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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
DOI: https://doi.org/10.3803/EnM.2015.30.4.557
  • 4,841 View
  • 44 Download
  • 13 Web of Science
  • 13 Crossref
AbstractAbstract PDFPubReader   
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.

Citations

Citations to this article as recorded by  
  • Epicardial Adipose Tissue in Myocardial Disease: From Physiology to Heart Failure Phenotypes
    Alexios S. Antonopoulos, Charalampos Papastamos, Dennis V. Cokkinos, Konstantinos Tsioufis, Dimitris Tousoulis
    Current Problems in Cardiology.2023; 48(10): 101841.     CrossRef
  • Metabolic mitochondrial alterations prevail in the female rat heart 8 weeks after exercise cessation
    Carolina Tocantins, João D. Martins, Óscar M. Rodrigues, Luís F. Grilo, Mariana S. Diniz, Jelena Stevanovic‐Silva, Jorge Beleza, Pedro Coxito, David Rizo‐Roca, Estela Santos‐Alves, Manoel Rios, Lina Carvalho, António J. Moreno, António Ascensão, José Maga
    European Journal of Clinical Investigation.2023;[Epub]     CrossRef
  • The link between obesity and aging - insights into cardiac energy metabolism
    Patricia Owesny, Tilman Grune
    Mechanisms of Ageing and Development.2023; 216: 111870.     CrossRef
  • Surgically Metabolic Resection of Pericardial Fat to Ameliorate Myocardial Mitochondrial Dysfunction in Acute Myocardial Infarction Obese Rats
    Ki-Woon Kang, Ju-Young Ko, Hyunghee Lee, Seung Yong Shin, Wang Soo Lee, Joonhwa Hong, Sang-Wook Kim, Seong-Kyu Lee, Min-Ho Oak
    Journal of Korean Medical Science.2022;[Epub]     CrossRef
  • Cilostazol attenuates cardiac oxidative stress and inflammation in hypercholesterolemic rats
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    Naunyn-Schmiedeberg's Archives of Pharmacology.2022; 395(7): 789.     CrossRef
  • The impact of diet upon mitochondrial physiology (Review)
    Ioannis Kyriazis, Eleni Vassi, Maria Alvanou, Christos Angelakis, Zoi Skaperda, Fotios Tekos, Venkata Garikipati, Demetrios Spandidos, Demetrios Kouretas
    International Journal of Molecular Medicine.2022;[Epub]     CrossRef
  • SIRT1 promotes lipid metabolism and mitochondrial biogenesis in adipocytes and coordinates adipogenesis by targeting key enzymatic pathways
    Yasser Majeed, Najeeb Halabi, Aisha Y. Madani, Rudolf Engelke, Aditya M. Bhagwat, Houari Abdesselem, Maha V. Agha, Muneera Vakayil, Raphael Courjaret, Neha Goswami, Hisham Ben Hamidane, Mohamed A. Elrayess, Arash Rafii, Johannes Graumann, Frank Schmidt, N
    Scientific Reports.2021;[Epub]     CrossRef
  • Physical Exercise Potentially Targets Epicardial Adipose Tissue to Reduce Cardiovascular Disease Risk in Patients with Metabolic Diseases: Oxidative Stress and Inflammation Emerge as Major Therapeutic Targets
    Thembeka A. Nyawo, Carmen Pheiffer, Sithandiwe E. Mazibuko-Mbeje, Sinenhlanhla X. H. Mthembu, Tawanda M. Nyambuya, Bongani B. Nkambule, Hanél Sadie-Van Gijsen, Hans Strijdom, Luca Tiano, Phiwayinkosi V. Dludla
    Antioxidants.2021; 10(11): 1758.     CrossRef
  • Potentially Critical Roles ofNDUFB5,TIMMDC1,and VDAC3in the Progression of Septic Cardiomyopathy Through Integrated Bioinformatics Analysis
    Kai Kang, Jingtian Li, Ruidong Li, Xiufeng Xu, Jianli Liu, Limin Qin, Tao Huang, Jinhua Wu, Min Jiao, Miaomiao Wei, Hongjie Wang, Tao Wang, Quan Zhang
    DNA and Cell Biology.2020; 39(1): 105.     CrossRef
  • Liraglutide shows superior cardiometabolic benefits than lorcaserin in a novel free choice diet-induced obese rat model
    François Briand, Emmanuel Brousseau, Julie Maupoint, Caroline Dubroca, Clément Costard, Natalia Breyner, Rémy Burcelin, Thierry Sulpice
    European Journal of Pharmacology.2020; 882: 173316.     CrossRef
  • Mitochondrial impairment following neonatal overfeeding: A comparison between normal and ischemic‐reperfused hearts
    Cristiane de Moura Freitas, Luciana Caroline Paulino do Nascimento, Glauber Rudá Feitoza Braz, Severina Cassia Andrade‐Silva, Nelson C. Lima‐Junior, Tercya de Araujo Silva, Mariana Pinheiro Fernandes, Diorginis José Soares Ferreira, Claudia Jacques Lagran
    Journal of Cellular Biochemistry.2019; 120(5): 7341.     CrossRef
  • Exercise training reverses age‐induced diastolic dysfunction and restores coronary microvascular function
    Kazuki Hotta, Bei Chen, Bradley J. Behnke, Payal Ghosh, John N. Stabley, Jeremy A. Bramy, Jaime L. Sepulveda, Michael D. Delp, Judy M. Muller‐Delp
    The Journal of Physiology.2017; 595(12): 3703.     CrossRef
  • Qiliqiangxin Enhances Cardiac Glucose Metabolism and Improves Diastolic Function in Spontaneously Hypertensive Rats
    Jingfeng Wang, Zhiming Li, Yanyan Wang, Jingjing Zhang, Weipeng Zhao, Mingqiang Fu, Xueting Han, Jingmin Zhou, Junbo Ge
    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
DOI: https://doi.org/10.3803/jkes.2008.23.5.332
  • 1,696 View
  • 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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