Diastolic Dysfunction Induced by a High-Fat Diet Is Associated with Mitochondrial Abnormality and Adenosine Triphosphate Levels in Rats
Autor: | Ok Kim, Ki Woon Kang, Seong-Kyu Lee, Yu Jeong Choi, Do Seon Lim, Sang Hyun Park, Jung Yeon Chin, Kyung Tae Jung, Jong Ho Shin, Won Ho Kim |
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Jazyk: | angličtina |
Rok vydání: | 2015 |
Předmět: |
medicine.medical_specialty
Mitochondrial DNA Endocrinology Diabetes and Metabolism Diastole Oxidative phosphorylation Mitochondrion Biology medicine.disease_cause lcsh:Diseases of the endocrine glands. Clinical endocrinology chemistry.chemical_compound Endocrinology Internal medicine medicine Endocrine Research Obesity Receptor lcsh:RC648-665 medicine.disease Mitochondria chemistry Heart failure Diastolic dysfunction Original Article Adenosine triphosphate Oxidative stress |
Zdroj: | Endocrinology and Metabolism Endocrinology and Metabolism, Vol 30, Iss 4, Pp 557-568 (2015) |
ISSN: | 2093-5978 2093-596X |
Popis: | 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. |
Databáze: | OpenAIRE |
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