- Retraction: Polymorphisms of Kir6.2 Gene are Associated with Type 2 Diabetes and Blood Pressure in the Korean Population.
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Bo Kyeong Koo, Hong Il Kim, Eu Jin Lee, Young Min Cho, Hyoung Doo Shin, Hak Chul Jang, Hong Kyu Lee, Kyong Soo Park
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Korean Diabetes J. 2007;31(2):185-185. Published online March 1, 2007
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DOI: https://doi.org/10.4093/jkda.2007.31.2.185
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- Polymorphisms of Kir6.2 Gene are Associated with Type 2 Diabetes and Blood Pressure in the Korean Population.
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Bo Kyeong Koo, Hong Il Kim, Eu Jin Lee, Young Min Cho, Hyoung Doo Shin, Hak Chul Jang, Hong Kyu Lee, Kyong Soo Park
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Korean Diabetes J. 2005;29(5):440-450. Published online September 1, 2005
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- BACKGOUND: ATP-sensitive potassium channels are a heterooctamer of SUR1 and Kir6.2, which are key components in the insulin secretory mechanism. Whether common variants in the Kir6.2 gene are associated with type 2 diabetes and/or its associated phenotypes was investigated. METHODS: The Kir6.2 gene was sequenced in 24Korean DNA samples to identify common polymorphisms (frequency > 0.05). The common variants found among these samples were genotyped in a larger population including type 2 diabetic patients and nondiabetic subjects. RESULTS: Thirteen single nucleotide polymorphisms and one insertion/deletion polymorphism were identified in the Kir6.2 gene, with six common variants(g.-1709A>T, g.-1525T>C, g.67G >A [E23K], g.570C>T [A190A], g.1009A>G [1337V], and g.1388C>T) genotyped in 761 type 2 diabetic patients and 675 nondiabetic subjects. Four individual polymorphisms(g.-1525T > C, g.67G>A, g.1009A>G and g.1388C>T) appeared to be associated with type 2 diabetes (age, sex and BMI-adjusted odds ratio[OR]=0.751[0.584-0.967] in the recessive model on g-1525T>C, 1.193 [1.020-1.394] in the additive model in g.67G>A, 1.195 [1.022-1.399] in the additive model on g.1009A>G, 0.835 [0.717-0.973] in the additive model in g.1388C >T). The haplotype "ATACGC" in the Kir6.2 gene, composed of rare allele in the g.67 and g.1009, was also associated with a higher prevalence of type 2 diabetes (age, sex, and BMI- adjusted OR = 1.256 [1.067-1.479], P for logistic regression = 0.006). In addition g.67G>A and g.1009A >G in the KCNJ11 were strongly associated with a high systolic blood pressure. CONCLUSION: Polymorphisms in the Kir6.2 gene are associated with type 2 diabetes and blood pressure in the Korean population.
- Increasing Trends of Metabolic Syndrome in Korea -Based on Korean National Health and Nutrition Examination Surveys-.
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Soo Lim, Eun Jung Lee, Bo Kyeong Koo, Sung Il Cho, Kyong Soo Park, Hak Chul Jang, Seong Yeon Kim, Hong Kyu Lee
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Korean Diabetes J. 2005;29(5):432-439. Published online September 1, 2005
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- BACKGOUND: The number of individuals with metabolic syndrome is increasing in Asian as well as in Western countries. The aim of this study was to compare the prevalence and patterns of metabolic syndrome as determined by the 1998 and 2001 Korean National Health and Nutrition Examination Surveys(KNHANES). METHODS: A total of 6,907 and 4,536 Koreans aged over 20 years participated in the KNHANES in 1998 and 2001, respectively. A stratified multistage probability sampling design and weighting adjustments were made to obtain a representative Korean population. The working definition of the National Cholesterol Education Program-Adult Treatment Panel III was used to define metabolic syndrome. The International Obesity Task Force criteria for the Asian-Pacific population were used to determine waist circumference criteria. RESULTS: The age-adjusted prevalence of metabolic syndrome significantly increased from 22.5 to 24.1% between 1998 and 2001(P<0.01). Of the five components composing metabolic syndrome, low HDL-cholesterolemia showed the highest increase(32.6%) over this period, followed by hypertriglyceridemia and abdominal obesity, with 15.9% and 4.3% increases, respectively. In contrast, the number of subjects with high blood pressure or elevated fasting glucose levels were reduced(37.1-->33.1% and 18.9-->15.4%, respectively, both P<0.01). CONCLUSION: Dyslipidemia and abdominal obesity were primarily responsible for the increase in metabolic syndrome in Korea over the period 1998 to 2001. Changes to diet patterns and a reduction in physical activity are likely to have contributed to the rapid increase in metabolic syndrome in Korea; therefore, national strategies will be needed to counteract this increase.
- Common Genetic Polymorphisms in the Promoter of Resistin Gene are Major Determinants of Plasma Resistin Concentrations in Humans.
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Young Min Cho, Byung Soo Youn, Sung Soo Chung, Ki Woo Kim, Bo Kyeong Koo, Kang Yeol Yu, Hong Je Park, Hyoung Doo Shin, Hak Chul Jang, Kyong Soo Park, Seong Yeon Kim, Hong Kyu Lee
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Korean Diabetes J. 2004;28(1):9-19. Published online February 1, 2004
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- BACKGROUND
Resistin has been postulated to be an important link between obesity and insulin resistance. Genetic polymorphisms in the resistin gene promotor have been suggested as a determinant of the expression of resistin mRNA, which is possibly associated with obesity and insulin resistance. In this study, the association between the genotype of the resistin promoter, and its plasma concentrations, were investigated. METHODS: The g.-537A>C and g.-420C>G polymorphisms in the resistin promoter were examined, and the levels of plasma resistin measured in the Korean subjects, both with and without type 2 diabetes. Haplotype-based promoter activity and the gel electrophoretic mobility-shift assays(EMSA) were also performed. RESULTS: The -420G and the -537A alleles, which were in linkage disequilibrium, were associated with higher plasma resistin concentrations. Individuals with the A-G(-537 A and -420G) haplotypes showed significantly higher plasma resistin levels than those that did not. The haplotypes A-G had modestly increased promoter activities compared to the other haplotypes. The EMSA revealed the -420 G allele to be specific for binding of the nuclear proteins from adipocytes and monocytes. However, neither polymorphism was associated with type 2 diabetes or obesity in our study subjects. CONCLUSION: Polymorphisms in the promoter of the resistin gene are major determinants of plasma resistin concentrations in humans
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