Key result
A UFA-rich diet caused myocardial oxidative stress, including higher lipid hydroperoxide levels (176 vs 158, P<0.0005), and mild structural alterations, but did not change mechanical function.
Why the study?
Does a UFA-rich diet affect myocardial performance, metabolism, and morphology in male Wistar rats?
Does a UFA-rich diet affect myocardial performance, metabolism, and morphology in male Wistar rats?
Absolute Event Rate: 176% vs 158%
p-value: p=<0.0005
A UFA-rich diet induces myocardial oxidative stress and mild structural alterations without affecting mechanical function in a rat model.
Does not support human dietary changes from rat data; leaves open UFA effects on myocardial function.
Diets rich in saturated fatty acids are one of the most important causes of atherosclerosis in men, and have been replaced with diets rich in unsaturated fatty acids (UFA) for the prevention of this disorder. However, the effect of UFA on myocardial performance, metabolism and morphology has not been completely characterized. The objective of the present investigation was to evaluate the effects of a UFA-rich diet on cardiac muscle function, oxidative stress, and morphology. Sixty-day-old male Wistar rats were fed a control (N = 8) or a UFA-rich diet (N = 8) for 60 days. Myocardial performance was studied in isolated papillary muscle by isometric and isotonic contractions under basal conditions after calcium chloride (5.2 mM) and ss-adrenergic stimulation with 1.0 microM isoproterenol. Fragments of the left ventricle free wall were used to study oxidative stress and were analyzed by light microscopy, and the myocardial ultrastructure was examined in left ventricle papillary muscle. After 60 days the UFA-rich diet did not change myocardial function. However, it caused high lipid hydroperoxide (176 +/- 5 vs 158 +/- 5, P < 0.0005) and low catalase (7 +/- 1 vs 9 +/- 1, P < 0.005) and superoxide-dismutase (18 +/- 2 vs 27 +/- 5, P < 0.005) levels, and discrete morphological changes in UFA-rich diet hearts such as lipid deposits and mitochondrial membrane alterations compared to control rats. These data show that a UFA-rich diet caused myocardial oxidative stress and mild structural alterations, but did not change mechanical function.
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Pinotti et al. (2006) studied this question. UFA-rich diet vs. control diet was evaluated on lipid hydroperoxide levels (p=<0.0005). A UFA-rich diet caused myocardial oxidative stress, including higher lipid hydroperoxide levels (176 vs 158, P<0.0005), and mild structural alterations, but did not change mechanical function.
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