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Eun Jung Kim  (Kim EJ) 3 Articles
Transcriptional Regulation of Insulin and CXCL10 Gene by Peroxisome Proliferator Activated Receptor gamma Coactivator-1alpha.
Won Gu Jang, In Kyu Lee, Eun Jung Kim, Seong Yeol Ryu, Bo Wan Kim, Jung Guk Kim
Korean Diabetes J. 2007;31(4):326-335.   Published online July 1, 2007
DOI: https://doi.org/10.4093/jkda.2007.31.4.326
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AbstractAbstract PDF
BACKGROUND
Peroxisome proliferator-activated receptor-gamma coactivator 1alpha (PGC-1alpha), which act as a coactivator of nuclear receptors and several other transcription factors. This study was performed to evaluate the expressional regulation of insulin and inflammatory response genes by PGC-1alpha. METHODS: Transient transfection assays were performed to measure the promoter activity of the insulin and CXCL10 gene. The insulin gene expression levels in INS-1 cells were determined by Northern blot analysis. Differentially expressed genes by PGC-1alpha overexpression in HASMCs were confirmed using DNA microarray, real-time PCR and Northen blot analysis. RESULTS: Insulin promoter activity and mRNA levels were suppressed by GR and Ad-PGC-1alpha. Northern blot analysis of the INS-1 cells revealed that infection with Ad-PGC-1alpha markedly reduced the amount of insulin mRNA and treatment of Dex enhanced this effect in an additive manner. The PGC-1alpha-specific siRNA decreased insulin expression that was induced by Dex in the GR-expressing INS-1 cells was nearly restored by this siRNA treatment. We found that when vascular smooth muscle cells (VSMCs) overexpressed PGC-1alpha, immune or inflammatory response genes were highly expressed. For example, promoter activity and mRNA level of CXCL10 gene were increased by PGC-1alpha. CONCLUSION: PGC-1alpha overexpression inhibited insulin promoter activity in INS-1 cells and enhanced expressions of inflammatory response genes (CXCL10, CXCL11, TNFLSF10) in VSMCs.
Relative Hyperglucagonemia and Its Related Factors in Patients with Type 2 Diabetes.
Kang Hyun Choi, Ki Ho Song, Sang Hoon Lee, Seong Hoon Chung, Eun Jung Kim, Seung Hyun Ko, Hyuk Sang Kwon, Yu Bae Ahn, Kun Ho Yoon, Bong Yun Cha, Kwang Woo Lee, Ho Young Son, Sung Koo Kang
Korean Diabetes J. 2004;28(4):338-345.   Published online August 1, 2004
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AbstractAbstract PDF
BACKGROUND
Excessive secretion of glucagon contributes to metabolic disturbance in type 2 diabetes. A hyperglucagonemic state is likely to be involved in increased hepatic glucose output resulting from both gluconeogenesis and glycogenolysis. The mechanism of hyperglucagonemia, though still unclear, is explained, in part, by the decreased sensitivity of cells to insulin or glucose and disturbances of the normal oscillatory secretory pattern of insulin. The aim of the study was to determine the extent of glucagon excess and its related factors in Korean patients with type 2 diabetes. METHODS: The subjects of this study were 21 controls and 102 type 2 diabetic patients. The blood glucose, glucagon and insulin concentrations were measured at 0, 30, 60, 90 and 120 min after ingestion of 75 g of glucose, and the areas under the curve (AUC) calculated. RESULTS: The AUC of plasma glucose (AUCgc) was significantly higher in the type 2 diabetic patients than in the controls (2,026.1585.8 vs. 854.8190.3 mmol/min, P<0.01), but there was no difference in the AUC of plasma glucagon (AUCgn) between the two groups. The AUCgn in the type 2 diabetic patients was positively correlated with the duration of diabetes (r=0.202, P<0.05) or HbA1c (r=0.208, P<0.05). The AUC of serum insulin (AUCin) was negatively correlated with the duration of diabetes (r=-0.291, P<001). AUCgn, AUCgc and HbA1c in long-term diabetic patients (duration of diabetes 10 years, n=32) were significantly higher compared with recently diagnosed patients (duration of diabetes <1 year, n=38) (11,362.35,981.9 vs. 9,097. 22,990.4 ng/min; 2,119.9519.0 vs. 1,832.2477.6 mmol/min; 9.52.0 vs. 8.32.1%, P<0.05). In addition, the AUCin and insulinogenic index in long-term patients were significantly lower compared with recently diagnosed patients. (Eds note: the highlighted figures are confusing, due to your various uses of commas and period marks, olease clarify?) CONCLUSIONS: Our results suggest that duration of diabetes and poor glycemic control might be closely associated with relative hyperglucagonemia in Korean type 2 diabetic paticnts.
A Case of MELAS(Mitochondrial Encephalomyopathy, Lactic Acidosis, Stroke-like Episodes) Syndrome Manifested by Diabetic Ketoacidosis.
Sung Hoon Jung, Eun Jung Kim, So Hi Im, Kang Ju, Kang hyun Choi, Seung Hyun Ko, Yu Bae Ahn, Ki Ho Song, Ho Young Son, Sung Kyung Park, Jeong Su Jun
Korean Diabetes J. 2004;28(3):231-237.   Published online June 1, 2004
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AbstractAbstract PDF
MELAS(mitochondrial encephalomyopathy, lactic acidosis, stroke-like episodes) syndrome is a rare cause of mitochondrial encephalomyopathy, with variable clinical features, such as encephalomyopathy, lactic acidosis, stroke, diabetes, short stature, sensorineural hearing loss and basal ganglia calci-fication, etc. It can be confirmed by molecular genetic analysis that reveals the mitochondrial A3243G point mutation. Among the clinical manifestations in MELAS syndrome, diabetes mellitus is associated with impaired insulin secretion and often misdiagnosed type 1 diabetes. Herein, a rare case for the MELAS syndrome, with diabetes mellitus that came from ketoacidosis, is introduced. A 21-year-old woman, carried to the emergency department had a stuporous mentality. She was thin(BMI 16.1kg/m(2)), and had difficulty with her hearing capacity. According to the initial laboratory results, she showed the metabolic acidosis, hyperglycemia, ketonemia, and ketonuria. She was diagnosed as diabetic ketoacidosis and treated with insulin and hydration. Brain imaging from MRI, and a CT scan showed basal ganglia calcification, hemorrhagic infarction and diffuse brain atrophy. The markers for beta-cell autoimmunity were negative. Her electromyography suggested proximal myopathy. In addition, a molecular genetic analysis identified A3243G point mutation in the peripheral blood leukocytes from her, her mother and her sister.

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