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Endocrinol Metab : Endocrinology and Metabolism


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Jung Yeon Chin  (Chin JY) 2 Articles
Endocrine Research
Diastolic Dysfunction Induced by a High-Fat Diet Is Associated with Mitochondrial Abnormality and Adenosine Triphosphate Levels in Rats
Ki-Woon Kang, Ok-Soon Kim, Jung Yeon Chin, Won Ho Kim, Sang Hyun Park, Yu Jeong Choi, Jong Ho Shin, Kyung Tae Jung, Do-Seon Lim, Seong-Kyu Lee
Endocrinol Metab. 2015;30(4):557-568.   Published online December 31, 2015
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  • 44 Download
  • 13 Web of Science
  • 13 Crossref
AbstractAbstract PDFPubReader   

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.


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.


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.


Diastolic dysfunction was accompanied by the mitochondrial abnormality and reduced ATP levels in the myocardium of 10 weeks-HFD-induced rats.


Citations to this article as recorded by  
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  • Qiliqiangxin Enhances Cardiac Glucose Metabolism and Improves Diastolic Function in Spontaneously Hypertensive Rats
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    Evidence-Based Complementary and Alternative Medicine.2017; 2017: 1.     CrossRef
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A Patient with Primary Amyloidosis Misrecognized as Thyrotoxicosis-induced Heart Failure.
Seok Ju Lee, Seung Hwan Lee, Jung Yeon Chin, Youn Mi Song, Sung Won Lee, Min Hee Kim, Mi Ja Kang, Kang Woo Lee, Hyuk Sang Kwon, Kun Ho Yoon, Ho Young Son, Bong Yun Cha
J Korean Endocr Soc. 2008;23(5):332-336.   Published online October 1, 2008
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  • 20 Download
AbstractAbstract PDF
Amyloidosis is caused by deposition of insoluble amyloid protein in the extracellular space of organs and tissues. The causes of amyloidosis are classified as primary, secondary, and hereditary, and symptoms develop according to which organ is involved. Cardiac amyloidosis induces cardiomyopathy and is developed by deposition of amyloid proteins in cardiac tissue. We diagnosed a patient with rhabdomyolysis and thyrotoxicosis with underlying Graves' disease 5 years ago. The patient was readmitted recently complaining of general weakness and mild dyspnea, and was diagnosed as relapsed thyrotoxicosis. An echocardiogram was performed for the evaluation of dyspnea and the findings were compatible with infiltrative cardiomyopathy due to amyloidosis. A biopsy of the abdominal subcutaneous fat and rectal mucosa was performed, and diagnosis was amyloidosis with histologic findings. The cause of heart failure was therefore cardiac amyloidosis rather than thyrotoxicosis. This case indicates the importance of evaluating the cause of heart failure in patients with thyrotoxicosis.
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Endocrinol Metab : Endocrinology and Metabolism