Key result
A high saturated fat diet following coronary artery ligation in rats increased mitochondrial oxidative phosphorylation and did not adversely affect left ventricular contractile function.
Why the study?
Does a high saturated fat diet exacerbate left ventricular dysfunction and inhibit mitochondrial function in a rat model of postinfarction heart failure?
Population
Rats with heart failure induced by coronary artery ligation (n=15) and sham-operated rats (n=8)
Comparison
High saturated fat diet for 8 weeks vs Normal diet (10% kcal from fat) for 8 weeks
Design
Preclinical, randomly assigned
Follow-up
8 weeks
Authors
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May inform post-MI dietary approaches in animal models; extends mitochondrial data but leaves open human translation.
RCT (n=23)
randomly assigned
Does a high saturated fat diet exacerbate left ventricular dysfunction and inhibit mitochondrial function in a rat model of postinfarction heart failure?
In a rat model of postinfarction heart failure, a high saturated fat diet enhanced mitochondrial function without exacerbating left ventricular dysfunction.
Rennison et al. (2006) conducted an RCT in Heart failure (n=23). High saturated fat diet vs. Normal diet (10% kcal from fat) was evaluated on Left ventricular contractile function, remodeling, and mitochondrial oxidative phosphorylation. A high saturated fat diet following coronary artery ligation in rats increased mitochondrial oxidative phosphorylation and did not adversely affect left ventricular contractile function.
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