Abstract 434: A Diet Rich in Oleic Acid, as Primary Lipid Source, Attenuates the Progressive Functional Decline in Hypertrophied Hearts During Pathological Stress

Abstract

Two major dietary long chain fatty acids (LCFA), oleate and palmitate, display differing capacities to induce transcriptional activation of metabolic genes, lipid trafficking, substrate metabolism, and contractile function in the failing heart. Perfusing isolated failing rat hearts with the unsaturated LCFA, oleate, improves contractile function and restores intracellular lipid dynamics vs. failing rat hearts perfused with the saturated LCFA, palmitate. We therefore investigated whether chronically feeding rats a diet of either high-oleate (as triolein) or high-palmitate (as tripalmitin) could alter the development of heart failure in response to chronic pressure overload induced by transverse aortic constriction (TAC). Following TAC or sham surgery rats were randomized to a diet rich in either triolein or tripalmitin as primary fat source (65% carbohydrate, 20% protein and 15% fat (210 Kcal/kg)). TAC induced similar increases in LV mass independent of diet, however rats fed tripalmitin showed a significant reduction in survival and a decline in ejection fraction and fractional shortening as well as LV dilation, evident at 6 and 10 weeks post TAC (Figure). In contrast, triolein diet attenuated declining systolic function and LV dilation (Figure) and eliminated the otherwise expected elevation of plasma BNP, as seen with tripalmitin diet (50%, P<0.05) after 14 weeks of TAC, indicating differential effects of these fats on both the heart and whole body metabolism and physiology during cardiac stress. The results suggest that a diet rich in oleic acid affords benefits in attenuating the development of cardiac decompensation independent of changes in hypertrophic growth.