ω-3 Polyunsaturated Fatty Acids Prevent Pressure Overload-Induced Ventricular Dilation and Decrease in Mitochondrial Enzymes Despite no Change in Adiponectin
O'Shea, Karen M
Chess, David J
Khairallah, Ramzi J
Hecker, Peter A
Des Rosiers, Christine
Stanley, William C
MetadataShow full item record
Citation (published version)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)
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.
RightsCopyright 2010 O'Shea et al; licensee BioMed Central Ltd.