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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 dysfuction devleops when rats are fed with a HFD for 10 weeks: additionally, we sought to investigate the association between mitochondrial abnormalities, adenosin triphosphate (ATP) levels and cardiac dysfuction.
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 phosphorlyation (OXPHOS) subunit gene, peroxisome-proliferator activated receptor gamma co-activator 1 alpha (PGC1 alpha) and anti-oxidant enzymes were assessed. Markers of oxidative stress damage, mitochindrial DNA compy number and myocardial ATP level were also examined.
After 10 weeks, the body weight of the HFD group (349+/-22g) was significantly higher than that of the SD group (286+/-14g), and perigonadal and epicardial fat weights of the HFD group were significantly higher than that of the SD group. Histomorphologic and electron microscopic images were slighty different between the two groups. However, in the myocardium of the HDF group, the expression level of OXPHOS subunit NDUFB5 in complex I and PGC1alpha, and the mitochondrial DNA compy number were decreased and the oxidative stress damage marker 8-hydroxydeoxyguanosine was increased, accompanied by reduced ATP levels.
Diastolic dysfuction was accompanied by the mitochondrial abnormality and reduced ATP levels in the myocardium of 10 weeks HFD-indcued rats.