- Endocrine Research
- Diastolic Dysfunction Induced by a High-Fat Diet Is Associated with Mitochondrial Abnormality and Adenosine Triphosphate Levels in Rats
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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
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Endocrinol Metab. 2015;30(4):557-568. Published online December 31, 2015
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DOI: https://doi.org/10.3803/EnM.2015.30.4.557
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Abstract
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- 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. MethodsWe 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. ResultsAfter 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. ConclusionDiastolic dysfunction was accompanied by the mitochondrial abnormality and reduced ATP levels in the myocardium of 10 weeks-HFD-induced rats.
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Citations
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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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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
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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
- A Case of Complete Agenesis of the Dorsal Pancreas in a Patient with Newly Diagnosed Diabetes Mellitus.
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Dong Pil Kim, Kang Seo Park, Dong Sun Kim, Bong Suk Ko, Ji Hae Lee, Jae Hyuk Lee, Jong Ho Shin, Byung Jun Kim, Hyun Jin Kim
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J Korean Endocr Soc. 2010;25(1):78-83. Published online March 1, 2010
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DOI: https://doi.org/10.3803/jkes.2010.25.1.78
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Abstract
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- Agenesis of the dorsal pancreas is a rare congenital anomaly caused by underdevelopment or agenesis of the dorsal pancreatic bud that forms the upper head, neck, body and tail of the pancreas. We report a case of agenesis of the dorsal pancreas, which was found under examination of diabetes mellitus (DM). A 16-year-old girl was transferred to our hospital because of a positive urine glucose reading during a school-conducted examination. Abdominal computed tomography and magnetic resonance cholangiopancreatography revealed the deficit of the pancreatic body and tail. Diabetes-associated autoimmune antibodies were negative in a blood test. Decreased beta-cell function was demonstrated by oral glucose tolerance and glucagon stimulation tests. Although the notion that agenesis of the dorsal pancreas leads to decreased endocrine or exocrine function is controversial, the results of this study suggest that we should consider these causes of diabetes mellitus. When treating a young patient with diabetes mellitus, we should consider causes of diabetes mellitus such as congenital anomaly or maturity onset diabetes, in addition to type 1 and type 2 diabetes mellitus.
- A Case of Graves' Disease with Pancytopenia.
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Jong Ho Shin, Hyun Jin Kim, Si Bum Kim, Dong Pil Kim, Bong Suk Ko, Dong Soon Kim, Ji Myung Kim, Soo Jung Gong, Jung Ae Lee
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J Korean Endocr Soc. 2009;24(4):272-276. Published online December 1, 2009
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DOI: https://doi.org/10.3803/jkes.2009.24.4.272
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2,026
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- Hematological disorders, and especially single lineage abnormalities, have been described in patients suffering with thyrotoxicosis, but pancytopenia is a rare complication of thyrotoxicosis. Pancytopenia with thyrotoxicosis has been reported to be totally reversible with antithyroid drug treatment. We experienced a case with pancytopenia associated with Graves' disease in a 57-year-old woman who had no specific cause of pancytopenia. She presented with dyspnea and palpitation. The laboratory findings revealed thyrotoxicosis and pancytopenia. Increased radioisotope uptake was seen on the thyroid scan and normal cellularity and maturation were found in the bone marrow aspiration biopsy. Based on these findings, she was diagnosed as suffering from Gravesyendisease with pancytopenia. After treatment with propylthiouracil, the blood cell counts were restored to normal as the patient achieved a euthyroid state. We report here on a case of Graves' disease that was complicated by pancytopenia, and all this was normalized after treatment for hyperthyroidism.
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Citations
Citations to this article as recorded by
- Non-myeloproliferative Pancytopenia: A Rare Presentation of Thyrotoxicosis
Izzathunnisa Rahmathullah, Maheswaran Umakanth, Suranga Singhapathirane Cureus.2023;[Epub] CrossRef - Pancytopenia in a surgical patient, a rare presentation of hyperthyroidism
Prabhat Jha, Yogendra Prasad Singh, Bikal Ghimire, Binit Kumar Jha BMC Surgery.2014;[Epub] CrossRef - A Case of Pancytopenia with Hyperthyroidism
Tae Hoon Kim, Ji Sung Yoon, Byung Sam Park, Dong Won Lee, Jae Ho Cho, Jun Sung Moon, Eui Hyun Kim, Kyu Chang Won, Hyoung Woo Lee Yeungnam University Journal of Medicine.2013; 30(1): 47. CrossRef
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