Abstract 5398: Eicosapentaenoic Acid (EPA) and Docosahexaenoic Acid (DHA) Supplementation, but not α-Linolenic Acid, Elevates Plasma Adiponectin Concentration and Prevents Pressure Overload Induced Ventricular Dysfunction and Remodeling
Coronary disease is reduced by intake of the ω-3 polyunsaturated fatty acids (ω-3PUFA) EPA and DHA. Recent evidence suggest EPA+DHA may also prevent development of heart failure. We previously showed that intake of fish oil rich in EPA+DHA up-regulates expression and plasma levels of adiponectin, a cardioprotective adipose-derived hormone. We examined the effects of dietary EPA+DHA on plasma adiponectin levels and development of left ventriclular (LV) dysfunction and remodeling in response to pressure overload induced by abdominal aorta banding. Rats were fed either a standard chow or diets supplemented with EPA+DHA from fish oil at 0.7%, 2.3% or 7% of energy intake. LV volumes were measured by echo. On the standard diet banding increased LV mass by 38%, LV end diastolic volume by 29%, and end diastolic volume by 101% compared to sham (p<0.05). EPA+DHA supplementation increased plasma adiponectin concentration in a dose dependent manner (see Fig.⇓), and prevented the increases in LV end diastolic volume and end systolic volume (p<0.05). Adiponectin levels were negatively correlated with LV end systolic and diastolic volumes (r=−0.78 and −0.71, respectively; p<0.001). The protective effect of adiponectin has been linked to AMPK activation and/or inhibition of pro-growth Akt, however there were no differences in AMPK or Akt activation by western blot. A parallel series of rats were fed with α-linolenic acid, a ω-3PUFA from flaxseed, over a similar dose range, and showed no increase in adiponectin or prevention of LV pathology. In conclusion, supplementation with EPA+DHA prevented LV remodeling and dysfunction, which was strongly associated with an elevation in plasma adiponectin.