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Joong Yeol Park  (Park JY) 35 Articles
Frequency of Silent Myocardial Ischemia Detected by Thallium-201 SPECT in Patients with Type 2 Diabetes.
Dong Woo Kim, Eun Hee Jung, Eun Hee Koh, Min Seon Kim, Joong Yeol Park, Seung Whan Lee, Seong Wook Park, Jin Sook Ryu, Ki Up Lee
Korean Diabetes J. 2009;33(3):225-231.   Published online June 1, 2009
DOI: https://doi.org/10.4093/kdj.2009.33.3.225
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BACKGROUND
Silent myocardial ischemia (SMI) is more common in diabetic patients than among the general population. It is not yet established whether a routine screening test for SMI is necessary, and which screening test would be most useful. The purpose of this study was to estimate the prevalence of SMI detected by Thallium-201 perfusion single photon emission computed tomography (SPECT) in type 2 diabetic patients. METHODS: A total of 173 asymptomatic type 2 diabetic patients were included in the study. Thallium-201 perfusion SPECT was performed to screen for SMI. RESULTS: Among the 173 patients, abnormal perfusion patterns were found in 11 patients. Coronary angiography was carried out for these patients, and significant coronary artery stenosis was found in ten of them (positive predictive value; 90.9%). There was a significant association between SMI and overt albuminuria (OR = 7.33, 95% CI, 1.825-29.437). CONCLUSION: Thallium-201 perfusion SPECT is not sensitive enough to identify SMI, but is accurate in detecting decreased myocardial perfusion. This may be a useful screening tool for detecting SMI in type 2 diabetic patients with impaired renal function.
Nitric Oxide Increases Insulin Sensitivity in Skeletal Muscle by Improving Mitochondrial Function and Insulin Signaling.
Woo Je Lee, Hyoun Sik Kim, Hye Sun Park, Mi Ok Kim, Mina Kim, Ji Young Yun, Eun Hee Kim, Sang Ah Lee, Seung Hun Lee, Eun Hee Koh, Joong Yeol Park, Ki Up Lee
Korean Diabetes J. 2009;33(3):198-205.   Published online June 1, 2009
DOI: https://doi.org/10.4093/kdj.2009.33.3.198
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  • 2 Crossref
AbstractAbstract PDF
BACKGROUND
Accumulating evidence has suggested that nitric oxide (NO) is involved in the regulation of insulin sensitivity in skeletal muscle. Recent studies also suggested NO as an important molecule regulating mitochondrial biogenesis. This study examined the effect of the NO donor, 3-morpholinosydnonimine (SIN-1), on glucose metabolism in skeletal muscle and tested the hypothesis that NO's effect on glucose metabolism is mediated by its effect on mitochondrial function. METHODS: In Sprague-Dawley (SD) rats treated with SIN-1 for 4 weeks, insulin sensitivity was measured by a glucose clamp study. Triglyceride content and fatty acid oxidation were measured in the skeletal muscle. In addition, mitochondrial DNA content and mRNA expression of mitochondrial biogenesis markers were assessed by real-time polymerase chain reaction and expression of insulin receptor substrate (IRS)-1 and Akt were examined by Western blot analysis in skeletal muscle. In C2C12 cells, insulin sensitivity was measured by 2-deoxyglucose uptake and Western blot analysis was used to examine the expression of IRS-1 and Akt. RESULTS: SIN-1 improved insulin sensitivity in C2C12 cells and skeletal muscles of SD rats. In addition, SIN-1 decreased triglyceride content and increased fatty acid oxidation in skeletal muscle. Mitochondrial DNA contents and biogenesis in the skeletal muscle were increased by SIN-1 treatment. Moreover, SIN-1 increased the expression of phosphor-IRS-1 and phosphor-Akt in the skeletal muscle and muscle cells. CONCLUSION: Our results suggest that NO mediates glucose uptake in skeletal muscle both in vitro and in vivo by improving mitochondrial function and stimulating insulin signaling pathways.

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  • NO-Rich Diet for Lifestyle-Related Diseases
    Jun Kobayashi, Kazuo Ohtake, Hiroyuki Uchida
    Nutrients.2015; 7(6): 4911.     CrossRef
  • Metformin Activates AMP Kinase through Inhibition of AMP Deaminase
    Jiangyong Ouyang, Rahulkumar A. Parakhia, Raymond S. Ochs
    Journal of Biological Chemistry.2011; 286(1): 1.     CrossRef
Anti-GAD Antibody in Patients with Adult-Onset Diabetes in Korea.
Sang Ah Lee, Eui Young Kim, Eun Hee Kim, Ji Yun Jeong, Eun Heui Jeong, Dong Woo Kim, Eun Hee Cho, Eun Hee Koh, Min Seon Kim, Joong Yeol Park, Ki Up Lee
Korean Diabetes J. 2009;33(1):16-23.   Published online February 1, 2009
DOI: https://doi.org/10.4093/kdj.2009.33.1.16
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  • 10 Crossref
AbstractAbstract PDF
BACKGROUND
It is well known that the clinical characteristics of diabetes mellitus in Korean people are different from those of Western people. The purpose of this study was to investigate the prevalence of the anti-GAD antibody (GADA) in a large number of Korean patients with adult-onset diabetes. METHODS: The GADA was measured by radioimmunoassay for 11,472 adult-onset diabetic patients who visited the Asan Medical Center from 1998 to 2007. According to the fasting C-peptide levels, we classified the patients into an insulin dependent diabetes mellitus group (IDDM; C-peptide < 0.6 ng/mL) and non-insulin dependent diabetes mellitus group (NIDDM; C-peptide > or = 1.0 ng/mL). Other clinical and laboratory data were obtained from medical records. RESULTS: Among the 11,147 diabetic patients, 9,250 patients were classified as NIDDM, 922 patients were classified as IDDM and 975 patients excluded. Within the latter group 472 patients were to absolute insulin deficient (C-peptide < 0.1 ng/mL). The prevalence of GADA was 22.0% in the IDDM group and 4.7% in the NIDDM group. GADA was more prevalent in younger-onset NIDDM patients (25~40 years of age; 12.4%) than in older-onset NIDDM patients (> or = 40 years of age; 3.8%). The GADA-positive NIDDM patients had lower C-peptide and BMI levels, and higher rates of typical diabetic symptoms and insulin treatment. CONCLUSION: The prevalence of GADA in Korean patients with IDDM and NIDDM was lower than that reported in Western populations. It is thus suggested that autoimmunity is a rarer cause of diabetes in Korean people. However, since over 10% of younger-onset NIDDM patients were positive for GADA, routine GADA measurement in such patients is recommended.

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Citations to this article as recorded by  
  • Distinct changes to pancreatic volume rather than pancreatic autoantibody positivity: insights into immune checkpoint inhibitors induced diabetes mellitus
    Hung-Hui Wei, Ying-Chieh Lai, Gigin Lin, Cheng-Wei Lin, Ya-Chu Chang, John Wen-Cheng Chang, Miaw-Jene Liou, I-Wen Chen
    Diabetology & Metabolic Syndrome.2024;[Epub]     CrossRef
  • Recent information on test utilization and intraindividual change in anti-glutamic acid decarboxylase antibody in Korea: a retrospective study
    Rihwa Choi, Wonseo Park, Gayoung Chun, Jiwon Lee, Sang Gon Lee, Eun Hee Lee
    BMJ Open Diabetes Research & Care.2022; 10(3): e002739.     CrossRef
  • The effect of glargine versus glimepiride on pancreatic β-cell function in patients with type 2 diabetes uncontrolled on metformin monotherapy: open-label, randomized, controlled study
    Jun Sung Moon, Kyoung Soo Ha, Ji Sung Yoon, Hyoung Woo Lee, Hyun Chul Lee, Kyu Chang Won
    Acta Diabetologica.2014; 51(2): 277.     CrossRef
  • Successful treatment of latent autoimmune diabetes in adults with Traditional Chinese Medicine: a case report
    Jiaxing Tian, Wenke Liu, Zhong Zhen, Xiaolin Tong
    Journal of Traditional Chinese Medicine.2013; 33(6): 766.     CrossRef
  • The prevalence and characteristics of latent autoimmune diabetes in adults (LADA) and its relation with chronic complications in a clinical department of a university hospital in Korea
    Mi-Oh Roh, Chan-Hee Jung, Bo-Yeon Kim, Ji-Oh Mok, Chul-Hee Kim
    Acta Diabetologica.2013; 50(2): 129.     CrossRef
  • Prevalence and Clinical Characteristics of Recently Diagnosed Type 2 Diabetes Patients with Positive Anti-Glutamic Acid Decarboxylase Antibody
    Yul Hwangbo, Jin Taek Kim, Eun Ky Kim, Ah Reum Khang, Tae Jung Oh, Hak Chul Jang, Kyong Soo Park, Seong Yeon Kim, Hong Kyu Lee, Young Min Cho
    Diabetes & Metabolism Journal.2012; 36(2): 136.     CrossRef
  • Body Composition Analysis in Newly Diagnosed Diabetic Adolescent Girls
    Yong Hyuk Kim, Min Kyoung Song, Sochung Chung
    Journal of Korean Society of Pediatric Endocrinology.2011; 16(3): 172.     CrossRef
  • Increasing Trend in the Number of Severe Hypoglycemia Patients in Korea
    Jin Taek Kim, Tae Jung Oh, Ye An Lee, Jun Ho Bae, Hyo Jeong Kim, Hye Seung Jung, Young Min Cho, Kyong Soo Park, Soo Lim, Hak Chul Jang, Hong Kyu Lee
    Diabetes & Metabolism Journal.2011; 35(2): 166.     CrossRef
  • Progression to insulin deficiency in Korean patients with Type 2 diabetes mellitus positive for anti‐GAD antibody
    S. A. Lee, W. J. Lee, E. H. Kim, J. H. Yu, C. H. Jung, E. H. Koh, M.‐S. Kim, J.‐Y. Park, K.‐U. Lee
    Diabetic Medicine.2011; 28(3): 319.     CrossRef
  • Anti-GAD Antibody in Patients with Adult-Onset Diabetes in Korea
    Eun-Gyoung Hong
    Korean Diabetes Journal.2009; 33(1): 13.     CrossRef
Retraction: Protective Effect of PGC-1 on Lipid Overload-induced Apoptosis in Vascular Endothelial Cell.
Eun Hee Koh, Youn Mi Kim, Ha Jung Kim, Woo Je Lee, Jong Chul Won, Min Seon Kim, Ki Up Lee, Joong Yeol Park
Korean Diabetes J. 2008;32(3):293-293.   Published online June 1, 2008
DOI: https://doi.org/10.4093/kdj.2008.32.3.293
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No absrtact available.
Changes in the Prevalence of Metabolic Syndrome in a Rural Area of Korea Defined by Two Criteria, Revised National Cholesterol Education Program and International Diabetes Federation.
Jong Chul Won, Joong Yeol Park, Kee Ho Song, Woo Je Lee, Eun Hee Koh, Il Sung Nam-Goong, Sung Min Han, Moo Song Lee, Min Seon Kim, Ki Up Lee
Korean Diabetes J. 2007;31(3):284-292.   Published online May 1, 2007
DOI: https://doi.org/10.4093/jkda.2007.31.3.284
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  • 3 Crossref
AbstractAbstract PDF
BACKGROUND
The prevalence of obesity is increasing in Korea, including rural areas. We examined the changes in the prevalence of metabolic syndrome (MetS), defined by revised National Cholesterol Education Program (NCEP) or International Diabetes Federation (IDF) criteria, in a rural area of Korea during the past 6 years. METHODS: A total of 1,119 subjects (424 men and 695 women) aged > or = 30 years were initially recruited in 1997. Baseline clinical data and various laboratory values were obtained. Six years later, we performed a follow-up study in 814 subjects (316 men and 498 women) of which 558 were original participants and 256 subjects were new. The prevalence of MetS was assessed by the criteria of NCEP or IDF. RESULTS: The prevalence of central obesity and impaired fasting glucose increased in both sexes during the period between 1997 and 2003. The prevalence of MetS according to the IDF criteria also increased. In men, the age-adjusted prevalence of MetS was 10.9% in 1997 and 23.3% in 2003. In women, it was 42.2% in 1997 and 43.4% in 2003. However, the prevalence of MetS according to the NCEP criteria increased only in men. CONCLUSION: There have been increases in the prevalence of central obesity and MetS according to the IDF criteria during the recent 6 years in a rural area of Korea.

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  • The Association between Midnight Salivary Cortisol and Metabolic Syndrome in Korean Adults
    Yun-Mi Jang, Eun Jung Lee, Dong Lim Kim, Suk Kyeong Kim, Kee-Ho Song
    Diabetes & Metabolism Journal.2012; 36(3): 245.     CrossRef
  • The Diagnostic Criteria of Metabolic Syndrome and the Risk of Coronary Heart Disease according to Definitions in Men
    Hyouk-Soo Seo, Sung-Hi Kim, Soon-Woo Park, Jong-Yeon Kim, Geon-Ho Lee, Hye-Mi Lee
    Korean Journal of Family Medicine.2010; 31(3): 198.     CrossRef
  • Metabolic syndrome is associated with erosive esophagitis
    Jung Ho Park, Dong IL Park, Hong Joo Kim, Yong Kyun Cho, Chong IL Sohn, Woo Kyu Jeon, Byung Ik Kim
    World Journal of Gastroenterology.2008; 14(35): 5442.     CrossRef
Protective Effect of PGC-1 on Lipid Overload-induced Apoptosis in Vascular Endothelial Cell.
Eun Hee Koh, Youn Mi Kim, Ha Jung Kim, Woo Je Lee, Jong Chul Won, Min Seon Kim, Ki Up Lee, Joong Yeol Park
Korean Diabetes J. 2006;30(3):151-160.   Published online May 1, 2006
DOI: https://doi.org/10.4093/jkda.2006.30.3.151
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BACKGROUND
Fatty acids contribute to endothelial cell dysfunction and apoptosis by inducing accumulation of long chain fatty acyl CoA (LCAC), which increases oxidative stress in vascular endothelial cells. Forced expression of PGC-1 was shown to induce mitochondrial biogenesis and to control expression of mitochondrial enzymes involved in fatty acid oxidation. This study was undertaken to test the hypothesis that PGC-1 overexpression could prevent endothelial cell apoptosis by enhancing fatty acid oxidation and relieving oxidative stress in vascular endothelium. METHODS: Adenoviruses containing human PGC-1 (Ad-PGC-1) and beta-galactosidase (Ad-beta-gal) were transfected to confluent human aortic endothelial cells (HAECs). To investigate the effect of adenoviral PGC-1 gene transfer on apoptosis, combined treatment of linoleic acid (LA), an unsaturated fatty acid, was performed. RESULTS: PGC-1 overexpression inhibited the increase in ROS production and apoptosis of HAECs induced by LA. Also, PGC-1 led to a significant increase in fatty acid oxidation and decrease in triglyceride content in HAECs. LA caused the decrease of adenine nucleotide translocase (ANT) activity and transient mitochondrial hyperpolarization, which was followed by depolarization. PGC-1 overexpression prevented these processes. CONCLUSION: In summary, PGC-1 overexpression inhibited mitochondrial dysfunction and apoptosis by facilitating fatty acid oxidation and protecting against the damage from oxidative stress in HAECs. The data collectively suggest that the regulation of intracellular PGC-1 expression might play a critical role in preventing atherosclerosis.
Increase in Fatty Acid Oxidation by AICAR: the Role of p38 MAPK.
Woo Je Lee, Jin Yob Kim, Sung Jin Bae, Eun Hee Koh, Sung Min Han, Hye Sun Park, Hyun Sik Kim, Min Seon Kim, Joong Yeol Park, Ki Up Lee
Korean Diabetes J. 2005;29(1):15-21.   Published online January 1, 2005
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BACKGROUND
AMPK is an enzyme that increases glucose transport and fatty acid oxidation in skeletal muscle. The activation of AMPK stimulates fatty acid oxidation by decreasing the acetyl CoA carboxylase (ACC) activity and the concentration of malonyl-CoA. However, a recent study has reported a dissociation of AMPK activity and ACC phosphorylation in skeletal muscle during periods of prolonged exercise. This suggested that there is an additional mechanism for AMPK-induced fatty acid oxidation in skeletal muscle. METHODS: Plamitate oxidation was measured via the generation of [3H]-water generation from 9,10[3H]-palmitate after treating various concentrations of AICAR on the C2C12 mouse skeletal muscle cell line. Western analysis was used to test for the possible activation of p38 MAPK by AICAR. Involvement of p38 MAPK in the AICAR-induced increase in fatty acid oxidation was tested for by using SB203580, a p38 MAPK inhibitor. RESULTS: C2C12 cell treated with AICAR exhibited a dose-dependent increase in fatty acid oxidation compared to the cells that were not treated with AICAR. Western blot analysis revealed that phosphorylation of p38 MAPK was increased 2.5 folds after AICAR treatment. The increase of fatty acid oxidation with AICAR treatment was significantly inhibited by a treatment of SB203580; this indicated the involvement of p38 MAPK on the AICAR-induced increase in fatty acid oxidation. CONCLUSION: AICAR stimulated the fatty acid oxidation by activating p38 MAPK. This is a novel pathway by which AMPK activation in skeletal muscle increases the fatty acid oxidation
AMPK Activator AICAR Inhibits Hepatic Gluconeogenesis and Fatty Acid Oxidation.
Jin Yob Kim, Eun Hee Koh, Woo Je Lee, Seong Min Han, Ji Young Youn, Hye Sun Park, Hyun Sik Kim, Min Seon Kim, Joong Yeol Park, Ki Up Lee
Korean Diabetes J. 2005;29(1):6-14.   Published online January 1, 2005
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BACKGROUND
Recent studies have demonstrated that adiponectin and metformin activate AMPK in the liver, and adiponectin and metformin stimulate fatty acid oxidation while inhibiting glucose production in liver. These results are in contrast to previous studies that have demonstrated that increased fatty acid oxidation in the liver is associated with increased gluconeogenesis. The present study was undertaken to reinvestigate the effects of AMPK activation by AICAR on hepatic fatty acid oxidation and gluconeogenesis. METHODS: HePG2 cells were treated with various concentrations of AICAR, and then the fatty acid oxidation and gluconeogenesis of the cells were determined. To investigate the in vivo effect of AICAR, Sprague-Dawely rats were infused with AICAR (bolus, 40 mg/g; constant, 7.5 mg/g/min-1) for 90min. RESULTS: Incubation of the HePG2 cells with higher concentrations (=1 mM) of AICAR increased fatty acid oxidation and gluconeogenesis. On the other hand, incubation of HePG2 cells with lower concentrations (0.05 and 0.1 mM) of AICAR decreased fatty acid oxidation and gluconeogenesis. Consistent with this in vitro data, the intravenous administration of AICAR to rats lowered their plasma glucose concentration and inhibited hepatic gluconeogenesis. Fatty acid oxidation in the liver tissue was significantly decreased by the administration of AICAR. CONCLUSION: The present study has demonstrated that AICAR decreased gluconeo-genesis in the liver. In contrast to previous studies, AICAR profoundly decreased hepatic fatty acid oxidation in rats and also in cultured hepatocytes
The Role of AMPK in Vascular Endothelium.
Woo Je Lee, Jin Yob Kim, Eun Hee Koh, Sung Min Han, Min Seon Kim, Ki Up Lee, Joong Yeol Park
Korean Diabetes J. 2005;29(1):1-5.   Published online January 1, 2005
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No abstract available.
Hypothalamic AMPK Activity in Diabetic Rats.
Churl Namkoong, Min Seon Kim, Woo Je Lee, Pil Geum Jang, Seong Min Han, Eun Hee Koh, Joong Yeol Park, Ki Up Lee
Korean Diabetes J. 2004;28(6):468-477.   Published online December 1, 2004
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BACKGROUND
AMP-activated protein kinase (AMPK) acts as a cellular energy sensor that is activated during states of low energy charge and it regulates the various metabolic pathways to reestablish the normal cellular energy balance. It has recently been demonstrated that AMPK activity is altered by the state of energy metabolism in the hypothalamic neurons and this mediates the feeding response. METHODS: Diabetes was induced by an intra-peritoneal injection of streptozotocin (STZ) in Sprague-Dawley rats. The diabetic rats were maintained for 3 weeks with or without insulin treatment. 3 weeks later, we collected hypothalamus and we then assayed the phosphorylation of AMPK and the activity of acetyl CoA carboxylase (ACC) and isoform-specfic AMPK. To determine the effect of hypothalamic AMPK inhibition on diabetic hyperphagia, we administered an AMPK inhibitor, compound C, into the third ventricle in the STZ-induced diabetic rats. RESULTS: Phosphorylation of AMPK, which is a marker of AMPK activation, increased in the hypothalamus of the STZ-induced diabetic rats (DR). Moreover, 2-AMPK activity, but not 1-AMPK activity, increased by 2-fold in hypothalamus of the DRs. Phosphorylation of hypothalamic acetyl CoA carboxylase (ACC), a key downstream enzyme of AMPK, also increased in the DRs and this caused a reduction in ACC activity. Insulin treatment completely reversed the diabetesinduced changes in the hypothalamic AMPK and ACC, suggesting that insulin deficiency was associated with the changes in hypothalamic AMPK and ACC. Inhibition of AMPK by an intracerebroventricular administration of AMPK inhibitor, compound C, attenuated the development of diabetic hyperphagia and reduced the blood glucose levels in DRs. CONCLUSION: We have demonstrated that hypothalamic AMPK activity increased in the DRs, and inhibition of hypothalamic AMPK activity attenuated the development of diabetic hyperphagia. These data indicate that the enhanced hypothalamic AMPK activity may contribute to the development of diabetic hyperphagia
Recent Advances in the Treatment of Obesity.
Woo Je Lee, Eun Hee Koh, Min Seon Kim, Joong Yeol Park, Ki Up Lee
Korean Diabetes J. 2004;28(5):347-355.   Published online October 1, 2004
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No Abstract available.
The Role of Plasma Adiponectin and Polymorphism of Adiponectin Gene in the Development of Type 2 Diabetes Mellitus.
Kee Ho Song, Joong Yeol Park
Korean Diabetes J. 2003;27(6):433-437.   Published online December 1, 2003
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No abstract available.
Potential Role of Leptin Resistance in Metabolic Syndrome.
Seong Min Han, Joong Yeol Park
Korean Diabetes J. 2003;27(4):304-312.   Published online August 1, 2003
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No abstract is available.
Association between Type 2 Diabetes and Genetic Variations in Uncoupling Protein 2, beta3-Adrenergic Receptor, and Peroxisome Proliferator-Activated Receptor gamma in Korean.
Min Kyong Moon, Young Min Cho, Hye Seung Jung, Tae Yong Kim, Yun Yong Lee, Joong Yeol Park, Ki Up Lee, Chan Soo Shin, Kyong Soo Park, Seong Yeon Kim, Hong Kyu Lee, Hyoung Doo Shin
Korean Diabetes J. 2002;26(6):469-480.   Published online December 1, 2002
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AbstractAbstract PDF
BACKGROUND
Type 2 diabetes mellitus is a multifactorial disease influenced by numerous genetic and environmental factors. The uncoupling proteins, 2 (UCP2), beta3-adrenergic receptor ADRB3, and peroxisome proliferator-activated receptor gamma PPAR gamma, are genes involved in energy expenditure and fatty acid metabolisms, ans are therefore regarded as candidate genes for type 2 diabetes. In this study, we examined whether the known polymorphisms of UCP2, ADRB3 and PPAR gamma are associated with type 2 diabetes in the Korean population. METHODS: We studied 516 type 2 diabetic patients and 147 control subjects. The enrollment criteria for the control subjects were as follows; age > 60 years, no family history of diabetes in their first-degree relatives, a fasting plasma glucose (FPG) < 6.1 mmol/L, and a HbA1C < 5.8%. Height, weight, waist and hip circumference, FPG, 2 hour-plasma glucose after 75g-glucose load (2h-PG), blood pressure, lipid profile, and fasting insulin level were measured. The Ala55Val polymorphism of the UCP2, Trp64Arg polymorphism of the ADRB3, and Pro12Ala polymorphism of the PPAR gamma were determined by single base extension method. RESULTS: The allele frequency of the Ala55Val variant of the UCP2 tended to be higher in the control subjects than in the type 2 diabetic patients (0.497 vs. 0.456, p=0.064). The allele frequencies of the Trp64Arg polymorphism of the ADRB3, and the Pro12Ala polymorphism of the PPAR gamma, were comparable between the diabetic patients and the control subjects (0.141 vs. 0.152 and 0.033 vs. 0.041, respectively). In the control subjects, the Ala55Val polymorphism of the UCP2 was associated with a significantly lower 2h-PG compared to the wild type (6.0 +/- 0.8 mmol/L vs. 6.6 +/- 0.7 mmol/L, p=0.002). The female control subjects, with the ADRB3 Trp64Arg variant, had a significantly lower triglyceride level than those without the variant (1.36 +/- 0.53 mmol/L vs. 1.74 +/- 0.82 mmol/L, p=0.020). The type 2 diabetic patients, with the ADRB3 Trp64Arg variant showed a significantly lower body mass index (23.6 +/- 2.6 kg/m2vs. 24.6 +/- 3.0 kg/m2, p=0.001). The PPAR gamma Pro12Ala variant, was not associated with any of the features of insulin resistance. The combined genotype of the Val allele of UCP2, Trp allele of ADRB3 and Ala allele of PPAR gamma was less frequent among the type 2 diabetes patients than the control subjects (0.020 vs. 0.056, p=0.039). CONCLUSION: The Ala55Val variant of the UCP2, the Trp64Arg variant of the ADRB3 and the Pro12Ala variant of the PPAR gamma, were not associated with type 2 diabetes in the Korean population. However, the Ala55Val variant of the UCP2 was associated with a lower 2h-PG in the control subjects and the Trp64Arg variant of the ADRB3 was associated with a lower triglyceride level in the female control subjects. Further study may be required to elucidate if the combined genotype of Val allele of UCP2, Trp allele of ADRB3 and Ala allele of PPAR gamma would be protective against type 2 diabetes.
Effect and Mechanism of Vascular Endothelial Growth Factor on Endothelial Nitric Oxide Synthase Expression in Aortic Endothelial Cells.
Soon Hee Lee, Jung Guk Kim, Joong Yeol Park, Sung Woo Ha, Bo Wan Kim
Korean Diabetes J. 2002;26(5):396-404.   Published online October 1, 2002
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BACKGROUND
Vascular endothelial growth factor (VEGF), a soluble angiogenic factor produced by many tumor and normal cells, is a potent angiogenic and vascular permeability factor. VEGF plays a key role in both pathological and physiological angiogenesis. There are many recent findings regarding the role of VEGF in diabetic microvascular and macrovascular diseases. Many approaches with VEGF-related therapies begin to treat and prevent these complications and have been used for the treatment of microvascular complications such as diabetic retinopathy, whereas VEGF agonists have been used to treat macrovascular complications such as myocardial infarction and peripheral limb ischemia. Nitric oxide (NO) is known to mediate many physiological and pathological functions, including modulation of vascular tone, permeability, and capillary growth. Recent reports indicate that NO may play an intimate role in VEGF signaling. Therefore, we hypothesized that the expression of eNOS may be regulated by VEGF. The objectives of the present study were to determine whether VEGF up-regulates the expression of endothelial NO synthase (eNOS) in endothelial cells and to elucidate the mechanism that mediate this response. METHODS: Endothelial cells were isolated from bovine aortae. The expression of eNOS was assessed by Northern blotting analysis. To evaluate the mechanism of VEGF-induced eNOS expression, endothelial cells were conditioned with VEGF and pretreated with phorbol-12-myristate acetate (PMA), a protein kinase C (PKC) activator, or GF109203X (GFX), a PKC inhibitor. The changes of eNOS gene expression. RESULTS: VEGF significantly increased the expression of eNOS mRNA in bovine aortic endothelial cells (BAEC) in time and dose dependent manners. PMA increased the expression of eNOS mRNA, as well as the VEGF-induced expression of eNOS mRNA in endothelial cells, while inhibition of the PKC activity, with the GFX blocked the upregulation of the VEGF-induced eNOS mRNA. CONCLUSION: The results suggest that VEGF upregulates eNOS gene expression in aortic endothelial cells, by a PKC dependent pathway and, eNOS may be important in the development of VEGF-induced angiopathy.
Endothelial Dysfunction in Type 2 Diabetes: Role of Alpha-lipoic Acid, an Antioxidant.
Ki Ho Song, Joong Yeol Park
Korean Diabetes J. 2002;26(4):238-241.   Published online August 1, 2002
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No abstract available.
Comparative Study about the Effects of Acarbose and Voglibose in Type 2 Diabetic Patients.
In Kyung Jeong, Jae Hoon Chung, Yong Ki Min, Myung Shik Lee, Moon Kyu Lee, Kwang Won Kim, Yun Ey Chung, Joong Yeol Park, Sung Kwan Hong, Ki Up Lee
Korean Diabetes J. 2002;26(2):134-145.   Published online April 1, 2002
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AbstractAbstract PDF
BACKGROUND
Acarbose and voglibose are alpha-glucosidase inhibitors. Although different pharmacological effects and adverse abdominal events associated with the two drugs have been reported, no study directly compared acarbose and voglibose in diabetes has been undertaken. To compare the pharmacological effects and gastrointestinal adverse events between two drugs, a randomized, placebo-controlled, double-blind study was performed in type 2 diabetes patients. METHODS: The period of study was 12 weeks (observation period: 4 weeks; treatment period: 8 weeks). Fifty-three patients were randomized into two groups (the acarbose group: 24 patients; the voglibose group: 29 patients). The serum glucose, insulin, fructosamine, HbA1c, cholesterol, triglyceride and the incidence of adverse events were measured. RESULTS: 1) The reduction of glucose from before treatment to 4 weeks after treatment was significantly higher in the acarbose group, but the change before treatment and 8 weeks after treatment in the two groups was similar (p = 0.569). 2) The insulin significantly decreased after voglibose treatment (p = 0.040). 3) HbA1c level tended to decrease in voglibose group, and there was a significant decrease after acarbose treatment. However, the change in HbA1c level before and after treatment was similar between the two groups (p = 0.412). 4) The two drugs did not cause any other changes in the total, HDL-cholesterol and triglyceride. 5) The number of patients with gastrointestinal adverse events was significantly low 4 weeks after voglibose treatment (p = 0.049), but the incidence in the two groups was similar after 8 weeks (p = 0.215). CONCLUSIONS: Acarbose and voglibose significantly improved postprandial hyperglycemia in diabetes. The incidence of gastrointestinal adverse events was low 4 weeks after voglibose treatment.
The Effects of Uncoupling Protein 3 Overexpression on Glucose Metabolism in OLETF Rats in Vivo and Cultured Skeletal Muscle Cells in Vitro.
Jeong Hee Han, Hye Seon Park, Jung Min Koh, Ha Young Kim, Ho Kyung Kang, In Kyu Lee, Joong Yeol Park, Sung Kwan Hong, Jae Dam Lee, Ki Up Lee
Korean Diabetes J. 2001;25(6):460-468.   Published online December 1, 2001
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BACKGROUND
UCP3 is a mitochondrial membrane protein expressed selectively in the skeletal muscle and brown adipose tissue. Since the skeletal muscle is the main organ determining insulin sensitivity in the body, it was hypothesized that UCP3 overexpression in skeletal muscle cells would improve glucose metabolism. METHODS: An adenovirus-UCP3 was produced by a recombinant DNA method. OLETF rats were divided into 2 groups. Four rats were injected with the adenovirus- UCP3 (UCP3 group) and others were injected with the adenovirus (control group) in the skeletal muscle. The UCP3 group was provided with the same quantity of food as that consumed by the control group on the previous day. Insulin sensitivity was evaluated by the euglycemic hyperinsulinemic clamp method. In a separate experiment, glucose transport and glycogen synthesis we evaluated in C2C12 cells transfected with ether an adenovirus or the adenovirus-UCP3. RESULTS: The insulin sensitivity improved significantly and the body weight decreased in the UCP3 group. The glucose transport and glycogen synthesis were higher in the UCP3-C2C12 skeletal muscle cells at the basal state. After insulin treatment, glucose transport and glycogen synthesis were also higher in the UCP3-C2C12 cells but the increments were reduced after treatment with wortmannin, a PI3K inhibitor. CONCLUSION: Insulin sensitivity was higher in the UCP3-overexpressed OLETF rats in the in vivo study. UCP3 transfection also increased glucose transport and glycogen synthesis in the cultured skeletal muscle cells by a PI3K dependent mechanism.
Effects of High Fat Diet on Lipolysis in Skeletal Muscle and Adipose Tissue in Rats.
Chul Hee Kim, Yun Ey Chung, Seong Jin Lee, Joong Yeol Park, Sung Kwan Hong, Hong Kyu Kim, Kyo Il Suh, Ki Up Lee
Korean Diabetes J. 2000;24(6):641-651.   Published online January 1, 2001
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BACKGROUND
It has been hypothesized that increased fat oxidation reduces glucose utilization in skeletal muscle, and is responsible for the insulin resistance associated with obesity or high-fat feeding. In contrast, there have been reports that fat oxidation capacity was decreased in skeletal muscles from insulin resistant subjects. This study was undertaken to examine whether insulin resistance in high- fat fed rats is associated with increased lipolysis in skeletal muscle and adipose tissue. METHODS: Two groups of Sprague-Dawley rats were fed either high-fat or low-fat diets for 4 weeks. Lipolysis in skeletal muscle and adipose tissue was determined by measurement of interstitial glycerol concentrations by a microdialysis method in basal and hyperinsulinemic-euglycemic clamp conditions. RESULTS: In basal state, plasma glycerol levels and interstitial glycerol concen trations of skeletal muscle, and adipose tissue were lower in high-fat fed than in low-fat fed rats. The degree of suppression of glycerol release by the hyperinsulinemia was smaller in the high-fat diet than in the low-fat diet group. However, plasma and interstitial glycerol concentrations during the hyperinsul inemic euglycemic clamps were also lower in the high-fat diet group. CONCLUSION: Lipolysis was decreased in skeletal muscle and adipose tissue of insulin resistant, high-fat fed rats. These results support the idea that limited fat oxidation capacity resulting in lipid accumulation in tissues, rather than increased fat oxida tion per se, is responsible for the insulin resistance associated with high-fat feeding.
Humoral Immunological Marks in Patients with Child-onset and Adult-onset Type 1 Diabetes.
Hyun Dae Yoon, Jae Hong Kim, Jung Hyun Oh, Jin Chul Park, Sang Yub Nam, Ji Soon Yoon, Kyu Chang Won, In Ho Cho, Choong Ki Lee, Joong Yeol Park, Sung Kwan Hong, Ki Up Lee, Hyoung Woo Lee
Korean Diabetes J. 2000;24(4):444-456.   Published online January 1, 2001
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BACKGROUND
Type 1 diabetes mellitus is an autoimmune disease in which serum antibodies against islet antigens have been recognized. These antibodies include cytoplasmic islet cell antibodies (ICA), and glutamic acid decarboxylase (GAD)65 antibodies and IA2 antibodies. It has been reported that the prevalence of these autoantibodies is different among Caucacian and Asian and Korean type 1 diabetes patients. And the natural course of type 1 diabetes can differ according to the age of onset. But, in contrast to the classic juvenile onset type 1 diabetes, the adult onset type 1 diabetes is poorly characterized about clinical and autoimmune differences at presentation. Thus, this study was perfomed to evaluate clinical and autoimmune characteristics at presentation in subjects with either child onset or adult onset type 1 diabetes and to establish an autoimmune pathogenesis in Korean type 1 diabetes. METHOD: We examined the clinical characteristics of child onset type 1 diabetes (n=32) and adult onset type 1 diabetes (n=40) retrospectively. At the same time, ICA from these patients was measured by standard indirect immunofluorescence, GADA and IA2A from these patients were measured by radioimmunoassay. RESULTS: The mean duration of disease was longer in the adult onset and their serum fasting C-peptide concentration at diagnosis were higer. The prevalence of ICA, GADA, IA2A in sera from 32 patients with child onset type 1 diabetes was 50%, 38% and 31% respectively. And, the prevalence of ICA, GADA and IA2A in sera from 40 patients with adult onset type 1 diabetes was 30%, 25% and 18% respectively.The prevalence of ICA, GADA and IA2A in sera from 39 patients with typical type 1 diabetes was 46%, 30% and 16% respectively. And, the prevalence of ICA, GADA and IA2A in sera from 33 patients with atypical type 1 diabetes was 30%, 30% and 25% respectively. The concordance rate of ICA and GADA in child onset and adult onset diabetes was 81% (26/32), 80% (32/40) respectively. In a subset of these patients with recent onset type 1 diabetes (duration of diabetes < or = 1 year), the prevalence of ICA, GADA and IA2A was 75% (3/4), 75% (3/4), 100% (1/1) respectively, in the child onset type 1 diabetes. CONCLUSION: These observations show that autoantibodies in Korean patients with child onset type 1 diabetes is similar compaired with other Asian groups but is lower than Caucasian patients with type 1 diabetes and the prevalence of humoral immunologic makers in child onset type 1 diabetes was higher than that of adult onset diabetes. These results suggest that autoimmune response is a significant cause of Korean type 1 diabetes but other factors except autoimmunity may play an important role in the pathogenesis of Korean type 1 diabetes.
Clustering of Risk Variables in Insulin Resistance Syndrome in Jungup District, Korea.
Sang Wook Kim, Myung Hoe Huh, Young Il Kim, Jin Yub Kim, Eun Sook Kim, Moo Song Lee, Joong Yeol Park, Sung Kwan Hong, Ki Up Lee
Korean Diabetes J. 1999;23(6):843-856.   Published online January 1, 2001
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BACKGROUND
Insulin resistance syndrome (IRS), a clustering of hypertension, impaired glucose tolerance, low HDL cholesterol and high triglyceride, is prevalent in Korea. We studied the correlational structure of IRS using factor analysis to evaluate whether a single process underlies in the clustering of these risk factors. METHODS: Factor analysis was performed using data from 1,018 non-diabetic subjects (388 men and 630 women) who participated in the Jungup epidemiological study. RESULTS: Factor analysis reduced 9 correlated risk factors to 4 independent factors, each reflecting a different aspect of IRS: hypertension factor (increased systolic and diastolic blood pressure), glucose intolerance factor (increased fasting and postload glucose), obesity factor (increased body mass index, waist circumference, and increased insulin), and dyslipidemia factor (increased trigly- cerides and decreased HDL cholesterol). Increased insulin was also loaded into dyslipidemia factor in men and glucose intolerance factor in women. These factors explained about 70% of the total variance in the data. Three factors such as the glucose intolerance factor, the dyslipidemia factor and the obesity factor, were linked through mutual association with hyperinsulinemia, while hypertension factor was not associated with hyperin- sulinemia. Age-adjusted mean BP by BMI tertile and fasting insulin level tertile for men and women increased progressively with increase in BMI in men and women. There was no significant elevation of mean BP according to increase in fasting insulin level. In contrast to premenopausal women in whom hyperinsulinemia show mutual association with the glucose intolerance factor, the dyslipidemia factor, and the obesity factor, hyperinsulinemia was only loaded into obesity factor in postmenopausal women. CONCLUSION: These results suggested that more than one process underlies the clustering of IRS. In sulin resistance alone did not seem to be the single underlying mechanism of IRS. Especially, hypertension was not correlated with hyperin- sulinemia.
Lack of Effectiveness of Glomerular Hyperfiltration on Development of Microalbuminuria in Type 2 Diabetic Patients: five Year Follow-up Study.
Eun Sook Kim, Sang Wook Kim, Jin Yub Kim, Joong Yeol Park, Sung Kwan Hong, Ki Up Lee
Korean Diabetes J. 1999;23(2):155-161.   Published online January 1, 2001
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BACKGROUND
Glomerular hyperfiltration (GHF) is found in 30-40% of patients with type 1 diabetes at the onset of the disease. Several lines of evidence suggest that this might be responsible for the development of diabetic nephropathy. However, it is still controversial whether GHF is a risk factor in patients with type 2 diabetes. This led us to perform a five-year-prospective study in normoalbuminuric type 2 diabetic patients. METHODS: A total of 68 patients with type 2 diabetes were studied prospectively, They were all normoalbuminuric initially. Glomerular filtration rate was determined by the 51Cr-EDTA single injection method and urinary albumin excretion rate by the radioimtnunoassay method. RESULTS: GHF was present in 19 out of 68 patients. At follow-up, l7 out of 49 patients of the normofiltration group and 3 out of 19 patients of GHF group progressed to microalbuminuria (p>0.05). Multiple logistic regression analysis revealed that the known duration of diabetes, systolic hypertension, and the presence of retinopathy were independently associated with the development of microalbuminuria. CONCLUSION: Our study suggests that GHF does not predict the subsequent development of diabetic nephropathy as indicated by the elevation of the urinary albumin excretion rate during the five year interval.
Effect of Decreased Plasma Free Fatty Acids by an Antilipolytic Agent on Plasma Glucose Level and Liver Glycogen Content in Streptozotocin - induced Diabetic Rat.
Yun Ey Chung, Sang Wook Kim, Jin Yub Kim, Eun Sook Kim, Joong Yeol Park, Sung Kwan Hong, Ki Up Lee
Korean Diabetes J. 1999;23(1):46-54.   Published online January 1, 2001
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BACKGROUND
Increased availability of plasma free fatty acid (FFA) leads to an inhibition of glucose utilization in peripheral tissue and to an increase of gluconeogenesis in the liver. A previous study has shown that a decrease in plasma FFA profoundly inhitbits hepatic gluconeogenesis, but total hepatic glucose production is maintained due to a com pensatory increase in glycogenolysis. It has been suggested that this hepatic autoregulatory mechanism is defective in the diabetic state, but there has been no firm evidence to confirm this. This study was performed to see the effect of decreasing plasma FFA on plasma glucose and hepatic glucose metabolism in diabetic rats, METHODS: Eight nondiabetic and 8 streptozotocin-induced diabetic rats were used. Blood sampling for plasma glucose and free fatty acid and liver biopsy for measurement of glycogen content were done after intravenous phenobarbital ancsthesia. Acipimox (50 mg/kg in saline) was administered via gastric tube. Plasma glucose and FFA were measured at 30, 60 and 120 min. Liver biopsy was repeated at 120 min. RESULTS: Baseline plasma glucose and FFA were higher in diabetic rats than in nondiabetic rats (18.8 +1.4 mmol/L vs. 6.9+0.8 mmol/L, 720+/-36 umol/L vs. 420+40 umol/L p<0.001 respectively). Hepatic glycogen content was higer in nondiabetic rats (31.8 +1.6mg/g liver vs. 26.02.Dmg/g liver, p<0.01). After acipimox administration, plasma glucose decreased profoundly in diabetic rats (18.8+1.4 mmol/L to 9.2+1.2 mmol/L, p<0.001) but not in nondiabetic rats. Glycogen content was significantly reduced in both groups (p<0.001). However, the difference in the contents was much smaller in the diabetic group compared with the nondiabetic group (6.5+2.1 mg/g liver vs. 19.2+ l.9 mg/g liver, p<0.001). CONCLUSION: 1t is suggested that the intrahepatic autoregulatory mechanism, which maintains hepatic glucose production constant in nondiabetic rats, is defective in diabetic rats.
The Effects of Metformin Given into the Brain on Food Intake and a Expressions of Hypothalamic Neurotransmitters in the Rats.
Eun Sook Kim, Jin Yub Kim, Sang Wook Kim, Joong Yeol Park, Ki Up Lee, Sung Kwan Hong
Korean Diabetes J. 1998;22(4):475-481.   Published online January 1, 2001
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BACKGROUND
Metformin, a biguanide agent, is an oral hypoglycemic agent frequently prescribed to non-insulin-dependent diabetic patients. In adclition to the glucose lowering effect, it is known to suppress fol intake, but the action mechanism for food intake suppression is not known yet. Hypothalamic neuropeptide Y (NPY) is recently identified that strongly stimulates food intake and melanin concentrating hormone (MCH) is also known to be involved in the ingestion of foods. The effects of mettormin on these substances are not known yet. We tried to define the effect of metformin administered into the lateral ventricle on the amount of food intake and mRNA expressions of NPY and MCH. METHODS: Each rat was housed in a separate cage, and brain cannula was set into the lateral ventricle and proper position was checked by the response to angiotensin-II injection. Metformin l ug (1 ug/uL) or normal saline (1 uL) were injected daily into the lateral ventricle for 4 days in the Metformin group (n=7) and Control group (n=6) respectively, and the amount of food intake and weight change were recrded. Expressions of corticotropin releasing hormone mRNA in paraventricular nucleus, NPY mRNA in arcuate nucleus, and MCH mRNA in lateral hypothalamus were measured by the in situ hybridization technique. RESULTS: The amount of food intake was lower in metformin group than that in control group by 14~35% during the study period (p<0.05). Changes of body weight was -18+9 g (mean+SD) in metformin group and -2+11 g in control group. But mRNA expressions of NPY, MCH and CRH were not different between the groups (p>0.05). CONCLUSION: Metformin injected into the brain reduced the amount of food intake and body weight without the changes of NPY and MCH mRNAs. This study suggests that metformin suppress food intake by directly acting in the brain, but these effects are not through the changes of NPY and MCH mRNA expressions.
Effects of Free Fatty Acids on Glutathione Redox Status in Cultured Endothelial Cells.
Joong Yeol Park, Chul Hee Kim, Yun Ey Chung, Hong Kyu Kim, Young Il Kim, Sung Kwan Hong, Jae Dam Lee, Ki Up Lee
Korean Diabetes J. 1998;22(3):262-270.   Published online January 1, 2001
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BACKGROUND
Although plasma free fatty acids (FFA) are frequently elevated in diabetes mellitus, its role in the pathogenesis of diabetic vascular complications has not been well investigated. Recent stuclies reported that FFA may cause endothelial dysfunction through an enhancement of oxidative damage by decreasing glutathione redox cycle, an important anti-oxidant defense system in endothelial cells. In this study, we examined the effects of increased availability of FFA on intracellular glutathione redox cycle. METHODS: Bovine pulonary endothelial cells were exposed to 90 umol/L linoleic acid with or without 0.1 mM 2-bromopalmitate, an inhibitor of mitochondrial fatty acid oxidation, for 6hr. Components of the glutathione redox cycle such as total glutathione, reduced glutathione(GSH) and oxidized glutathione(GSSG) concentrations were measured by HPLC. RESULTS: Total glutathione concentration in cultured endothelial cells exposed to linoleic acid was significantly lower than that in control cells (10.8+ 0.5 vs 14.1+0.8 umol/g protein, P<0.05). Linoleic acid significantly decreased GSH concentrations (10.5+0.4 vs. 13.8+0.5 pmol/g protein, P<0.05) and the ratio of GSH/GSSG(26.3+1.3 vs. 47.0+2,1, P<0.05). Compared to cells exposed linoleic acid alone, total glutathione(13.5+0.5umol/g protein, P<0.05) and GSH concentration(13.2+0.4 pmol/g protein, P<0.05) significantly increased in cells treated with 2-bromopalmitate and linoleic acid. The ratio of GSH/GSSG in cells treated with 2-bromopalmitate and linoleic acid was higher th.an that in cells exposed to linoleic acid alone(44.1+1.3, P<0.05). CONCLUSION: Increased provision of FFA resulted in a derangement of glutathione redox cycle in cultured endothelial cells, which appears to be related to an increase in mitochondrial FFA oxidation. These results suggested that FFA can increase the risk of diabetic vascular complications.
Effect of Exercise Training on Insulin Sensitivity and Intracellular Glucose Metabolism in Skeletal Muscle of High Fat-fed Rats.
Chul Hee Kim, Joong Yeol Park, Sung Kwan Hong, Kyong Soo Park, Hong Kyu Lee, Ki Up Lee
Korean Diabetes J. 1998;22(2):231-242.   Published online January 1, 2001
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AbstractAbstract PDF
BACKGROUND
Insulin resistance is a major characteristic of non-insulin-dependent diabetes mellitus and obesity. Many studies have indicated that increased intake of fat are associated with obesity and insulin resistance. On the other hand, chronic exercise is known to improve insulin sensitivity. However, the mechanisms by which high fat diet induces insulin resistance and exercise trainmg improves insulin sensitivity are not established. This study was undertaken to examine the mechanisms by which high fat diet and exercise training affect the insulin sensitivity in the whole body and in skeletal muscles. METHODS: Male Sprague-Dawley rats were divided into three groups: high fat sedentary group, high fat exercise group, and control(low fat sedentary) group. High fat diet consists of 66.5% fat and 12.5% carbohydrate, and control(low fat) diet consists of 12 5% fat and 66.5% carbohydrate. Exercise training was performed by swimming three hours per day. After 3 weeks, animals underwent hyperinsulinemic euglycemic clamp study to measure whole body glucose metabolic fluxes. Glycogen synthase activity and glucose-6-phosphate (G-6-P) levels were measured in skeletal muscle at the end of the clamp study. RESULTS: In the high fat diet group, whole body glycolysis and glycogen synthesis were decreased. Exercise training reversed the insulin resistance induced by high fat diet by increasing both glycolysis and glycogen synthesis. Glycogen synthase activity in skeletal muscle was reduced in high fat diet group, and it was partially reversed by exercise training. G-6-P level in skeletal muscle was increased in high fat diet group, and it was further increased by exercise training. CONCLUSION: These results suggested that the insulin resistance in high fat diet-fed rats is due to the impairment in glucose metabolism at sites distal to G-6-P, i.e. glycolysis and glycogen synthesis. In contrast, the improvement in insulin sensitivity by exercise training in high fat-fed rats is primarily due to the increased glucose metabolic flux proximal to G-6-P, i.e. glucose transport and phosphorylation.
Changes in Serum True Insulin and C-peptide Levels during Oral Glucose Tolerance Test in Koreans with Glucose Intolerance.
Young Il Kim, Chul Soo Choi, Sang Wook Kim, Hong Kyu Kim, Chul Hee Kim, Joong Yeol Park, Sung Kwan Hong, Ki Up Lee
Korean Diabetes J. 1998;22(2):192-198.   Published online January 1, 2001
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BACKGROUND
Previous studies have shown that progression from normal glucose tolerance(NGT) to impaired glucose tolerance(IGT) is associated with the development of insulin resistance and hyper-insulinemia, while further progression from IGT to NIDDM results from an inability of the 8-cell to maintain high rate of insulin secretion. However, it is not established whether similar findings are also observed in Korean subjects with glucose intolerance. The aim of this study was to examine insulin secretory response after oral glucose stimulation in obese and non-obese Korean subjects according to varying degree of glucose intolerance. METHODS: Eighty eight Korean men underwent 75g oral glucose tolerance test. The subjects were classified into NGT(n=30), IGT(n=23), NIDDM(n= 35) according to National Diabetes Data Group criteria. Obesity was defined as body mass index (BMI) > 25 kg/m . Serum true insulin and C-peptide concentrations were measured by radioimmunoassay. RESULTS: Fasting serum true insulin and C-peptide levels were not different from each other among NGT, IGT and NIDDM groups, both in obese and non-obese subjects. Obese subjects with IGT had significantly higher serum true insulin and C-peptide levels at 120 min than those in NGT subjects, but the levels at 30 and 60 min were not different. On the other hand, non-obese subjects with IGT had lower serum true insulin level at 30 min and lower serum C-pepitde level at 60 min compared to those in NGT subjects. True insulin and C-pepitde levels at 30 and 60 min were significantly lower in patients with NIDDM than in those with NGT, both in obese and non-obese subjects. CONCLUSION: Hyperinsulinemia, especially at a later phase of oral glucose tolerance test, is apparent in obese subjects with IGT. On the other hand, early phase insulin secretory defect is prominent in non-obese subjects with IGT. These results suggest that impaired insulin secretion may play a primary role in the pathogenesis of non-obese NIDDM in Korea.
Changes of Glomerular Filtration Rate and Urinary Albumin Excretion Rate in NIDDM patients with Microalbuminuria.
Hyo Jung Kim, Jung Min Koh, Eun Sug Shin, Yun Ey Chung, Young Il Kim, Chul Hee Kim, Joong Yeol Park, Sung Kwan Hong, Ki Up Lee
Korean Diabetes J. 1997;21(4):414-424.   Published online January 1, 2001
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AbstractAbstract PDF
BACKGROUND
We previously suggested that micro-albuminuria in the presence of retinopathy may represent a state of real incipient diabetic nephropathy with declining glomerular filtration rate(GFR), while the meaning of microalbuminuria in the absence of retinopathy may be more heterogeneous. This study was performed to further test this hypothesis. METHODS: We prospectively followed up the changes in GFR and urinary albumin excretinn rate (UAE) in microalbuminuric NIDDM patients with or without diabetic retinopathy for 3.1 years. RESULTS: 1) Among 45 patients who completed the followup, 27 had retinopathy from the baseline(group A), while 18 patients did not have retinopathy throughout the study(group B). 2) UAE at baseline was not statistically different between the group A and group B. During follow-up, VAE remained stable in the group B patients(40.0 [20.5 ~ 158.0) to 60.0[20.2 ~ 231.0] ug/min, NS). On the other hand, UAE significantly increased in the group A patients(47.9[20.0~186.0] to 140.0[24.5~2862.0] ug/min, P <0.001). 3) Thirty percent of the group A patients(8/27) progressed to overt proteinuria, while 11%(2/18) of the group B patients developed overt proteinuria(NS). 4) GFR significantly decreased both in the group A (113.0+21.2 to 89.1+24.0 mL/min/1.73 m, P < 0,001) and in the group B patients(134.1+27.2 to 121.5+27.3 mL/min/1.73 m, P<0.01). However, the magnitude of change in GFR was significantly higher in the group A than in the group B patients(7.7+7.6 vs 3.9+4.2 mL/min/1.73 m /year, P <0.05), 5) Multiple logistic regression analysis revealed that the presence of retinopathy was a independent risk factor for faster decline in GFR. CONCLUSION: It appears that clinical course is different in NIDDM patients with microalbuminuria, according to the presence or absence of diabetic retinopathy. Microalbuminuria in the presence of retinopathy predicts aggravation of albuminuria and decline in GFR. In contrast, the renal function in microalbuminuric NIDDM patients in the absence of retinopathy may remain stable for years.
Plasminogen Activator Inhibitor ( PAI-1 ) Levels in Patients with non-insulin Dependent Diabetes Mellitus ( NIDDM ).
Hong Kyu Kim, Chul Hee Kim, Eun Sug Shin, Hyo Jung Kim, Joong Yeol Park, Sung Kwan Hong, Hyun Sook Chi, Ki Up Lee
Korean Diabetes J. 1997;21(1):29-38.   Published online January 1, 2001
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BACKGROUND
Conventional cardiovascular risk factors cannot fully explain high risk of cardiovascular disease in patients with non-insulin dependent diabetes mellitus(NIDDM). This study was undertaken to know whether plasma PAI-1 levels are increased in NIDDM patients, and to identify factors intluencing Pal-1 levels. METHODS: Forty three microalbuminuric, 41 normoalbuminuric NIDDM patients and 39 normal controls matched with age, sex and body mass index (BMI) participated in this study. Clinical characteristies and laboratory findings such as lipid profile, fasting serum C-peptide and PAI-1 levels were evaluated, RESULTS: NIDDM patients showed significantly higher PAI-1 levels than normal controls(44.3+17.4 ng/mL vs. 26.3+12.6ng/mL, p<0.05). However, we failed to show the differences in PAI-1 levels between NIDDM patients with microalbuminuria and normoalbuminuria. PAI-1 levels were significantly correlated to BMI, fasting plasma glucose, HbA1, triglyceride and serum C-peptide levels. Multiple regression analysis showed that serum triglyceride and fasting serum C-peptied levels were independently related to PAI-1 levels. Conclusion; These findings suggested that elevated PAI-1 levels may contribute to increased risk of cardiovascular disease in patients with NIDDM.
The prevalence of micro-and macrovascular complications of korean niddm patients.
Joong Yeol Park, Sang Wook Kim, Goo Yeong Cho, Mee Hwa Lee, Soo Jung Je, Ki Up Lee, Ghi Su Kim
Korean Diabetes J. 1993;17(4):377-385.   Published online January 1, 2001
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AbstractAbstract PDF
No abstract available.
Biological activity of in-vitro glycosylated insulin in diabetic patients.
Joong Yeol Park, Jae Joon Koh, Kyong Soo Park, Moon Kyu Lee, Seong Yeon Kim, Bo Youn Cho, Hong Kyu Lee, Chang Soon Koh, Hun Ki Min, Sung Wan Kim
Korean Diabetes J. 1993;17(3):253-258.   Published online January 1, 2001
  • 852 View
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AbstractAbstract PDF
No abstract available.
Follow-up of glomerular hyperfiltration in non-insulin-dependent diabetes mellitus.
Il Ran Hwang, Ki Up Lee, Joong Yeol Park, Dae Hyuk Moon, Ghi Su Kim
Korean Diabetes J. 1993;17(2):169-174.   Published online January 1, 2001
  • 700 View
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AbstractAbstract PDF
No abstract available.
Effect of acipimox(olbetam)treatment on plasma lipids and glucose in hyperlipidemic patients with type 2 diabetes mellitus.
Ki Up Lee, Soojung Je, Joong Yeol Park, Ghi Su Kim, Mun Ho Lee
Korean Diabetes J. 1993;17(1):105-110.   Published online January 1, 2001
  • 818 View
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AbstractAbstract PDF
No abstract available.
Body weight changes of non-insulin dependent diabetic patients in korea.
Joong yeol Park, Hyeon Kyu Kim, Min Sun Kim, Kyong Soo Park, Seong Yeon Kim, Bo Youn Cho, Hong Kyu Lee, Chang Soon Koh, Hun Ki Min
Korean Diabetes J. 1993;17(1):51-58.   Published online January 1, 2001
  • 864 View
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AbstractAbstract PDF
No abstract available.
Transplantation of microencapsulated canine pancreatic islets to streptozotocin-induced diabetic rats.
Chul Hee Kim, Joo Jun Koh, Joong Yeol Park, Kyong Soo Park, Seong Yeon Kim, Bo Youn Cho, Hong Kyu Lee, Chang Soon Koh, Hun Ki Min, Seung Eun Yang, Seng Jin Lee
Korean Diabetes J. 1992;16(2):129-135.   Published online January 1, 2001
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AbstractAbstract PDF
No abstract available.

Diabetes Metab J : Diabetes & Metabolism Journal