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Volume 31(3); May 2007
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Review
Mitochondrial Gene Therapy.
Kyung Soo Ko
Korean Diabetes J. 2007;31(3):187-192.   Published online May 1, 2007
DOI: https://doi.org/10.4093/jkda.2007.31.3.187
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AbstractAbstract PDF
Mitochondrial dysfunction contributes to a large variety of human disorders, ranging from neurodegenerative and neuromuscular diseases, obesity, and diabetes to ischemia-reperfusion injury and cancer. Increasing pharmacological efforts toward therapeutic interventions have been made leading to the emergence of 'Mitochondrial Medicine' as a new field of biomedical research. The identification of molecular mitochondrial drugs targets in combination with the development of methods for selectively delivering biologically active molecules to the site of mitochondria will eventually launch a multitude of new therapies for the treatment of mitochondria-related diseases, which are based either on the selective protection, repair, or eradication of cells. Yet, while tremendous efforts are being undertaken to identify new mitochondrial drugs and drug targets, the development of mitochondria-specific drug carrier systems is lagging behind. To ensure a high efficiency of current and future mitochondrial therapeutics, delivery systems need to be developed, which are able to selectively transport biologically active molecules to and into mitochondria within living cells.
Original Articles
Microarray Analysis of Short Heterodimer Partner (SHP)-induced Changes in Gene Expression in INS-1 Cells.
Eui Dal Jung, Ji Hyun Lee, Won Gu Jang, Jung Guk Kim, Bo Wan Kim, In Kyu Lee
Korean Diabetes J. 2007;31(3):193-199.   Published online May 1, 2007
DOI: https://doi.org/10.4093/jkda.2007.31.3.193
  • 1,765 View
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AbstractAbstract PDF
BACKGROUND
Nuclear receptors are involved in the cell growth, development, differentiation, and metabolism. The orphan nuclear receptor SHP which lacks a DNA-binding domain is a negative regulator of nuclear receptor signaling pathways. In pancreas, SHP regulate transcriptional activity of HNF3 and HNF4 through binding them and BETA2 which is involved in beta cell differentiation and insulin production. Here, we examined transcriptional activity changes of genes expressed in beta cell when SHP was overexpressed. METHOD: INS-1 cells of passage number 24 - 30 were prepared. Affimetrix DNA chip was used to examine gene expression in INS-1 cell when SHP was overexpressed. INS-1 cells were infected with adenovirus-SHP to overexpress SHP. To confirm the result of DNA chip, we used real time RT-PCR. RESULT: When SHP was overexpressed by adenovirus-SHP transfection, FXR, Transforming growth factor, beta 2, fructose-1,6-bisphosphatase 2, bone morphogenetic protein 4 genes expression were increased. Contrarily, Activating transcription factor 2, Glycogen synthase kinase 3 alpha, Nur 77, fibroblast growth factor 14 genes expression were decreased. We confirmed DNA microarray analysis by real time RT-PCR. FXR, tribbles homolog 3 (Drosophila), fructose-1,6-bisphosphatase 2, CD36 genes expression were increased in real time RT-PCR. Nur 77 and cAMP response element modulator genes expression were decreased in real time RT-PCR. CONCLUSION: we identified several genes which expression are regulated by SHP in pancreas beta cell. These results help to explain how SHP act in the various metabolism of pancreas beta cell.
The Effect of Alpha-lipoic Acid on the Cell Cycle Arrest and Apoptosis in Rat Vascular Smooth Muscle Cells.
Hye Jin Kim, In Kyu Lee, Young Ho Kim, Soon Young Shin, Young Han Lee, Jung Guk Kim, Bo Wan Kim, Hye Soon Kim, Mi Kyoung Kim, Keun Gyu Park, Seong Yeol Ryu
Korean Diabetes J. 2007;31(3):200-207.   Published online May 1, 2007
DOI: https://doi.org/10.4093/jkda.2007.31.3.200
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AbstractAbstract PDF
BACKGROUND
The proliferation of vascular smooth muscle cells (VSMCs) is a hallmark of atheroscelrosis and post-angioplasty restenosis. We previously showed that alpha-lipoic acid (ALA) inhibited neointimal hyperplasia and has potential anti-atherosclerosis effect in rat carotid artery balloon injured model. Here, we investigated whether alpha-lipoic acid inhibited proliferation of cells and induced apoptosis in rat vascular smooth muscle cells. METHODS: VSMCs were treated with ALA under each condition, harvested and protein was extracted. Same amount of protein was loaded into SDS-PAGE and western blot analysis was performed with various cell cycle regulation protein. To examine ALA induce apoptosis in VSMCs, FACS and DNA fragmentation assay were performed. Antioxidant effect of ALA was determined by DCF-DA staining. RESULTS: ALA induced VSMCs cell cycle arrest and induced p21, p27 and p53 proteins. Also ALA induced PTEN expression and AMPK phosphorylation. Increased AMPK phosphorylation reduced Erk-2 phosphorylation and finally arrested cell cycle promotion. The apoptotic effect was also shown by ALA treatment. Also we confirmed that ALA reduced ROS generation in VSMCs. CONCLUSION: The present data suggest that ALA has anti-proliferative effect and arrests cell proliferation. Therefore, ALA may provide new strategies for the prevention of neointimal hyperplasia after angioplasty.
Proliferation and Differentiation of Pancreatic beta Cells in L-type Calcium Channel alpha(1D) Subunit (Ca(v)1.3) Heterozygous Knock Out Mice After Partial Pancreatectomy.
Yoon Hee Choi, Il Hee Yun, Sun Hee Suh, Dong Jun Lim, Jae Hyuung Cho, Hyuk Sang Kwon, Bong Yun Cha, Ho Young Son, Chung Gyu Park, Kun Ho Yoon
Korean Diabetes J. 2007;31(3):208-219.   Published online May 1, 2007
DOI: https://doi.org/10.4093/jkda.2007.31.3.208
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AbstractAbstract PDF
BACKGROUND
S: L-type voltage-dependent calcium channel (LTCC) plays a crucial role in insulin secretion from pancreatic beta cells through Ca2+ influx. In the recent report, LTCC Ca(v)1.3 subtype homozygous knock out mice showed impairment of postnatal pancreatic beta cell development as well as insulin secretion. METHODS: We performed 90% partial pancreatectomy in heterozygous Ca(v)1.3 knock out mice to investigate the effect of partial deficiency of Ca(v)1.3 gene on beta cell regeneration in the adult. Glucose homeostasis, metabolic profiles including serum insulin and lipid levels and morphologic changes of pancreatic islets were studied. RESULTS: 90% Partial pancreatectomy induced glucose intolerance only in the heterozygous knock out mice at 8 weeks after surgery. Distribution of islet size was significantly different between two groups after partial pancreatectomy; median value of islet size of heterozygote was larger than that of wild type (642.8 micrometer2 vs 1459.8 micrometer2, P < 0.01). The frequency of single beta cell unit, considered as a unit of beta cell neogenesis, was much lower in heterozygote than that of wild type (41% vs 23.3%, P < 0.05). CONCLUSION: These data suggest that Ca(v)1.3 gene deficiency is specifically associated with impairment of beta cell regeneration, especially neogensis and eventual glucose intolerance in the 90% partial pancreatectomized mice.
Effects of Troglitazone on the Expression of VEGF and TGF-beta in Cultured Rat Mesangial Cells.
Dong Lim Kim, Nan Hee Kim, Dong Seop Choi
Korean Diabetes J. 2007;31(3):220-229.   Published online May 1, 2007
DOI: https://doi.org/10.4093/jkda.2007.31.3.220
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AbstractAbstract PDF
BACKGROUND
Clinical study reported that troglitazone ameliorated microalbuminuria in diabetic nephropathy. However, the mechanism of action is not fully understood. Vascular endothelial growth factor (VEGF) is known as vascular permeability factor and it is considered the most likely cause of glomerular hyperfiltration and proteinuria in diabetic nephropathy. Transforming growth factor-beta (TGF-beta) is a potent inducer of extracellular matrix production and fibrosis in renal cells and one of the important cytokine in the pathogenesis of diabetic nephropathy. To determine whether troglitazone affects VEGF and TGF-beta production in diabetic nephropathy, we examined the effects of troglitazone on the VEGF and TGF-beta expression in cultured rat mesangial cells exposed to high glucose concentration. METHODS: Rat mesangial cells were cultured in media with D-glucose 5.5 mM (NG) or D-glucose 30 mM (HG), or D-glucose 30 mM/troglitazone 20 micrometer(HTz) and for 6, 24, or 72 hours, respectively. VEGF and TGF-beta expression were assessed by semiquantitative RT-PCR and western blot analysis. RESULTS: Troglitazone decreased the VEGF164 and VEGF120 mRNA expressions in cultured rat mesangial cells exposed to high glucose concentration with incubation for 24 and 72 hours, respectively. VEGF protein was also decreased in experimental group treated with troglitazone (HTz) than in those with HG for 24 and 72 hours. However troglitazone had no effect on the expression of TGF-beta mRNA in mesangial cells. CONCLUSION: This study suggested that troglitazone may modulate the development and progression of diabetic nephropathy by reducing the expression of VEGF in mesangial cells
Effects of Lovastatin on Free Fatty Acid Oxidation in Cultured L6 Rat Skeletal Muscle Cells.
Dong Lim Kim, Kee Ho Song, Hae Rim Kim, Suk Kyeong Kim
Korean Diabetes J. 2007;31(3):230-235.   Published online May 1, 2007
DOI: https://doi.org/10.4093/jkda.2007.31.3.230
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  • 1 Crossref
AbstractAbstract PDF
BACKGROUND
Recent clinical studies suggest that statins improve insulin resistance and glucose metabolism in patients with metabolic syndrome and type 2 diabetes. To evaluate the possible mechanism of this action, we measured free fatty acid oxidation in cultured L6 rat skeletal muscle cell line. METHODS: Cultured L6 myotubes were treated with or without lovastatin (1, 5, 20 micrometer) for 24 hours or 48 hours and palmitate oxidation was measured. We also measured protein concentration of the cells. RESULTS: Lovastain increased palmitate oxidation in dose and time dependent manner in L6 myotubes (24 hr; 1 micrometer 119.2 +/- 11.9% of control, 5 micrometer 140.9 +/- 8.1%, 20 micrometer 150 +/- 5%, P = 0.05 vs control, respectively, 48 hr 1 micrometer 120.9 +/- 14.5%, 5 micrometer 176.6 +/- 28.2%, 20 micrometer 196.0 +/- 19.9%, P < 0.01 vs control, respectively). However, lovastatin decreased total cellular protein (24 hr: 1 micrometer 89.2 +/- 6.1% of control, 5 micrometer 79.3 +/- 7.6%, 20 micrometer 65.4 +/- 4.2%, P = 0.05 vs control, respectively, 48 hr: 1 micrometer 81.7 +/- 5.1%, 5 micrometer 58.6 +/- 11.9%, 20 micrometer 48.1 +/- 6.9%, P < 0.01 vs control, respectively). CONCLUSION: Lovastatin increased skeletal muscle free fatty acid oxidation in L6 rat skeletal muscle cells. This would be one of the mechanisms which lovastatin improves insulin resistance.

Citations

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  • Characterization and Mechanisms of Action of Avocado Extract Enriched in Mannoheptulose as a Candidate Calorie Restriction Mimetic
    Donald K. Ingram, Paul J. Pistell, Zhong Q. Wang, Yongmei Yu, Stefan Massimino, Gary M. Davenport, Michael Hayek, George S. Roth
    Journal of Agricultural and Food Chemistry.2021; 69(26): 7367.     CrossRef
Differentiation of Pancreatic beta Cells from Human Pancreatic Duct Cells Derived from a Partial Pancreas Tissue.
Ki Ho Song, Myung Mee Kim, Min Kyung Lee, Gyeong Ryul Ryu, Seung Hyun Ko, Sung Dae Moon, Yu Bae Ahn, Kun Ho Yoon, Bong Yun Cha, Kwang Woo Lee, Ho Young Son, Sung Koo Kang, Hyung Min Chin
Korean Diabetes J. 2007;31(3):236-242.   Published online May 1, 2007
DOI: https://doi.org/10.4093/jkda.2007.31.3.236
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  • 1 Crossref
AbstractAbstract PDF
BACKGROUND
Despite a recent breakthrough in human islet transplantation for treating diabetes mellitus, the limited availability of insulin-producing tissue is still a major obstacle. This has led to a search for alternative sources of transplantable insulin-producing cells including pancreatic duct cells. We aimed to establish in vitro culture of pancreatic duct cells from a partial pancreas tissue in human, which could be harnessed to differentiate into pancreatic beta cells. METHODS: We isolated pancreatic duct cells from small pieces of pancreas tissue (1~3 g) derived from non-diabetic humans (n = 8) undergoing pancreatic surgery due to cancer. Pancreas tissue was finely minced after injection of collagenase P into the parenchyma. The mince was incubated in a shaking water bath at 37degrees C for 25 min and passed through a 150 micrometer mesh. The released cells were recovered, washed, and plated in a dish containing CMRL culture medium with serum. RESULTS: Isolated pancreatic cells grew in monolayer and became confluent in 1~2 wks showing typical epithelial cobblestone morphology. Immunochemistry demonstrated that ~90% of the cultured cells were cytokeratin7-positive duct cells. To induce beta cell differentiation, the cells were incubated in DMEM/F12 culture medium without serum. In addition, treatment with Matrigel overlay, exendin-4, cholera toxin or forskolin was done. Though beta cell differentiation was found by immunostaining and RT-PCR, the differentiation efficiency was very low. Over-expression of neurogenin-3 by recombinant adenovirus did not increase beta cell differentiation of the cultured duct cells significantly. CONCLUSION: We established in vitro culture of pancreatic duct cells from a partial pancreas tissue in human, which differentiate into pancreatic cells. However, a strategy to optimize beta cell differentiation in this model is needed.

Citations

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  • Transdifferentiation of Enteroendocrine K-cells into Insulin-expressing Cells
    Esder Lee, Jun Mo Yu, Min Kyung Lee, Gyeong Ryul Ryu, Seung-Hyun Ko, Yu-Bae Ahn, Sung-Dae Moon, Ki-Ho Song
    Korean Diabetes Journal.2009; 33(6): 475.     CrossRef
The Differences of Circulating Adiponectin Levels and Multimerization According to Obesity in Type 2 Diabetes Mellitus of Men.
Sang Ah Chang, Ho Young Son, Jung Min Lee, Tae Seo Sohn, Hyuk Sang Kwon, Hyun Shik Son, Kun Ho Yoon, Hee Seung Kim, Bong Yun Cha, Kwang Woo Lee
Korean Diabetes J. 2007;31(3):243-252.   Published online May 1, 2007
DOI: https://doi.org/10.4093/jkda.2007.31.3.243
  • 1,764 View
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AbstractAbstract PDF
BACKGROUND
Adiponectin is adipose tissue derived hormone, which has been shown to play an important role in the regulation of glucose and lipid metabolism. Low adiponectin levels are associated with obesity and diabetes and coronary artery disease. In addition to adiponectin level, the adiponectin multimerization and its ratio to total adiponectin have also affect on metabolic risk factors and insulin resistance. However, the adiponectin multimerization pattern in type 2 diabetes of Korean has not been established. We investigated adiponectin levels and adiponectin multimerization pattern according to obesity in type 2 diabetes males of Korean. METHOD: The subjects of this study were 86 of diabetes patients and 89 of control subjects whose fasting blood glucose was below 110 mg/dL. They were divided into two subgroup, non-obese and obese, according to BMI (non-obese 25 < BMI). Anthropometric parameter and other metabolic risk factors were measured. Insulin resistance was presented by HOMA-IR. Plasma adiponectin level was measured by radioimmunoassay method. Adiponectin multimerization was fractionated by SDS-PAGE under non-reducing and non-heat denaturing state and performed immunoblotting. RESULT: Serum adiponectin levels were significantly reduced in obese than non obese group in diabetes patients (7.73 +/- 5.2 versus 12.56 +/- 8 microgram/mL, P = 0.003). Correlational analyses demonstrated that BMI, body weight, waist circumference, diastolic pressure, glucose and height correlated significantly with adiponectin levels in the diabetes patients. The HOMA-IR did not affect the plasma adiponectin levels in diabetic patients. There were no differences in adiponectin multimerization distribution and ratio between obese and non-obese group in the diabetes, however middle molecular weight multimers (MMW, ~110~160 Kda, hexamer) ratio in the control subjects were significantly reduced in obese group than non-obese group (49 +/- 9 versus 56 +/- 11%, P < 0.05). CONCLUSION: The adipoenctin levels were lower in obese than non-obese group of diabetes males in Korea. Aiponectin levels correlated with BMI and weight but not insulin resistance. The differences of adiponectin multimerization distribution and ratio between obese and non-obese group in diabetes were not detected.
Alcohol Consumption, Liver Enzymes, and Prevalence of Metabolic Syndrome in Korean Adult Men.
Soo Min Nam, Ho Yeol Yu, Mi Young Lee, Jang Hyun Koh, Jang Yel Shin, Young Goo Shin, Choon Hee Chung
Korean Diabetes J. 2007;31(3):253-260.   Published online May 1, 2007
DOI: https://doi.org/10.4093/jkda.2007.31.3.253
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  • 8 Crossref
AbstractAbstract PDF
BACKGROUND
Metabolic syndrome is associated with an increasing incidence of diabetes and cardiovascular disease. The relationship between the amount of alcohol consumption and the prevalence of metabolic syndrome is controversial. Our study was performed to evaluate the relationship between alcohol consumption and the prevalence of metabolic syndrome in Korean men. Also we examined the correlation of liver markers, including alanine transaminase (ALT) and gamma-glutamyl transferase (GGT) with the development of metabolic syndrome. METHODS: We enrolled 1,775 Korean men (mean age 40.0 +/- 5.8 years) who were undergone health check-ups in our hospital. Each component of metabolic syndrome was measured by using the American Association of Clinical Endocrinologists (AACE) criteria. The subjects were divided into 4 subgroups according to the amount of alcohol consumption; Group 1: no consumption, 2 (mild): those consumed less than 200 g/week, 3 (moderate): those consumed 200~399 g/week, 4 (heavy): those consumed more than 400 g/week. RESULTS: The prevalence of metabolic syndrome was 24.6%. There were significant positive correlations between the amount of alcohol consumption blood pressure, triglyceride, fasting blood glucose, GGT levels and HDL cholesterol levels. But the odds ratios for metabolic syndrome were not significantly increased in subjects with moderate alcohol consumption. The odds ratios for the metabolic syndrome significantly increased in proportion to the increasing levels of ALT and GGT. CONCLUSION: Although alcohol consumption didn't increase the prevalence of metabolic syndrome, the amount of alcohol consumption had significant positive correlation with components of metabolic syndrome in Korean men, and elevated ALT and GGT levels could strongly associate with the prevalence of metabolic syndrome.

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  • Association of Seaweed Consumption with Metabolic Syndrome and Its Components: Findings from the Korean Genome and Epidemiology Study
    Haeun Park, Kyung Won Lee, Dayeon Shin
    Foods.2022; 11(11): 1635.     CrossRef
  • Association between Amount of Alcohol Consumption and Serum Fasting Glucose Level in Korean Male in their 40s and 50s: The Seventh Korea National Health and Nutrition Examination Survey 2016-2018
    Jihyun Kim
    Korean Journal of Family Practice.2022; 12(5): 320.     CrossRef
  • The association of dietary patterns with insulin resistance in Korean adults: based on the 2015 Korea National Health and Nutrition Examination Survey
    I Seul Kim, Yoon Jung Yang
    Journal of Nutrition and Health.2021; 54(3): 247.     CrossRef
  • Resting Heart Rate, QTc Interval, and Laboratory Variables in Relation to Risk Factors of Metabolic Syndrome in Korean Adult Male
    Chul-Gyu Kim, Sun Kyung Cha
    Journal of Health Informatics and Statistics.2017; 42(4): 322.     CrossRef
  • An Investigation on the Metabolic Syndromes and Health-Related Risk Factors among Male Workers
    Sun-Young Choi, Na-Eun Kang, Sung-Hee Kim
    The Korean Journal of Food And Nutrition.2013; 26(4): 975.     CrossRef
  • The Association of Metabolic Syndrome and Serum γ-Glutamyl Transpeptidase: A 4-Year Cohort Study of 3,698 Korean Male Workers
    Jung Hyun Lee, Mi Hyang Um, Yoo Kyoung Park
    Clinical Nutrition Research.2013; 2(1): 67.     CrossRef
  • The incidence of metabolic syndrome and its risk factor in who under went medical check-up in a health promotion center
    Hae-Kyung Cheon, Tae-Yong Lee, In-Sun Kwon
    Journal of the Korea Academia-Industrial cooperation Society.2012; 13(3): 1186.     CrossRef
  • Metabolic Syndrome and Serum Alanine Aminotransferase Levels in Korean Adults : The Third Korea National Health and Nutrition Examination Survey (KNHANES III), 2005.
    Mi Ah Han, So Yeon Ryu, Jong Park, Myung Geun Kang, Ki Soon Kim
    Korean Journal of Epidemiology.2008; 30(1): 25.     CrossRef
Activation of NF-kappaB and AP-1 in Peripheral Blood Mononuclear Cells Isolated from Patients with Diabetic Nephropathy.
Jisun Nam, Min Ho Cho, Jong Suk Park, Geun Taek Lee, Hai Jin Kim, Eun Seok Kang, Yu Mie Lee, Chul Woo Ahn, Bong Soo Cha, Eun Jig Lee, Sung Kil Lim, Kyung Rae Kim, Hun Joo Ha, Hyun Chul Lee
Korean Diabetes J. 2007;31(3):261-273.   Published online May 1, 2007
DOI: https://doi.org/10.4093/jkda.2007.31.3.261
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AbstractAbstract PDF
BACKGROUND
We evaluated the role of oxidative stress in diabetic nephropathy by measuring intracellular reactive oxygen species (ROS) and redox-sensitive transcription factors in isolated peripheral mononuclear cells (PBMC). METHODS: From 66 diabetic patients with or without diabetic nephropathy (Group III and II, respectively) and 49 normal control subjects (Group I), spontaneous and stimulated ROS levels, activities of nuclear factor-kappa B (NF-kappaB), activator protein-1 (AP-1), and specificity protein1 (Sp1) in PBMC, urinary and PBMC TGF-beta1 (transforming growth factor-beta1), and 24-hour urinary albumin excretion (UAE) were measured. RESULTS: Spontaneous ROS was significantly higher in group III and II than group I (60.7 +/- 3.3 vs. 60.0 +/- 3.0 vs. 41.1 +/- 2.4%, respectively), and stimulated ROS were significantly higher in Group III compared to Group II (Increment of H2O2-induced ROS production: 21.8 +/- 2.2 vs. 11.1 +/- 2.0%, respectively; increment of PMA-induced ROS production 23.5 +/- 4.5 vs. 21.6 +/- 2.2%, respectively). The activities of NF-kappaB and AP-1, but not of Sp1, were significantly higher in Group III than in Group II (2.53 vs. 2.0 vs. 1.43-fold, respectively). Both PBMC- and urinary TGF-beta1 levels were higher in Group III than Group II (3.23 +/- 0.39 vs. 1.99 +/- 0.68 ng/mg in PBMCs, 16.88 +/- 6.84 vs. 5.61 +/- 1.57 ng/mL in urine, both respectively), and they were significantly correlated with activities of NF-kappaB and AP-1 and 24-hour UAE. CONCLUSIONS: Increased intracellular ROS generation in PBMCs of diabetic patients is involved in the pathogenesis of diabetic nephropathy through activation of NF-kappaB and AP-1, but not Sp1, and increased expression of TGF-beta1.
The Association of Aldose Reductase Gene Polymorphisms with Neuropathy in Patients with Type 2 Diabetes.
In Kyong Jeong, Kyong Soo Park, Min Kyong Moon, Jae Hyeon Kim, Chan Soo Shin, Seong Yeon Kim, Hong Kyu Lee
Korean Diabetes J. 2007;31(3):274-283.   Published online May 1, 2007
DOI: https://doi.org/10.4093/jkda.2007.31.3.274
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  • 1 Crossref
AbstractAbstract PDF
BACKGROUND
Previous studies have suggested that polymorphisms in and around the aldose reductase (AR) gene are associated with the development of diabetic microvascular disease. This study explored the hypothesis that the polymorphisms of the (A-C)n dinucleotide repeat sequence, located at 2.1 kilobase (kb) upstream of the transcription start site of AR gene, modulate the risk of diabetic neuropathy (DN). METHODS: 66 patients with DN, 30 without microvascular complications (MC) after 20 years of diabetes, and 87 normal healthy controls were studied. To test highly polymorphic microsatellite marker 2.1 kb upstream of the initiation site of the AR gene, we performed polymerase chain reaction using the primer labeled with fluorescent dye and GeneScan by ABI prism 377 automated DNA sequencer and ABI Genotyper software 2.0. RESULTS: Seven alleles (Z-6, Z-4, Z-2, Z, Z+2, Z+4 and Z+6) were identified. Z-2 allele was more frequently observed in patients with DN (77.3%) than in those without MC (43.3%, P = 0.007). The subgroup of patients who developed DN within 5 years after the diagnosis of diabetes also had higher frequency of Z-2 allele (91.7%) compared to those without MC (43.3%, P = 0.028). On the contrary, Z+6 allele tended to be more frequent in patients without MC (10.0%) than in those with DN (0%, P = 0.063). CONCLUSION: These results support the hypothesis that environmental-genetic interactions may modulate the risk of neuropathy in patients with diabetes. Particularly, the Z-2 allele, in the presence of diabetes, may be associated with the development of DN.

Citations

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  • The Association between Serum GGT Concentration and Diabetic Peripheral Polyneuropathy in Type 2 Diabetic Patients
    Ho Chan Cho
    Korean Diabetes Journal.2010; 34(2): 111.     CrossRef
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
  • 2,061 View
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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.

Citations

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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
Case Report
A Case of Ketosis-Prone Type 2 Diabetes Mellitus.
Dong Lim Kim, Suk Kyeong Kim, Kee Ho Song
Korean Diabetes J. 2007;31(3):293-296.   Published online May 1, 2007
DOI: https://doi.org/10.4093/jkda.2007.31.3.293
  • 1,858 View
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  • 1 Crossref
AbstractAbstract PDF
Ketosis-prone type 2 diabetes (KPD) has been characterized as diabetes with severe insulin deficiency at diagnosis associated with ketosis or ketoacidosis without a precipitating cause. Improvement in beta-cell function and insulin sensitivity by aggressive diabetic management could allow discontinuation of insulin therapy within a few month of therapy. These subjects are usually obese, have a strong family history of diabetes, absence of beta-cell autoimmune markers and lack of human leukocyte antigen genetic association. This clinical presentation has been reported primarily in African and African Americans, but rare in Asian and white person. We recently experienced a case of KPD in Korea and present it with literature review.

Citations

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  • A Case of Autoantibody-Positive Ketosis-Prone Diabetes Mellitus
    Bora Yoon, Gyuri Kim, Jae Hyun Bae, Yu Jung Yun, Yong Ho Lee, Byung Wan Lee, Chul Woo Ahn, Bong Soo Cha, Hyun Chul Lee, Eun Seok Kang
    The Journal of Korean Diabetes.2016; 17(1): 60.     CrossRef

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