrial Enzymes Despite no Change in Adiponectin en_US
dc.type article en_US
dc.identifier.doi 10.1186/1476-511X-9-95 en_US
dc.identifier.pubmedid 20819225 en_US
dc.identifier.pmcid 2939588 en_US

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