Long-term high-fat feeding in C57BL/6J mice induced cardiac hypertrophy and altered systemic metabolism but did not impair left ventricular ejection fraction or contractile function.
Does dietary fat overload induce cardiac contractile and mitochondrial dysfunction in C57BL/6J mice?
Long-term dietary fat overload in C57BL/6J mice induces cardiac hypertrophy and systemic metabolic changes but does not cause contractile or mitochondrial dysfunction, challenging its utility as a model for diabetic cardiomyopathy.
Absolute Event Rate: 0.78% vs 0.81%
p-value: p=ns
Dietary fat overload (DFO) is widely used to model diabetic cardiomyopathy but the utility of this model is controversial. We comprehensively characterized cardiac contractile and mitochondrial function in C57BL6/J mice fed with lard-based or saturated fat-enriched diets initiated at two ages. Despite cardiac hypertrophy, contractile and mitochondrial function is preserved, and molecular adaptations likely limit lipotoxicity. The resilience of these hearts to DFO underscores the need to develop robust alternative models of diabetic cardiomyopathy.
Tadinada et al. (Fri,) conducted a other in Diabetic cardiomyopathy model (diet-induced obesity). High-fat diet vs. Low-fat diet (10% fat or low-fat low-sucrose) was evaluated on Left ventricular ejection fraction (LVEF) (p=ns). Long-term high-fat feeding in C57BL/6J mice induced cardiac hypertrophy and altered systemic metabolism but did not impair left ventricular ejection fraction or contractile function.