Key result
A high-fat diet for 10 weeks induced diastolic dysfunction in rats, evidenced by a significantly reduced E/A ratio (0.42 vs 1.33, p<0.001), accompanied by mitochondrial abnormalities and reduced ATP levels.
Why the study?
Does a high-fat diet induce diastolic dysfunction associated with mitochondrial abnormalities and reduced ATP levels in rats?
Does a high-fat diet induce diastolic dysfunction associated with mitochondrial abnormalities and reduced ATP levels in rats?
Absolute Event Rate: 0.42% vs 1.33%
p-value: p=<0.001
A 10-week high-fat diet in rats induces diastolic dysfunction associated with mitochondrial abnormalities, increased oxidative stress, and reduced myocardial ATP levels without striking structural changes.
High-fat diet effects on rat diastolic function remain preclinical; leaves open mitochondrial mechanisms for human HFpEF research.
BACKGROUND: Obesity is well-known as a risk factor for heart failure, including diastolic dysfunction. However, this mechanism in high-fat diet (HFD)-induced obese rats remain controversial. The purpose of this study was to investigate whether cardiac dysfunction develops when rats are fed with a HFD for 10 weeks; additionally, we sought to investigate the association between mitochondrial abnormalities, adenosine triphosphate (ATP) levels and cardiac dysfunction. METHODS: We examined myocardia in Wistar rats after 10 weeks of HFD (45 kcal% fat, n=6) or standard diet (SD, n=6). Echocardiography, histomorphologic analysis, and electron microscopy were performed. The expression levels of mitochondrial oxidative phosphorylation (OXPHOS) subunit genes, peroxisome-proliferator-activated receptor γ co-activator-1α (PGC1α) and anti-oxidant enzymes were assessed. Markers of oxidative stress damage, mitochondrial DNA copy number and myocardial ATP level were also examined. RESULTS: After 10 weeks, the body weight of the HFD group (349.6±22.7 g) was significantly higher than that of the SD group (286.8±14.9 g), and the perigonadal and epicardial fat weights of the HFD group were significantly higher than that of the SD group. Histomorphologic and electron microscopic images were similar between the two groups. However, in the myocardium of the HFD group, the expression levels of OXPHOS subunit NDUFB5 in complex I and PGC1α, and the mitochondrial DNA copy number were decreased and the oxidative stress damage marker 8-hydroxydeoxyguanosine was increased, accompanied by reduced ATP levels. CONCLUSION: Diastolic dysfunction was accompanied by the mitochondrial abnormality and reduced ATP levels in the myocardium of 10 weeks-HFD-induced rats.
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Kang et al. (2015) studied Obesity and diastolic dysfunction (n=12). High-fat diet vs. Standard diet (10 kcal% fat) was evaluated on E/A ratio (early to late peak transmitral flow velocity ratio) (p=<0.001). A high-fat diet for 10 weeks induced diastolic dysfunction in rats, evidenced by a significantly reduced E/A ratio (0.42 vs 1.33, p<0.001), accompanied by mitochondrial abnormalities and reduced ATP levels.
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