Diabetes & Metabolism Journal

Hong Kyu Lee (Lee HK)

57 Articles

Effect of Adipose Differentiation-Related Protein (ADRP) on Glucose Uptake of Skeletal Muscle.: Yun Hyi Ku, Min Kim, Sena Kim, Ho Seon Park, Han Jong Kim, In Kyu Lee, Dong Hoon Shin, Sung Soo Chung, Sang Gyu Park, Young Min Cho, Hong Kyu Lee, Kyong Soo Park; Korean Diabetes J. 2009;33(3):206-214. Published online June 1, 2009; DOI: https://doi.org/10.4093/kdj.2009.33.3.206

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Abstract PDF: BACKGROUND
Skeletal muscle is the most important tissue contributing to insulin resistance. Several studies have shown that accumulation of intramyocellular lipid is associated with the development of insulin resistance. Thus, proteins involved in lipid transport, storage and metabolism might also be involved in insulin action in skeletal muscle. Adipose differentiation-related protein (ADRP), which is localized at the surface of lipid droplets, is known to be regulated by peroxisome proliferator activated receptor gamma (PPARgamma). However, it is not known whether ADRP plays a role in regulating glucose uptake and insulin action in skeletal muscle. METHODS: ADRP expression in skeletal muscle was measured by RT-PCR and western blot in db/db mice with and without PPARgamma agonist. The effect of PPARgamma agonist or high lipid concentration (0.4% intralipos) on ADRP expression was also obtained in cultured human skeletal muscle cells. Glucose uptake was measured when ADRP was down-regulated with siRNA or when ADRP was overexpressed with adenovirus. RESULTS: ADRP expression increased in the skeletal muscle of db/db mice in comparison with normal controls and tended to increase with the treatment of PPARgamma agonist. In cultured human skeletal muscle cells, the treatment of PPARgamma agonist or high lipid concentration increased ADRP expression. siADRP treatment decreased both basal and insulin-stimulated glucose uptake whereas ADRP overexpression increased glucose uptake in cultured human skeletal muscle cells. CONCLUSION: ADRP expression in skeletal muscle is increased by PPARgamma agonist or exposure to high lipid concentration. In these conditions, increased ADRP contributed to increase glucose uptake. These results suggest that insulin-sensitizing effects of PPARgamma are at least partially achieved by the increase of ADRP expression, and ADRP has a protective effect against intramyocellular lipid-induced insulin resistance.

Prevalence and Clinical Characteristics of Aspirin Resistance in the Patients with Type 2 Diabetes Mellitus.: Mi Yeon Kang, Young Min Cho, Hyun Kyung Kim, Jee Hyun An, Hwa Young Ahn, Ji Won Yoon, Hoon Sung Choi, Jie Seon Lee, Kyong Soo Park, Seong Yeon Kim, Hong Kyu Lee; Korean Diabetes J. 2008;32(1):53-59. Published online February 1, 2008; DOI: https://doi.org/10.4093/kdj.2008.32.1.53

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BACKGROUND
We examined the prevalence and clinical characteristics of aspirin resistance in the Korean patients with type 2 diabetes mellitus. METHODS: We studied 181 Korean patients with type 2 diabetes mellitus who were taking aspirin (100 mg/day for > or = 3 months) and no other antiplatelet agents. The VerifyNow System was used to determine aspirin responsiveness. Aspirin resistance was defined as an aspirin reaction unit (ARU) > or = 550. We measured the cardio-ankle vascular index (CAVI) and ankle-brachial index (ABI) to evaluate arteriosclerosis. The anthropometric parameters, electrocardiogram, blood pressure, fasting plasma glucose, lipid profiles, hemoglobin A1c, highly sensitive C-reactive protein (hsCRP), homocysteine, and microalbuminuria were measured in each patient. RESULTS: The prevalence of aspirin resistance in type 2 diabetic patients was 9.4% (17 of 181). Those who had aspirin resistance were older than those without aspirin resistance (64.6 +/- 10.6 vs. 59.8 +/- 8.1, P = 0.024). Aspirin resistance was not associated with fasting plasma glucose, total cholesterol, triglyceride, LDL-cholesterol, HDL-cholesterol, hemoglobin A1c, hsCRP, homocysteine, microalbuminuria, ABI, CAVI, and body mass index. CONCLUSION: Prevalence of aspirin resistance in the Korean patients with type 2 diabetes mellitus was 9.4%. Although aspirin resistance was associated with old age, we could not find any good clinical parameter to predict it. Therefore, aspirin resistance should be evaluated in diabetic patients taking aspirin for prevention of cardiovascular complications.

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Long Non-Coding RNA H19 Positively Associates With Aspirin Resistance in the Patients of Cerebral Ischemic Stroke
Jue Wang, Bin Cao, Yan Gao, Dong Han, Haiping Zhao, Yuhua Chen, Yumin Luo, Juan Feng, Yanxia Guo
Frontiers in Pharmacology.2020;[Epub] CrossRef
6^th Asian PAD Workshop

Annals of Vascular Diseases.2015; 8(2): 135. CrossRef
Non-HDL cholesterol is an independent risk factor for aspirin resistance in obese patients with type 2 diabetes
Jong Dai Kim, Cheol-Young Park, Kue Jeong Ahn, Jae Hyoung Cho, Kyung Mook Choi, Jun Goo Kang, Jae Hyeon Kim, Ki Young Lee, Byung Wan Lee, Ji Oh Mok, Min Kyong Moon, Joong Yeol Park, Sung Woo Park
Atherosclerosis.2014; 234(1): 146. CrossRef

Two Cases of Autoantibody Negative Fulminant Type 1 Diabetes Mellitus.: Hwa Young Cho, Young Min Cho, Myoung Hee Park, Mi Yeon Kang, Ki Hwan Kim, Yun Hyi Ku, Eun Kyung Lee, Do Joon Park, Chan Soo Shin, Kyong Soo Park, Seong Yeon Kim, Bo Youn Cho, Hong Kyu Lee; Korean Diabetes J. 2007;31(4):372-376. Published online July 1, 2007; DOI: https://doi.org/10.4093/jkda.2007.31.4.372

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Abstract PDF: Autoantibody negative fulminant type 1 diabetes mellitus is a novel subtype of type 1 diabetes, which is characterized by a remarkably abrupt onset, metabolic derangement such as diabetic ketoacidosis at diagnosis, low HbA1c level at onset and a negative islet-related autoantibodies. The prevalence of fulminant type 1 diabetes has large difference between Japan and other countries. The precise reason for this regional variation remains to be clarified. One of the possible explanations is genetic background such as genotype of class II HLA molecule. In addition, environment factors including viral infection are suggested as possible pathogenesis of the disease. Only a few cases with fulminant type 1 diabetes have been reported outside Japan, and most of these cases with definite diagnosis have been reported in Korea. We report here on two Korean patients that met the criteria for diagnosis of fulminant type 1 diabetes in accordance with their HLA genotypes.

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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Abstract 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.

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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

Retraction: Polymorphisms of Kir6.2 Gene are Associated with Type 2 Diabetes and Blood Pressure in the Korean Population.: Bo Kyeong Koo, Hong Il Kim, Eu Jin Lee, Young Min Cho, Hyoung Doo Shin, Hak Chul Jang, Hong Kyu Lee, Kyong Soo Park; Korean Diabetes J. 2007;31(2):185-185. Published online March 1, 2007; 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.: Bo Kyeong Koo, Hong Il Kim, Eu Jin Lee, Young Min Cho, Hyoung Doo Shin, Hak Chul Jang, Hong Kyu Lee, Kyong Soo Park; Korean Diabetes J. 2005;29(5):440-450. Published online September 1, 2005

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Abstract PDF: 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-.: Soo Lim, Eun Jung Lee, Bo Kyeong Koo, Sung Il Cho, Kyong Soo Park, Hak Chul Jang, Seong Yeon Kim, Hong Kyu Lee; Korean Diabetes J. 2005;29(5):432-439. Published online September 1, 2005

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Abstract PDF: 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.

Glutathion S-Transferase M1 Gene Polymorphism is Associated with Type 2 Diabetic Nephropathy.: Jae Hyeon Kim, Min Kyong Moon, Sang Wan Kim, Hyoung Doo Shin, Young Hwan Hwang, Curie Ahn, Hak Cheol Jang, Kyong Soo Park, Seong Yeon Kim, Hong Kyu Lee; Korean Diabetes J. 2005;29(4):315-321. Published online July 1, 2005

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Abstract PDF: BACKGROUND
Oxidative stress may be a determinant of the development of diabetic nephropathy. Glutathione S-transferases(GST) can work as an endogenous antioxidant to protect cells from oxidative stress. Homozygous deletion of the mu and theta subclasses of GST(GST-M1 and GST-T1), and Val105Ile polymorphism of the pi subclass of GST(GST-P1) are associated with antioxidant enzyme activity. In this study, whether the Val105Ile of GST-P1, null genotype of GST-M1 and GST-T1 are associated with type 2 diabetic nephropathy were examined. METHODS: These GST subclasses were genotyped in 361 type 2 diabetic patients with retinopathy; the subjects were divided into two groups, those with an end stage renal disease(ESRD)(the case group n=177) and those(the control group, n=184) showing no signs of renal involvement. RESULTS: The frequencies of the GST-P1 Ile105Val and GST-T1 null genotypes were no different between the cases and controls. However, the frequency of the GST-M1 null genotype was significantly higher in the cases than the controls(61.7% vs. 51.1%, chi-square=4.09, P=0.043), which was still significant after correction for age, sex and duration of diabetes (P= 0.044). In addition, the GST-M1 null genotype showed an increased frequency between the controls and the cases with long and short durations of type 2 diabetes until the onset of ESRD(51.1, 58.9 and 65.5%, respectively; chi-square for trend=5.12, P=0.024). CONCLUSION: This is the first study to suggest that the GST-M1 gene polymorphism might contribute to the development of ESRD in type 2 diabetic patients.

Pregnancy Outcome in Korean Women with Gestational Diabetes Mellitus Diagnosed by the Carpenter-Coustan Criteria.: Hak Chul Jang, Young Min Cho, Kyong Soo Park, Seong Yeon Kim, Hong Kyu Lee, Moon Young Kim, Jae Hyug Yang, Son Moon Shin; Korean Diabetes J. 2004;28(2):122-130. Published online April 1, 2004

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Abstract PDF: BACKGROUND
The American Diabetes Association recently proposed the Carpenter-Coustan criteria for the diagnosis of gestational diabetes mellitus(GDM) based on the results of the Toronto Tri-Hospital Study. The prevalence of GDM in Korean women increased, on average, by 60% when the Carpenter-Coustan criteria were applied. However, the pregnancy outcome of Korean women with GDM with regard to the Carpenter-Coustan criteria tremains to be reported. The pregnancy outcomes of those Korean women with GDM by the Carpenter- Coustan criteria, but not by the NDDG criteria were assessed. METHODS: In this study, a total of 2776 pregnant women underwent universal screening for GDM, between January 1993 and December 1994, as recommended by the Third International Workshop-Conference on Gestational Diabetes Mellitus with minor modifications. The primary pregnancy outcomes were preeclampsia, premature delivery, delivery by C-section, birth weight and LGA infants. RESULTS: Of the 2776 women, 656 screened-positive for GDM. Of these, 37 and 74 had GDM by the Carpenter-Coustan and NDDG criteria, respectively. With increasing glucose intolerance, there was a stepwise increase in premature deliveries, deliveries by C-section and preeclampsia from those screening negative to GDM by the NDDG criteria, with a similar trend for the frequency of LGA infants. The LGA infant screening-negative and positive were 13.5 and 16.1%, but those with a normal glucose tolerance were 27.0 and 33.8% in those screening positive to GDM by the Carpenter-Coustan and NDDG criteria, respectively(P<0.001). CONCLUSION: Our study demonstrated that increasing glucose tolerance was associated with increasing frequencies of adverse pregnancy outcomes in Korean women. The maternally complicated and LGA infants were significantly higher in women with GDM by the Carpenter-Coustan criteria. Thus the Carpenter- Coustan criteria are recommended for the diagnosis of GDM in Korean Women.

Common Genetic Polymorphisms in the Promoter of Resistin Gene are Major Determinants of Plasma Resistin Concentrations in Humans.: 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; Korean Diabetes J. 2004;28(1):9-19. Published online February 1, 2004

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Abstract PDF: 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

The Effects of Insulin Sensitizers on the Plasma Concentrations of Adipokines in Type 2 Diabetic Patients.: Hye Seung Jung, Young Min Cho, Kyung Won Kim, Byung Soo Youn, Kang Yeol Yu, Hong Je Park, Chan Soo Shin, Seong Yeon Kim, Hong Kyu Lee, Kyong Soo Park; Korean Diabetes J. 2003;27(6):476-489. Published online December 1, 2003

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Abstract PDF: BACKGROUND
Resistin, leptin and adiponectin are proteins secreted from adipose tissue, and have been suggested to play roles in insulin sensitivity. The effects of the circulating levels of two different types of insulin sensitizer, rosiglitazone and metformin, in type 2 diabetic patients were examined to elucidate the relationship between adipokines and insulin resistance. METHODS: Thirty type 2 diabetic patients, who showed poor glycemic control when administered 4 mg glimepiride a day, without severe diabetic complications or medical illness, were randomized to receive an additional 4mg rosiglitazone or 1000 mg metformin a day. The plasma resistin, leptin and adiponectin concentrations were measured at the baseline and after 6 months of treatment. The anthropometric parameters, fasting plasma glucose, HbA1C, total cholesterol, triglyceride, HDL-cholesterol and free fatty acids were also measured. Certain single nucleotide polymorphisms of adipokine genes were also identified. RESULTS: There were no significant differences in the reductions of the plasma glucose and HbA1C levels, after 6 months of treatment, between the two groups. The plasma resistin concentrations decreased, the adiponectin significantly increased and the leptin showed a tendency to increase in the rosiglitazone group. In the metformin group, only the resistin concentration significantly increased. However, the changes in the adipokines did not correlate with the HOMA-IR in either group. The reduction in the HbA1C due to rosiglitazone was greater if the initial leptin level was high, if there was a G allele on the -420th locus of the resistin gene, or the 45th locus of the APM1 (adiponectin gene) was the T-homozygote or there was a T allele on the 276th locus of the APM1. Those due to metfromin were greater with high initial adiponectin levels. CONCLUSION: In type 2 diabetic patients, showing poor glycemic control with sulfonylurea therapy, rosiglitazone or metformin treatment changed some of the adipokine concentrations, but these changes were not clearly related with insulin resistance. Polymorphisms of certain adipokine genes seem to have a relation to the susceptibility of rosiglitazone.

Genetic Association of Adiponectin Polymorphisms with Risk of Type 2 Diabetes Mellitus.: Yun Yong Lee, Nam Seok Lee, Young Min Cho, Min Kyong Moon, Hye Seung Jung, Young Joo Park, Hong Je Park, Byoung Soo Youn, Hong Kyu Lee, Kyong Soo Park, Hyoung Doo Shin; Korean Diabetes J. 2003;27(6):438-448. Published online December 1, 2003

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Abstract PDF: BACKGROUND
Adiponectin, an adipocyte-secreted protein, is known to modulate insulin sensitivity, glucose homeostasis and the development of atherosclerosis. Recently, several single nucleotide polymorphisms (SNPs) in the adiponectin gene have been reported to be associated with type 2 diabetes and components of the insulin resistance syndrome. METHODS: The frequencies of SNP T45G and G276T of the adiponectin gene was examined in 493 unrelated type 2 diabetic and 136 non-diabetic control Korean subjects. The clinical characteristics and plasma adiponectin levels of the subjects were compared within these genotypes. RESULTS: The T allele at SNP45 was significantly more frequent in the type 2 diabetes than in the control subjects (71.6 vs. 64.3%, p=0.013). The subjects with the G/G genotype of SNP45 were at reduced risk for type 2 diabetes (OR: 0.495, 95% CI 0.246-0.995, p=0.048) compared with those having the T/T genotype. However, there were no statistically significant differences in allele the frequencies (G frequency in the control vs. the diabetic group 73.9 vs. 68.9%, p=0.106) and genotype frequencies at SNP276 between groups. The subjects with the T/T genotype at SNP45 had higher a body mass index (24.6+/- 3.1 vs. 24.1+/-2.8 kg/m2, p=0.036) and serum triglyceride levels (2.03+/-1.31 vs. 1.87+/-1.38 mmol/1, p=0.041) than the T/G+G/G genotypes in the diabetic group. Those with the T/T genotype also had lower plasma adiponectin levels than those without T/T genotype at SNP45 in the control group (6.11+/-3.10 vs. 8.24+/-4.24 g/mL, p=0.043). There was a similar trend in diabetic group, but this did not reach statistical significance (4.32+/-2.81 vs. 4.96+/-3.26 g/mL, p=0.097). The SNP276 had no association with the clinical features of insulin resistance or plasma adiponectin level. CONCLUSION: The T/T genotype of SNP45 in the adiponectin gene was associated with a low adiponectin level, high body mass index, the serum triglyceride level and risk of type 2 diabetes mellitus. The SNP276 in the adiponectin gene may not be an important determinant of insulin resistance or type 2 diabetes in Korean subjects.

Plasminogen Activator Inhibitor-1 (PAI-1)/tissue Plasminogen Activator (t-PA) Levels and PAI-1 4G/5G Promoter Polymorphism in Type 2 Diabetes with Microalbuminuria.: Seong Hee Kwon, Young Joo Park, In Kyong Jeong, Jae Joon Koh, Kyong Soo Park, Seong Yeon Kim, Hong Kyu Lee; Korean Diabetes J. 2003;27(3):186-198. Published online June 1, 2003

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Abstract PDF: BACKGROUND
Persistent microalbuminuria in diabetic patients is a risk factor of cardiovascular mortality. Increased plasma plasminogen activator inhibitor type-1 (PAI-1) levels have been observed in diabetic patients with overt nephropathy. However, there have been few studies on diabetic patients with microalbuminuria. The expression of PAI-1 may be influenced by the polymorphism of the PAI-1 genotype promoter. The aim of this study was to investigate the relationship between the plasma PAI-1/t-PA levels, polymorphism of the PAI-1 4G/5G promoter and microalbuminuria in type 2 diabetes. METHODS: The plasma PAI-1/t-PA levels and polymorphisms of the PAI-1 promoter were measured in type 2 diabetic patients without nephropathy (n=30), and with microalbuminuria (n=30) and overt proteinuria (n=20). The correlation between the amount of urinary albumin excretion and plasma PAI-1/t-PA levels were investigated using Pearson's correlation analyses. RESULTS: The plasma PAI-1/t-PA levels and polymorphisms of the PAI-1 promoter showed no significant difference between the three groups in relation to the urinary albumin excretion. There were no differences in the plasma PAI-1/t-PA levels between the genotypes of the polymorphism of the PAI-1 promoter. No association was found between the amount of urinary albumin excretion and the plasma PAI-1/t-PA levels and genotypes of the polymorphism of the PAI-1 promoter. CONCLUSION: These results show that there was no decrease in the fibrinolytic state in type 2 diabetics with microalbuminuria, compared to normoalbuminuria, which also suggest that polymorphisms of the PAI-1 4G/5G promoter do not affect the plasma PAI-1/t-PA levels in type 2 diabetic patients with microalbuminuria.

Fetal Protein Deficiency Causes Long Term Changes in Mitochondrial DNA Content of Liver and Muscle in Female Sprague-Dawley Rats.: Suk Kyeong Kim, Min Seon Kim, Youn Young Kim, Do Joon Park, Kyong Soo Park, Ki Up Lee, Hong Kyu Lee; Korean Diabetes J. 2003;27(2):115-122. Published online April 1, 2003

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Abstract PDF: BACKGROUND
Epidemiological data suggest a strong association between low birth weight and the increased risk of metabolic syndrome, including type 2 diabetes, hypertension and cardiovascular disease, in adult life. However, the underlying mechanisms are largely unknown. In our previous study, the mitochondrial DNA (mtDNA) copy number in peripheral blood leukocytes was decreased in patients with type 2 diabetes and insulin resistance. To test the hypothesis that mitochondrial changes may serve as a link between fetal under nutrition and insulin resistance in later life, the effects of fetal protein malnutrition on the mitochondria of the liver and skeletal muscle, the main sites of insulin action in adulthood, were investigated. METHODS: Eight-week old female rats were divided into 2 groups and fed on either a control diet (casein 180 g/kg diet) (n=5) or a low protein diet (casein 80 g/kg diet) (n=7) for 15 days prior to mating. They were mated with 10 week-old male Sprague Dawley rats that had been fed on the control diet. The female offspring, born to the mothers fed the low protein diet, were randomly divided into 2 groups 4 weeks after birth, and weaned on either the low protein (low protein group, n=48) or control diet (resuscitated group, n=48). As a control group, the offspring born to the mothers fed the control diet were weaned on the control diet (n=48). The animals in each group were again randomly divided into 4 groups, and sacrificed at 5, 10, 15 and 20 weeks of age, respectively (n=12 per group). The body weight, liver and muscle mtDNA content were measured at weeks 5, 10, 15 and 20. RESULTS: The mtDNA contents of the liver and skeletal muscle were reduced in fetal malnourished adult rats, and were not restored to normal levels even when proper nutrition was supplied after weaning. CONCLUSION: Our findings indicate that under nutrition in early life causes long lasting changes in the mitochondria DNA content of the liver and muscles, which may contribute to the development of insulin resistance in later life.

Clinical Characteristics of Post-transplantation Diabetes Mellitus associated with Tacrolimus Therapy after Kidney Transplantation.: Young Min Cho, Hye Seung Jung, Yun Yong Lee, Min Kyong Moon, Suk Kyung Kim, Hyun Jung Jeon, Curie Ahn, Jong Won Ha, Sang Joon Kim, Kyong Soo Park, Seong Yeon Kim, Hong Kyu Lee; Korean Diabetes J. 2002;26(6):509-519. Published online December 1, 2002

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Abstract PDF: BACKGROUND
Post-transplantion diabetes mellitus (PTDM) is a major metabolic complication of transplantation and shows a variable incidence among studies with different population or different definition. We examined the incidence and the risk factors of PTDM in the Korean patients with tacrolimus-based immunosuppression following kidney transplantation, and also investigated the change of insulin secretory capacity. METHODS: Twenty-one patients using tacrolimus as primary immunosuppressant were recruited and tested with serial 75-g oral glucose tolerance test (OGTT) at 0, 1, 3, and 6 months after kidney transplantation. RESULTS: According to the American Diabetes Association criteria, the incidence of PTDM was 57.1% (12 of 21). Baseline characteristics of PTDM group were old age (especially > 40 yr), high body mass index, high fasting glucose, high plasma insulin, and increased insulin resistance. The insulin secretory capacity in PTDM group was maximally suppressed 3 months after transplantation and was gradually restored thereafter along with dose reduction of tacrolimus. CONCLUSIONS: Attention should be paid to the patients, especially who are over 40 yr of age, throughout the high dose tacrolimus therapy.

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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Abstract 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.

Clinical Characteristics of S20G Mutation of Amylin Gene in Korean Type 2 Diabetic Patients.: Young Min Cho, Min Kim, Yun Yong Lee, Min Kyong Moon, Kyong Soo Park, Seong Yeon Kim, Hong Kyu Lee; Korean Diabetes J. 2002;26(5):377-382. Published online October 1, 2002

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Abstract PDF: BACKGROUND
Islet amyloid deposition, which is mainly composed of amylin, is a characteristic pathological finding in patients with type 2 diabetes mellitus. A missense mutation of amylin at amino acid 20, from Serine to Glycine (S20G), has been shown to be associated with type 2 diabetes in Japanese. In this study, we examined the frequency and clinical characteristics of the S20G mutation in Korean type 2 diabetic patients. METHODS: We studied 364 unrelated patients with type 2 diabetes from Seoul National University Hospital and compared them with 70 non-diabetic subjects. We measured their weight, height, blood pressure and the circumferences of their waist and hips, in order to obtain their prediabetic maximal body weight. Their Fasting plasma glucose, HbA1c, total cholesterol, triglyceride and high-density-lipoprotein (HDL) cholesterol were measured. To detect the S20G mutation, we used the polymerase chain reaction-restriction fragment length polymorphism method. The clinical features of the patients with the S20G mutation were compared with those without the mutation. RESULTS: The S20G mutation was found in 7 of the 364 diabetic patients (1.9 %) and in 1 of the 70 non-diabetic control subjects (1.4 %). The body mass index (BMI) of the patients with the S20G mutation was lower than in those with wild type (21.2+/-1.8 vs. 24.3+/-3.0 kg/m2; p<0.01). The prediabetic maximal BMI was also lower in the patients with S20G mutation (22.4+/-2.3 vs. 26.4+/-3.2 kg/m2; p<0.01) than in those with the wild type. The patients with the S20G mutation had a higher HbA1c level compared to those with the wild type (9.3+/-1.4 vs. 7.7+/-1.3%; p<0.01). CONCLUSION: The frequency of the S20G mutation of the amylin gene was 1.9% in the unrelated type 2 diabetic Korean patients. The S20G mutation is associated with a lower BMI and poor glycemic control.

Expression of ghrelin and its receptor according to feeding state in rats.: Min Seon Kim, Cho Ya Yoon, Young Joo Park, Hyung Kyu Park, Chen Ji Jin, Kyong Han Park, Chan Soo Shin, Kyong Soo Park, Seong Youn Kim, Bo Youn Cho, Hong Kyu Lee; Korean Diabetes J. 2002;26(3):169-178. Published online June 1, 2002

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Abstract PDF: BACKGROUND
Ghrelin is a newly discovered gut peptide, produced mainly in the stomach, which is secreted into the circulating blood and acts on the hypothalamus and the pituitary gland. Although ghrelin was originally identified as an endogenous growth hormone secretagogue, recent studies have suggested its role is in the regulation of food intake and energy homeostasis. The aim of this study was to investigate changes in the expression of ghrelin in the stomach, and of its receptors in the hypothalamus and the pituitary gland in relation to the feeding state. METHODS: Sprague Dawley male rats, divided into 3 groups, freely fed, fasted for 48 hrs and fasted for 48 hrs followed by feeding for 24 hrs, were investigated. The stomach fundus, the hypothalamus and the pituitary glands were collected. The gastric ghrelin mRNA expression was determined by Northern blot analysis and the ghrelin protein by immunohistochemistry. The ghrelin receptor mRNA levels in the hypothalamus and anterior pituitary gland were determined by real time PCR. RESULTS: The ghrelin mRNA levels in the stomach were increased by fasting but reduced again by allowing feeding. The number of ghrelin-immunoreactive gastric epithelial cells tended to increase with fasting. Moreover, the ghrelin receptor mRNA levels increased fold in the hypothalamus, and about 3 fold in the anterior pituitary gland harvested from the rats that had fasted for 48 hrs compared to those that were freely fed. CONCLUSION: Our data demonstrate that expression of both ghrelin in stomach and its receptor in target organs increased in the fasted state, which would be helpful for magnifying the orexigenic effect of ghrelin in the negative energy balance state. Dynamic changes in ghrelin and ghrelin receptor according to altered metabolic state may suggest a physiologic role of ghrelin in the regulation of energy homeostasis.

Pancreatic beta-cell Function and Development in Male Offspring of Protein-Malnourished Rats.: Hyeong Kyu Park, Cheng Ji Jin, Do Joon Park, Chan Soo Shin, Kyong Soo Park, Seong Yeon Kim, Hong Kyu Lee; Korean Diabetes J. 2002;26(1):21-30. Published online February 1, 2002

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Abstract PDF: BACKGROUND
Nutritional deprivation of the fetus and infant may be associated with susceptibility to impaired glucose tolerance or type 2 diabetes in adult life. This association has been interpreted as a long-term effects of nutritional factors that reduce fetal growth and impair the development of tissues that regulate glucose metabolism. This study aimed to investigate the effect of protein malnutrition in a fetus and early life on the pancreatic beta-cell function and development. METHODS: Sprague-Dawley rats were fed a low-protein (8% casein) diet during pregnancy and lactation. Their male offspring were weaned onto either a control (18% casein) diet (recuperated group, R) or a low-protein diet (low-protein group, LP). The offspring of the rats fed control diet were weaned onto control diet (control group, C). Glucose tolerance tests and morphometry of the pancreas were performed to evaluate the pancreatic beta-cell function and development at the 25th week of age. RESULTS: Offspring of the protein-malnourished rats had a significantly lower body weights than the controls. The R and LP showed no major impairment in glucose tolerance, but the plasma insulin concentrations in the R (0.24+/-.03 nmol/L) and LP (0.28+/-.02 nmol/L) groups were lower at 20 min during IVGTT than the C (0.43+/-.05 nmol/L) groups. The areas under the curve for insulin (AUC insulin) during IVGTT were significantly lower in R and LP (0.39+/-.03 nmol/L/min, 0.43+/-.02 nmol/L/min) groups than the C (0.54+/-.03 nmol/L/min) group. In particular, the rats with fetal protein malnutrition showed severe impairment in late-phase insulin secretion to a glucose load. Both the pancreas weight and the proportion of the pancreas weight to the body weight were significantly lower in the R and LP groups than the C group. The proportion of beta-cells to pancreatic cells was lower in the LP (0.91+/-.14%) group than the C (2.19+/-.23%) and R (1.79+/-.25%) group. The relative beta-cell mass was significantly lower in the LP (by 62%) group that the C group. CONCLUSION: Rats with fetal protein malnutrition showed persistently impaired pancreatic beta-cell development and reduced insulin secretion capacity. These findings suggest that in utero protein malnutrition can contribute to the development of type 2 diabetes in adult life along with other deleterious environmental or genetic conditions.

Mortality in Adults with and without Diabetes in Yonchon, Korea.: Kang Woo Bae, Youn Jhin Ahnn, Yong Su Park, Kyoung Soo Park, Byung Goog Yang, Hong Kyu Lee; Korean Diabetes J. 2001;25(5):384-398. Published online October 1, 2001

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Abstract PDF: BACKGROUND
This study is designed to estimate the mortality rate and to assess the relation between other risk factors for mortality and death in adults with diabetes by analysis of death certificates in Yonchon cohort population. METHODS: A population-based cross-sectional study was conducted in 1993 in Yonchon county to estimate the prevalence and risk factors of diabetes. This study population consists of respondents (2,463 persons) from Yonchon study and followed for 6 years from 1993 to 1998. Status of death and causes of death were determined from death certificates from National Statistical Office. RESULTS: During the 6 year follow-up, 18 deaths (10%) occurred in the 184 persons with diabetes and 69 deaths (3.3%) occurred in the 2,113 persons without diabetes. After adjustment for multiple variable (age, sex, total cholesterol, systolic blood pressure, smoking and body mass index (BMI)), mortality rate was significantly higher for diabetic adults than non-diabetic adults (RR, 2.03). The proportional hazard analysis for all-cause mortality in the 190 persons with diabetes showed that smoking, high total cholesterol, and high LDL-cholesterol were significantly associated with increased risk for mortality (p value < 0.05), but BMI, HDL-cholesterol, and high systolic blood pressure were not significantly associated with increased risk for mortality. CONCLUSIONS: This study was a prospective cohort study that followed 2,463 persons of Yonchon cohort for 6 years and showed that diabetic adults had higher mortality than non-diabetic adults. The strength of the association between risk factors and mortality was less clear because follow-up period was short and study population size was small, therefore further follow-up study are needed.

Oxidative Stress and Antioxidative Defense System in Offspring of Protein-Malnourished Rats.: Eun Young Cho, Hyeong Kyu Park, Hyeon Jeong Jeon, Suk Kyeong Kim, Kyong Soo Park, Chong Ho Lee, Seong Yeon Kim, Hong Kyu Lee; Korean Diabetes J. 2001;25(3):190-199. Published online June 1, 2001

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Abstract PDF: BACKGROUND
Free radical-mediated oxidative damage has been implicated in a variety of pathological processes such as diabetes mellitus, aging and atherosclerosis. The susceptibility of a given organism to oxidative damage is influenced by the overall balance between the degree of oxidative stress and antioxidative capabilities. Nutrition plays an important role in determining the cellular antioxidative defense mechanism. Thus, the aim of this study is to investigate the effects of fetal protein malnutrition on oxidative stress and antioxidative capabilities. METHOD: Rats were fed a low-protein (8% casein) diet throughout pregnancy and lactation. Male offspring were weaned onto either a control (18% casein) diet (group 2) or a low-protein diet (group 3). Offspring from rats fed a control diet were weaned onto a control diet (group 1). The activities of superoxide dismutase (SOD), glutathione peroxidase (GPx) and the concentration of thiobarbituric acid- reactive substances (TBARS) were determined at 10 and 15 wk in liver and skeletal muscle from offspring. RESULTS: SOD activities of liver in group 3 were significantly lower than those in group 1 at 10 wk (4.14+/-0.65 U/mg protein, 9.09+/-0.85 U/mg protein) and 15 wk (4.18+/-0.58 U/mg protein, 7.63+/-0.74 U/mg protein), respectively. But SOD activities of skeletal muscle were not different between groups. Whilst GPx activities of liver were not different at 10 wk, GPx activities in group 2 (1.80+/-0.16 U/mg protein) were significant higher than those in group 1 (1.24+/-0.15 U/mg protein) at 15 wk. GPx activities of skeletal muscle were not different between groups. The TBARS concentrations in liver or skeletal muscle were not different between groups at 10 and 15 wk. There was a significant negative correlation between SOD activities and TBARS concentrations in liver (r=-0.359). CONCLUSION: In offspring of rats fed a low-protein diet throughout pregnancy and lactation, the antioxidant enzyme activities were significantly decreased, compared with offspring of rats fed a control diet. These alterations were not fully restored in low-protein offspring even when weaned onto a control diet. These results suggest that fetal protein malnutrition impair the antioxidative defense system.

Correlation between Basal Insulin Requirements and Daily Administered Insulin Dosage in Diabetes.: Min Kyong Moon, Jong Ho Ahn, Tae Yong Kim, Won Shik Shinn, Soo Lim, Young Min Cho, Kyong Soo Park, Seong Yeon Kim, Hong Kyu Lee; Korean Diabetes J. 2000;24(5):552-559. Published online January 1, 2001

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Abstract: BACKGROUND
In patients who need insulin therapy, it is difficult to assess insulin requirements because of individual variability in insulin sensitivity and secretion. The aim of this study is to know that it is possible to achieve rapidly and efficiently normoglycemia based on insulin infusion algorithm and whether there is correlation between basal insulin requirements and daily administered total insulin dose. METHODS: Total 34 patients were enrolled. Insulin infusion was begun at 2:00 p.m., and bedside blood glucose concentration was measured at hourly intervals. The rate of insulin infusion was adjusted according to blood glucose levels. We compared insulin requirements to maintain normoglycemia (basal insulin requirements) with daily administered total insulin dose. RESULTS: At start, the mean blood glucose concentration was 14.9+/-4.7 mmol/L; by the first hour, it was 10.7+/-3.6 mmol/L; by the second hour, it was 7.4+/-3.1 mmol/L; when the infusion was discontinued, it was 5.7+/-1.0 mmol/L. This algorithm successfully inducted normoglycemia in all patients within 3.5+/-1.8 h. There was significant correlation between basal insulin requirements and daily administered total insulin dosage. And, daily administered insulin dose had significant correlation with first hour glucose concentration, first hour insulin infusion rate, second hour glucose concentration, second hour insulin infusion rate, and glucose concentration at the end. CONCLUSIONS: We concluded that normoglycemia can be achieved rapidly and efficiently based on insulin infusion algorithm. The present study suggested that we could predict daily insulin requirements through basal insulin requirements that we measured.

Regulation of mFABP (fatty acid binding protein) Expression by PPAR in Cultured Human Skeletal Muscle Cell.: Hyeosn Jeong Jeon, Won Shik Shinn, Jeong Mi Kim, Hye Kyung Hong, Kyong Soo Park, Seong Yeon Kim, Hong Kyu Lee; Korean Diabetes J. 2000;24(4):413-420. Published online January 1, 2001

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Abstract PDF: BACKGROUND
Fatty acid binding protein (FABP), putative mammalian fatty acid transporter, plays a role in fatty acid transport, the modulation of cellular signal transduction pathways and the protection against detergent like effects of fatty acids. FABP found in liver, adipose tissue, heart, skeletal muscle and FABP in skeletal muscle accounts for 2% of total protein mass. FABP expression has shown to be up-regulated by PPAR in liver and adipocyte. Adipocyte and liver FABP genes have a functional PPRE (PPAR responsive element) in their promoter region. This evidence led us to investigate for a possible the regulation of mFABP expression by PPAR in cultured human skeletal muscle cell. METHODS: Myoblast were cultured in SkGM for 4weeks and were differentiated into myocyte in MEM for 4days. The myocytes were treated with PPAR ligand (troglitazone: 5 g/mL) or transduction with adenovirus-PPAR 1 (Ad-PPAR 1). mFABP expression was identified by northern blot. RESULTS: mFABP expression was up-regulated by 4.0+/-1.2 fold in the PPAR ligand (p<0.05). There was increased in mFABP expression with transduction with adenovirus-PPAR 1 while there was no change in mFABP expression which transducted with adenovirus - -galactosidase. CONCLUSION: These results demonstrates that mFABP expression is up-regulated by both PPAR ligand and by PPAR 1 over expression in cultured human skeletal muscle cells.

Metabolic Phenotype of Glycogen Synthase Gene Inhibition in Human Skeletal Muscle Cells.: Jae Joon Koh, Kyong Soo Park, Jeong Mi Kim, Seong Yeon Kim, Hong Kyu Lee, Theodore P Ciaraldi, Robert R Henry; Korean Diabetes J. 2000;24(3):331-339. Published online January 1, 2001

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Abstract PDF: BACKGROUND
Glycogen synthase (GS) is the rate-limiting enzyme controlling non-oxidative glucose disposal in skeletal muscle. Reduction in GS activity and impaired insulin responsiveness are characteristic features of skeletal muscle in type 2 diabetes that contribute to glucose intolerance. These properties also exist in human skeletal muscle cell cultures from type 2 diabetic subjects. The aim of study is to determine the effect of an isolated reduction in GS on glucose metabolism and if this change can generate a diabetes-like state. METHODS: Cultured skeletal muscle cells from non-diabetic subjects were treated with antisense oligodeoxynucleotides (ODN) to GS to interfere with expression of the gene for 6 days. GS activity, protein expression, glycogen synthesis and cellular glycogen content were measured. RESULTS: Treatment with antisense ODN reduced GS protein expression by 70% compared to control (scrambled) ODN (p<0.01). Both total GS activity and that measured at 0.1 mM G-6-P were reduced by antisense ODN treatment. Insulin responsiveness of GS was also halved. Basal GS FV0.1 was decreased in both antisense ODN and control ODN treated cells and antisense treated cells did not show increase in GS FV0.1 in response to insulin stimulation. Glucose incorporation into glycogen under basal conditions was unaltered after antisense ODN treatment, though no further stimulation in response to insulin was observed. Yet both cellular glycogen content and glycogen synthesis were lower in antisense ODN treated cells compared to control ODN treated cells. CONCLUSIONS: Reduction in GS expression in human skeletal muscle cell impair GS activity and insulin responsiveness but does not replicate the abnormalities of glycogen synthesis found in cultured diabetic skeletal muscle cells.

Expression of Gal alpha1,3 Gal Antigen and Galactosyl Transferase mRNA in Porcine Neonatal Pancreatic Tissue.: Kyong Soo Park, Yoon Young Kim, Jeong Mi Kim, Yu Bae Ahn, Kun Ho Yoon, Bong Yun Cha, Ho Young Son, Hong Kyu Lee; Korean Diabetes J. 2000;24(3):323-330. Published online January 1, 2001

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Abstract PDF: BACKGROUND
Neonatal porcine pancreatic tissue may be a potential source of islet transplantation in patients with type 1 diabetes. Gal 1,3 Gal antigen (Gal epitope) is a xenoantigen which is responsible for hyperacute xenograft rejection. The aim of this study is to evaluate the expression of Gal epitope and galactosyl transferase mRNA in porcine neonatal pancreatic tissue. METHOD: Porcine neonatal pancreatic cell clusters (NPCCs) were isolated using collagenase and incubated in various culture condition. They were stained with Gal specific lectin for the detection of Gal epitope. Expression of 1,3 galactosyl transferase mRNA was assessed by semiquantitative RT-PCR. RESULTS: Gal epitope was expressed in both neonatal porcine pancreas and cell clusters. Most of Gal epitope expressed cells were endothelial cells and ductal epithelial cells. A small number of cells stained positive for insulin were also positive for Gal epitope. In some area of monolayer culture of porcine neonatal islet cluster, scattered insulin positive cells coexpressed the Gal epitope. The expression of 1,3 galactosyl transferase mRNA were lower in islet than other tissues. Culture using extracelluar matrix or 3D gel increased the expression of 1,3 galactosyl transferase mRNA levels. CONCLUSION: Gal epitope was expressed in ductal epithelial cells and some of beta cells of porcine neonatal pancreatic tissue. Expression of Gal epitope in porcine neonatal pancreatic cell cluster may be a problem that needs to be solved before porcine NPCCs can be used in human.

Devrease of Mitochondrial DNA Content in Non-Insulin Dependent Diabetic Rats.: Ji Hyun Song, Sun Hee Yim, Bok Ghee Han, Hong Kyu Lee, Young Mi Kim, Kyong Soo Park, S Suzuki; Korean Diabetes J. 2000;24(2):202-215. Published online January 1, 2001

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Abstract PDF: BACKGROUND
Although genetic disorder in diabetes mellitus (DM) is not well understood, it has been suggested that the maternally inherited mitochondrial DNA which does not follow the Mendel's laws is a genetic factor for DM. It was reported that the mitochondrial DNA contents in DM patients were decreased compared to the normal control. Similar decrease in mitochondrial DNA content before DM development was tested in animal models. METHOD: The mitochondrial DNA (mtDNA) content in various tissues obtained from two types of non-insulin dependent diabetic rats, Goto-Kakizaki (GK) and Otsuka Long-Evans Tokushima Fatty (OLETF) rats at different ages were quantified. We also determined the quantity of hepatic COX subunit lll(COX III) mRNA, and the enzyme activities of succinate dehydrogenase (SDH) and cytochrome c oxidase (COX) in mitochondria isolated from liver and skeletal muscle were measured. RESULTS: At 6 weeks, mtDNA content of GK rat liver was 20% decreased compared to the Wistar control, The mtDNA content of Wistar rat liver was decreased to aging from 6 weeks to 24 weeks while mtDNA in GK rat liver remains relatively constant. In case of skeletal muscle, however, mtDNA contents in GK rats were 50% decreased compared to the control at 12 and 24 week old, Similarly, OLETF and LETO control rats showed the age-dependent decrease of mtDNA content in liver and pancreas. Especially the mtDNA contents in OLETF rat tissues were reduced at the younger age than the LETO control content. That is, at 6 weeks old mtDNA contents in OLETF rat pancreas and liver were only 50% of the control. The level of mitochondrial coded hepatic CDX subunit III mRNA tends to decrease with age. Despite the decrease of mtDNA content, hepatic COX lll mRNA level and COX activities and SDH activities were not altered significantly, implying that the change of mtDNA contents did not damage the mitochondrial gene transcription and mitochondrial function dramatically. CONCLUSIONS: This results suggest that mtDNA contents in pancreas and liver decrease age-dependently but it occurs at younger age in NIDDM. The decrease of mtDNA content at young age may be a cause of NIODM.

Comparison of Clinical Characteristics of Impaired Fasting Glucose with Impaired Glucose Tolerance in Yonchon County.: In Kyong Jeong, Min Kyong Moon, Sang Wan Kim, Young Joo Park, Sun Yuk Kim, Chan Soo Shin, Do Joon Park, Kyong Soo Park, Seong Yeon Kim, Bo Youn Cho, Noe Kyeong Kim, Hong Kyu Lee; Korean Diabetes J. 2000;24(1):71-77. Published online January 1, 2001

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Abstract PDF: BACKGROUND
To compare the clinical characteristics of 1997 American Diabetes Association (ADA) impaired fasting glucose (IFG) based on fasting plasma glucose (FPG) with World Health Organization (WHO) impaired glucose tolerance (IGT) based on oral glucose tolerance test (OGTT) in a Korean population. METHODS: The analyses were based on the data of 2,251 subjects aged 30-80 years obtained from the surveys of Yonchon County in Korea in 1993, and the data of 1084 subjects participated in the follow-up survey in 1995. Prevalence of glucose tolerance categories was obtained by using WHO and ADA criteria, and the level of agreement was estimated by index. Cardiovascular risk profile and the incidence of diabetes based on the ADA criteria after 2 years were compared by focusing on the discordant ctiagnostic categories namely IGT/NFS in which the subjects were diagnosed as IGT by WHO criteria but normal fasting glucose(NFG) by ADA criteria and NGT/IFG diagnosed as normal glucose tolerance(NGT) by WHO but IFG by ADA. Results The ADA criteria failed to diagnose 69% of IGT patients, that is 62% of them were considered normal and 7% as diabetes. The overall agreement was poor (x statistics = 0.32, p<0.05). Subjects classified into IGT/NFG or NGT/IFG showed the worse cardiovascular risk profile and higher incidence of diabetes than NGT/NFG. Especially, subjects with NGT/IFG exhibited higher incidence of diabetes than those with IGT/NFG. CONCLUSION: Although IFG predicts subsequent development of diabetes much better than IGT, the vast majority of the subjects with IGT will be missed according to ADA criteria based on FPG only. Consequently FPG alone could be an inadequate substitute for the OGTT.

Prevalence of Islet Cell Autoantibodies and Mitochondrial DNA Mutation among Typical and Atypical Type 1 Diabetic Patients in Korea.: Hong kyu Lee, Kee Up Lee, Sung Kwan Hong, Byuong Doo Rhee, Dong Seop Choi, Hyoung Woo Lee, Sang Wook Kim, Hee Jin Kim, Nan Hee Kim, Kyong Soo Park, Woo Je Lee, Kyung Soo Ko; Korean Diabetes J. 1999;23(4):541-551. Published online January 1, 2001

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Abstract PDF: BACKGROUND
American Diabetes Association (ADA) proposed new criteria for the classification of diabetic patients, which were mainly based on the presence of autoimmune markers. But it is questionable if we can apply the new ADA criteria to Korean type 1 diabetic patients directly. In this study, we measured several autoantibodies to islet cell in Korean subjects with typical and atypical clinical manifestations of type 1 diabetes mellitus. And mutation of mitochondrial DNA was analyzed in the same patients. METHODS: We measured fasting serum C-peptide in 1870 diabetic patients attending the diabetes clinic of Asan Medical Center. Among the 117 patients with fasting serum C-peptide less than 0.6 ng/mL, glucagon-stimulated C-peptide was measured, and 57 Patients showed the level less than 1 ng/mL and they were diagnosed as type 1 diabetic patients. They were subgrouped into typical (n=26, needed insulin injection within 1 year after diagnosis) and atypical (n=30, did not need insulin for more than l year after diagnosis) type 1 diabetic patients. ICA was measured by indirect immunofluorescence method. Anti-GAD antibody was measured by radioimmunoassay. Anti-ICA512 antibody was measured by western blotting. Mitochondrial DNA 3243 mutation was detected using restriction enzyme Apa-I digestion of the amplified genomic DNA from the subjects. RESULTS: 1) Median age of onset was 40 years for atypical type 1 diabetes patients, while it was 27.5 years for typical type 1 diabetes patients. Average duration of insulin requirement was 0.18 years for typical group and 5.73 years for atypical group. In this series, only typical type 1 diabetic patients experienced diabetic ketoacidosis. 2) Only 50 % of typical type 1 diabetic patients and 47 % of atypical type 1 diabetic patients had at least one autoantibody among ICA, anti-GAD antibody and anti-ICA512 antibody. 3) Mitochondrial DNA 3243 point mutation was detected in 3 patients with atypical type 1 diabetes (10 %), but it was not found in patients with typical type 1 diabetes. CONCLUSION: These results suggest that the prevalence of autoantibodies in Korean type 1 diabetic patients was lower than that reported in Caucasians irrespective of clinical features. Therefore, it may not be easy to apply this new diabetes classification of ADA to Korean type 1 diabetic patients. In addition, mitochondrial DNA mutation may be responsible for some of the Korean atypical type 1 diabetic patients.

Efficacy and Safety of Glimepiride: A Novel Sulfonylurea Drug compared with Gliclazide in the Treatment of Type 2 Diabetes Mellitus: an Open , Randomized Comparative Multi - Center Clinical Study.: Sung Kwan Hong, Ki Up Lee, Yeon Sang Oh, Ho Young Son, Kwang Won Kim, Hyun Chul Lee, Kyung Rae Kim, Dong Seop Choi, Ie Byung Park, Young Seol Kim, Kwan Woo Lee, Hong Kyu Lee, Soon Hyun Shin; Korean Diabetes J. 1999;23(1):87-97. Published online January 1, 2001

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Abstract PDF: BACKGROUND
Glimepiride (HOE490, Amaryl (R)) is a new, third generation sulfonylurea, which binds to a different protein of the sulfonylurea receptor than other sulfonylureas. Although there have been many studies proving the efficacy of glimepiride on Caucasian diabetic patients, only a few studies are available on Asian diabetic patients. We performed an open, randomized, comparative multicenter clinical trial to assess the efficacy and safety of glimepiride in Korean type 2 diabetic patients. METHOD: We recruited 262 type 2 cliabetic patients at 12 different university hospitals whose blood glucose was not controlled effectively with diet alone. Patients were randomized to 1~2mg glimepiride or 40~80mg gliclazide depending on the fasting blood glucose level. Doses were increased stepwise, up to 8mg for glimepiride (once-daily) and 320mg for gliclazide (>80 mg as dividedose) respectively, until metabolic control (fasting blood glucose < 7.9 mmol/L) or maximum dose was achieved. The quality of rnetabolic control was assessed by fasting blood glucose and HbA 1c as primary variables. Insulin, C-peptide and weight were monitored as secondary variables. Safety was assessed by obtaining patient history and laboratory values of relevant variables. RESULTS: Of the 262 patients randomized to treatment, 160(61%) patients completed the 18-week study. The rate of successful blood glucose control (3.9

Relationship of Insulin-like Growth Factor(IGF)-1, IGF-2, IGF Binding Protein(IGFBP)-3, and Mitochondrial DNA Amount in the Umbilical Cord Blood to Birth Weight.: Yun Yong Lee, Do Joon Park, Chan Soo Shin, Kyong Soo Park, Hong Kyu Lee, Jong Kwan Jun, Boh Yun Yoon, Jih Yeun Song, Bong Sun Kang; Korean Diabetes J. 1999;23(1):36-45. Published online January 1, 2001

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Abstract PDF: BACKGROUND
Reaven proposed a syndrome (syndrome X), consisting of glucose intolerance, hypertension, hyperinsulinemia, dyslipidemia, as a clinical entity. The fundamental metabolic defect of this syndrome was recognized as insulin resistance, but the pathophysiology of insulin resistance is not clarified as of yet. Recent evidence, suggests that non-insulin dependent diabetes mellitus (NIDDM) ancl lipid and cardiovascular abnormalities-syndrome X-are associated with intrauterine growth retar- dation (IUGR). Recently Shin reported that the amounts of mitochondrial DNA (mtDNA) in a given amount of genomic DNA were lower in NIDDM patients than in healthy controls, and the amount of mtDNA is negatively correlated with blood pressure ancl waist-hip ratio. Birth weight is known to be correlated with levels of insulin-like growth factors (IGFs). The purpose of this study was to identify the correlation of low birth weight with reduced mtDNA and syndrome X. We investigated the relationship of birth weight to IGFs and the amount of mtDNA METHODS: 72 singleton pregnancy babies and their mathers admitted in Seoul National University Hospital from March to May, 1997 were studied. After delivery, the cord blcxxl and maternal venous blood sampling was done. Using the imnnmoradiometric assay (IRMA) the IGF-l, IGF-2, IGFBP-3 was measured from cord and maternal plasma. Among them only 27 pairs samples were measured mtDNA amount with competitive PCR method in their buffy coat. Then statistical analysis was done within these paratneters. RESULTS: Birth weight is correlated significantly with cord plasma IGF-1 (r=0.32, p<0.01), IGFBP-3 (r=0.44, p<0.01), prepregnancy maternal body weight (r=0.45, p<0.01), maternal mtDNA amount (r=0.63, p<0.01). Cord blood mtDNA is correlated with maternal mtDNA amount (r=0.55, p<0,01). In multiple regression analysis, the maternal mtDNA was found to be the only independent factor related to birth weight (p<0.01). COMCLUSION: We have found the correlation between birth weight and maternal prepregnancy body weight and mtDNA amount. The clinical implications of this result remain yet to be deiermined.

Evaluation of Fasting Plasma Glucose to Diagnose Diabetes in Yonchon County.: Young Joo Park, In Kyoung Chung, Chan Soo Shin, Kyong Soo Park, Seong Yeon Kim, Hong Kyu Lee, Sun Ja Kwon; Korean Diabetes J. 1998;22(3):372-380. Published online January 1, 2001

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Abstract PDF: BACKGROUND
Recently, many studies were performed to evaluate the diagnostic value of fasting plasma glucose to diagnose diabetes, and the diagnostic criteria were revised by ADA in 1997 to avoid discrepancy between the fasting plasma glucose (FPG) and 2 hour post-load plasma glucose(2hPG) cutpoint values after 75g oral glucose loading and to alsc facilitate and encourage the use of test for diagnosing diabetes. This study was performed to assess the performance of different cutpoint of fasting plasma glucose in the diagnosis of diabetes and to compare the prevalence and incidence of diabetes using revised 1997 ADA FPG criterion with those using 1985 WHO criteria in Yonchon County of Korea. METHODS: Two thousand three hundred fifty-six subjects who participated in population based cross-sectional study in Yonchon County in 1993. We have also analysed the data from 1141 subjects who were non-diabetic in 1993 and participated in the follow-up survey in 1995. The relationship between FPG and 2hPG were determined using sensitivity, specificity and the prevalence of diabetes according to FPG and/or 2hPG values. We have determined the prevalence and the incidence of diabetes using the ADA criterion. RESULTS: Based on WHO criteria, a FPG of 6.1 mmol/L(110mg/dL) was determined to yield optimal sensitivity(83.6%) and specificity(82.4%), but it showed low positive predictive value(27.2%) and high prevalence(24.5%). The FPG cutpoint which showed same prevalence with the criterion ot the 2hPG >11.1mmol/L(87 in 2251) was 7.4mmol/L (133mg/dL, 87 in 2251), The crude prevalence of diabetes and impaired fasting glucose by ADA criterion were 9.6% and 14.9%, respectively, where as the crude prevalence of diabetes and IGT were 9.4% and 11.5% by WHO criteria. The crude incidence of diabetes was 5.1% as defined by ADA criterion and 34.4% of subjects who showed impaired fasting glucose in 1993 converted to diabetes in 1995, whereas the incidence was 2.5% by WHO criteria and 13% of IGT subjeets converted to diabetes in 2 years. Conclusions: The adequate cutpoint for FPG seems to lie between 6.1mmol/L and 7.4mmol/L. The 1997 ADA criterion of the FPG > 7.0mmol/L produced similar prevalence and higher incidence than those obtained from 1985 WHO criteria and the former seems to be better to detect the risk group who may progress to diabetes.

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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Abstract 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.

Effect of Troglitazone on Glucose Transport in Human Skeletal Muscle Cell Cultures from Obese Non-diabetic and Obese Non-insulin Dependent Diabetes Mellitus.: Theodore Ciaraldi, Robert R Henry, Kyong Soo Park, Hong Kyu Lee; Korean Diabetes J. 1998;22(2):164-172. Published online January 1, 2001

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Abstract PDF: BACKGROUND
Skeletal muscle is the principal tissue of insulin resistance in obese non-diabetic and non-insulin dependent diabetic(NIDDM) subjects. Troglitazone(Tgz), a member of thiazolidinedione class of compounds, has been shown to improve glucose tolerance in insulin resistant state. At the celluar level, troglitazone has been shown to improve insulin action in skeletal muscle, liver and adipose tissue. However, there has been little knowledge about the mechanism of this drug in human skeletal muscle from insulin resistant subjects. METHODS: To determine the effect of troglitzone on glucose transport(GT) in skeletal muscle of obese non-diabetic and obese NIDDM patients, muscle cultures from 7 obese nondiabetic and 8 obese NlDDM subjects were grown for 4 weeks and then fused for 4 days either with or without Tgz (05ug/mL). At the end of fusion, GT activity was measured and cells were harvested for the measurement of glucose transporter protein expression. RESULTS: Tgz treatment(4 days) increased GT activity dose-dependently in skeletal muscle cell culture of both obese non-diabetic and obese NIDDM subjects. 5ug/mL troglitazone increased basal GT by 2.3 +0.3 fold in obese non-diabetic and 5.7+1.3 fold in obese NIDDM subjects (p <0.05, respectively) Absolute rate of insulin-stimulated GT was significantly increased following Tgz treatment with no enhancement of the incremental response above basal value in either group. Total memhrane GLUTl protein increased 1.7+0.3 fold(p<0.05) following troglitazone treatment(5ug/mL) in NIDDM but were unchhanged in obese non-diabetic cells. GLUT4 protein levels were not affected by Tgz treatment in either group. CONCLUSION: Troglitazone increased both basal and insulin-stimulated GT activity without enhancing the incremental insulin response above basal value in muscle cultures from insulin resistant subjects. These results indicate that troglitazone is not an insulin sensitizer in muscle cultures but acts primarily by mimicking insulin's ability to stimulate basal glucose metabolism in the insulin resistant state of obesity and NlDDM

NcoI Restriction Fragment Length Polymorphism(RFLP) on the TNF-beta gene in Korean Patients with Type 1(insulin-dependent) Diabetes Mellitus.: Suk Kyeong Kim, Chan Soo Shin, Kyong Soo Park, Seong Yeon Kim, Hong Kyu Lee, Hun Ki Min, Tae Gun O; Korean Diabetes J. 1998;22(2):155-163. Published online January 1, 2001

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Abstract PDF: BACKGROUND
To investigate whether a TNF-g gene polymorphism is associated with the development of insulin-dependent diabetes mellitus, we analyzed the TNF-g gene polymorphism with restriction enzyme Ncol in 38 Korean patients with insulin -dependent diabetes mellitus(IDDM) and in 150 healthy controls. METHODS: Genomic DNA was extracted from white blood cells, and amplified by polymerase chain reaction(PCR) on 735 base pairs fragment of TNF-g gene with NcoI polymorpnic site. 735 bp PCR product was digested with NcoI restriction endonuclease, then analyzed by agarose gel electrophoresis to detect the NcoI restriction fragment length polymorphism(RFLP). The TNF-g alleles were divided into two types according to the electrophoresis patterns. TNF-b*1 allele, which contains the Ncol restriction site(CCATGG), should be digested 539 bp and 196 bp fragments. On the other hand, TNF-g*2 allele, which lacks the restriction site, only showed 735 bp fragment. RESULTS: Six out of 38(15.8%) IDDM patients were homozygous for the TNF-b*1 allele, 11(28.9%) were homozygous for the TNF-b*2 alleie, and 21 (55.3%) were TNF-b*1/*2 heterozygous compared to 21.7%, 30.7% and 49.3%(p=0.83), respectively, in control subjects. CONCLUSION: The TNF-b gene polymorphism was not associated with insulin-dependent diabetes mellitus in Korean subjects.

Measurement of Anti-38kD Antibody in Korean patients with Insulin-Dependent Diabetes Mellitus by Western Blot Analysis.: Sun Ja Kwon, Hong Kyu Lee, Hyeon Kyu Kim; Korean Diabetes J. 1998;22(2):135-144. Published online January 1, 2001

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Abstract PDF: BACKGROUND
Insulin-dependent diabetes mellitus (IDDM) is characterized by the destruction of pancreatic b-cells, which is associated with the genetic susceptibility and the production of antibodies to a numter of islet cell antigens(ICA). A possible target antigen, 38kD antigen, was suggested by the proliferation of CD4 T cells frorn a newly diagnosed patient in response to a 38kD polypeptide of the insulin-secretory-granule membrane. Autoantibody to a rat islet cell -protein of 38kD was detectable in the sera of diabetes-prone biobreeding rats by both immunoprecipitation and differential Westem blot analysis. Anti-38kD antibodies were also found to have a 76% sensitivity at the time of diagnosis in diabetic children by immunoprecipitation. In the Asian populations, it has been reported that clinical and immunologic characteristics of IDDM are quite different from those of Caucasians, say low prevalence of ICA. In Korean, there has never been reported the presence of the anti-38kD antibody. Moreover, the time-consuming and laborious nature of assay, such as T-cell proliferation and immuno-precipitation, makes it difficult to use for large population screenings. In the present study, we aimed to evaluate the prevalence of anti-38kD antibody as a immunologic marker in Korean IDDM patients by Western blot analysis. METHODS: Anti-38kD antibody was detected by Western blot analysis using the lysate of rat insulinoma cell line(RINmSF) as an antigenic source. ICA was determined by enzymatic immunohistochemical analysis. The prevalence of anti-38kD antibody and ICA was measured in 38 cases of IDDM, whose mean age at diagnosis and mean duration of IDDM were 25.2+14.2 years and 0.66+0.97 years, respectively. RESULTS: Using Western blot analysis with the lysate fraction of RIN cell, the prevalence of anti-38kD autoantibody(21.1%) in the IDDM paients was significantly higher than that in the control subjects(0.0%, P<0.05). Clinical characteristics between anti-38kD antibody-positive and -negative IDDM patients were not different. In immunohisto-chemical staining, ICA was detected in 18.2% of the IDDM patients, but not in the control subjects. The prevalence of anti-38kD antibody was 21.7%, 28.6% and 12.5% in the patients of less 1 year, 1 year and 2~4 years, respectively, showing no statistically significant difference in the prevalence according to the duration of IDDM. As previously reported, however, the prevalence of ICA decreased with increasing duration of IDDM. CONCLUSION: These results suggested that the anti-38kD autoantibody is a candidate of autoantibodies for the immunologic markers of Korean IDDM We expect the development of the more methods for the detection of anti-38kD in the future.

The Characteristics of Insulin-resistance Syndrome in the Korean Population.: Jin Sung Kim, Gun Sang Park, Yun Yong Lee, Do Joon Park, Chan Soo Shin, Kyong Soo Park, Seong Yeon Kim, Bo Youn Cho, Hong Kyu Lee, Chang Soon Koh, Hyeon Kyu Kim, Yong Soo Park, Soon Ja Kwon; Korean Diabetes J. 1998;22(1):84-92. Published online January 1, 2001

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Abstract PDF: BACKGROUND
Insulin-resistance syndrome or syndrome X which includes diabetes mellitus, hypertension, dyslipidemia, and obesity has been regarded as one of the mechanisms involved in the atherosclerotic disease. This study was performed to evaluate the prevalence of each camponent of insulin-resistance syndrome. We have also analyzed the clustering of insulin-resistance syndrome according to fasting insulin levels in subjects who participated in the Younchon county diabetes prevalence study in 1993. METHOD: One thousand, eight hundred and eleven subjects among 2520 subjects over 30 years-old were enrolled, We investigated the prevalence of 5 metabolic syndromes: glucose intolerance(impaired glucose tolerance and diabetes mellitus by WHO criteria), hypertension(diastolic blood pressure >95 mmHg), Hypertriglyceridemia(triglyceride >2.26 mmol/L), low HDL cholesterolemia(HDL cholesterol <0.91 mmol/ L) and obesity(body mass index >25 kg/m) according to fasting serum insulin level. RESULTS: The prevalence of glucose intolerance (diabetes mellitus and impaired glueose tolerance), hypertension, hypertriglyceridemia, low HDI, cholesterolemia and obestiy were 18.2%, 21.3%, 10.9%, 45.6% and 36.3%, respectively. According to the four quartiles(quartile 1, 2, 3, 4) of fasting serum insulin level, the prevalence rate of each metaboic syndrome was as follows: 9.5%, 15.6%, 22.8% and 25.0% for glucose intolerance; 18.7%, 17.5%, 21.1% and 27.9% for hypertension; 5.0%, 8.1%, 13 8% and 16.9% for hypertriglyceridemia; 37.9%, 46.6%, 46.5% and 51.6% for low HDL cholesterolemia; 19.2%, 30.1%, 40.8% and 55.4% for obesity. As the fasting insulin levels increase, the clustering of 2 or more disease increase. CONCLUSION: Metabolic syndromes associated with insulin-resistance are relatively common disorders in the Korean population. The prevalence and clustering of metabolic abnormalities also increase as serum insulin level increases in Korean population.

Decreased Mitochondrial DNA Content in Peripheral Blood Leukocyte procedes the Development of Type 2 Diabetes Mellitus.: Jae Joon Koh, Jong Ho Ahn, Soon Ja Kwon, Ji Hyun Song, Chan Soo Shin, Do Joon Park, Kyong Soo Park, Seong Yeon Kim, Hong Kyu Lee; Korean Diabetes J. 1998;22(1):56-64. Published online January 1, 2001

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Abstract PDF: BACKGROUND
Mitochondrial mutations and deletions, have been implicated in the pathogenesis of diabetes mellitus. This can explain only a very small proportion of the patients with diabetes mellitus. Mitochondrial DNA(mtDNA) is vulnerable to oxidative stress, resulting in both qualitative and quantitative changes. We reported that the amount of mtBNA decreased in the peripheral blood leukocyte of patients with NIDDM. In this study, we examined that decreased mtDNA content preceded the development of NIDDM{Non-insulin dependent diabetes mellitus) and correlated with various insulin resistance parameters.In this study, we demonstrated that the amount of mtDNA decreased in peripheral blood leukocyte of patients with NIDDM. Furthermore, we found that lower mtDNA levels preceded the development of diabetes mellitus. METHODS: We utilized the stored blood samples from two community-based survey conducted in Yonchon County, Korea in 1993 and 1995. We selected 23 newly diagnosed diabetic patients and 22 age- and sex-matched control subjects. The buffy coats of peripheral blood samples were used for the competitive PCR and the products pairs were separated by gel EP. The content of mtDNA was calculated with the densitometry. RESULTS: There were no difference in the initial anthropometric parameters, blood pressure and lipid profiles between subjects who became diabetic converters and non converters. The mean quantity of mtDNA was lower in the converters, with 102.8+ 41.5 copies/pg template DNA compared to 137.8+ 67.7 copies/pg template DNA of the controls(p 0.05). The significant inverse correlations were noted between mtDNA content and WHR(r=0.31, p<0.05) in the first, and fasting glucose level(r=-0.35, p<0.05), diastolic blood pressures(r=-0.36, p<0.05), and WHR(r=-0.40, p<0.01) in the second survey. The correlations with the serum levels of total and high density cholesterol, triglyceride, insulin and proinsulin were not statistically significant. CONCLUSION: Although a relationship between diabetes and mitochondrial dysfunction has been suspected. This study showed that decreased mtDNA content in peripheral blood proceded the development of NIDDM. This is the first study to demonstrate that quantitative changes in mtDNA precede the development of NIDDM.

The Effect of Elevated Plasma Free Fatty Acids on Non-Insulin-Mediated Glucose Uptake and Insulin Resistance.: Yong Ki Min, Jong Ho Ahn, Jae Joon Koh, Hong Kyu Lee, Hun Ki Min; Korean Diabetes J. 1998;22(1):47-55. Published online January 1, 2001

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Abstract PDF: BACKGROUND
In vivo glucose uptake occurs via two mechanisms, namely insulin-mediated glucose uptake(IMGU) and non-insulin-mediated glucose up-take(NIMGU). NIMGU accaunts for about 70~85% of postabsorptive glucose uptake. Despite many studies, it is still controversial how an increase in lipolysis affects glucose metabolism in man. More specifically, the effect of free fatty acid(FFA) on NIMGU has not been exanuned. METHOD: Two-step(euglycemia- hyperglycemia) glucose clamp techique with [3-H]-glucose infusion was performed in 6 normal men. Each man was studied twice, with(test experiement) and without (control experiment) the administration of lipid and heparin at an interval of at least 4 weeks in random order. The subjects received an insulin infusion at 1.1 pmol/kg. min in conjuction with the infusion of somatostatin(step 1, 153 nmol/h; step 2, 458 nmol/h). Result: Plasma glucose levels during step 1 were 5.4+0.1 mmol/L(control experiment), 5.4+0.1 mmol/ L(test experiment), and were raised to 14.7+0.2 mmol/L, 14.6+0.1 mmol/L, respectively, during step 2. Plasma insulin levels during step 1 were 56+4 pmol/L(control experiment), 52+4 pmol/L(test experiment), and were 65+3 pmol/L, 62+4 pmol/L, respectively, during step 2. In control experiment, plasma FFA levels were 0.24+0.02 mmol/L during step 1 and 0.11+0.01 mmol/L during step 2. In test experiment, plasma FFA levels increased significantly to 1.08+0.06 mmol/L during step 1 and 1.01 +0.04 mmol/L during step 2, respectively(p<0.01). Glucose infusion rate(GIR) to increase glucose concentrations to the desired levels were 7.7+0.8 pnol/ kg,min during step 1 and 29.7+3.7 pmol/kg.min during step 2 in control experiment. In test experiment, GIR decreawd significantly to 3.8+0.9 pmol/ kg.min during step 1 and 20.7+1.2 pmol/kg.min during step 2, respectively(p<0.05). There was no significant difference between NIMGU, estimated by the difference between glucose disapperance rate of step 1 and step 2 of lipid infusion test experiment and that of control experiment. CONCLUSION: These results showed that artificial elevation of plasma FFA levels led to a state of insulin resistance, however, the change of FFA level did not influence NIMGU in man.

The Effect of Acarbose as an Adjuvant Therapy in Sulfonylurea-Treated NIDDM Patients.: Yun Yong Lee, Geon Sang Park, Jin Seong Kim, Byeong Sool Mun, Do Joon Park, Chan Soo Shin, Kyeong Soo Park, Seong Yeon Kim, Hong Kyu Lee; Korean Diabetes J. 1997;21(4):484-492. Published online January 1, 2001

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Abstract PDF: BACKGROUND
Acarbose-an aglucosidase inhibitor-is known to have a glucose lowering effect by delaying the digestion of complex carbohydrates in the small intestine. Acarbose especially prevents the abnormally high increment of postprandial blood glucose, reduces postprandial hyperinsulinemia and probably, alleviates insulin resistance. The aim of this study is to evaluate the glucose lowering effect of acarbose as an adjunt with a sulfonylurea in the treatment of NIDDM patients who have been poorly controlled with the use of sulfonylurea alone. METHODS: Forty NIDDM patients, who were poorly controlled with sulfonylurea alone, were randomly selected frorn outpatient diabetic clinic for study. For 16 weeks, they recieved either acarbose or placebo in additian to sulfonylurea under double blind method. RESULTS: 1) The metabohc parameters measured before initiation of either treatment regimen were similiar. 2) The HbAlc in placebo group increased from 8.9% to 9.0%. In contrast, in the acarbose group, HbAlc value decreased from 9.3% to 8.1%(p<0.05). 3) Mean fasting plasma glucose and 1-h postprandial glucose levels were reduced significantly in the acarbose group(p<0.001), especially in I-h postpandial glucose level in comparison with placebo group(p <0.0001). 4) Mean fasting, 1-h postprandial insulin levels decreased with time in the acarbose group in comparison with placebo group, but the decrease was not statistically significant. 5) Lipid profiles did not change during 16weeks of treatment period. 6) Adverse effects were observed in 3 patients on acarbose and 2 patients on placebo. CONCLUSION: Acarbose can be used as an effective adjuvant therapy to sulfonylurea in NIDDM patients who are poorly controlled with sulfonylurea alone.

Hyperfibrinogenemia as an Important Risk Factor for Microvascular Complications in NIDDM Patients.: Suk Kyeong Kim, Hyeong Kyu Park, Sun Wook Kim, Do Joon Park, Chan Soo Shin, Seong Yeon Kim, Bo Youn Cho, Hong Kyu Lee; Korean Diabetes J. 1997;21(4):406-413. Published online January 1, 2001

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Abstract PDF: BACKGROUND
Abundant evidences have accumulated to suggest that atherosclerosis is accelerated in both type I and type Il diabetes but, traditional risk factors(hyperlipidemia, hypertension, smoking, age, obesity) do not account fully for the increased prevalence and severity of vascular diseases in diabetes. In this study, we examined the relationship of plasma fibrinogen to microvascular complications in NIDDM patients METHODS: In this cross-sectional study, 104 NIDDM patients were chosen from subjects who were attending the metabolic ward of Seoul National University Hospital. None of them were smokers, nor had any clinical evidences of acute infections, cancers or liver diseases. Arnong 104 patients, 55 patients (male 26, fernale 29) had no evidence of microvascular complications and 49(male 30, female 19) had one or moe microvascular complications. Their mean age(55.7+11.6 and 57.2+8.9 years old) and BMI (23.34+2.98 kg/m and 23.74+3.41 kg/m) were similar between two groups. This study defined microvascular complications as follows: 1) retinopathy classified based on fundoscopic and fluorescein angiographic assessmeot to background and proliferative, 2) nephropathy defined by 24 hour urine protein over 500mg, and 3) pheripheral neuropathy assessed by symptoms or NCV. RESULTS: 1) Clinically, there was no differences between two groups with respect to diastolic BP, C-peptide, HbA1c, and triglyceride level. However statistically significant differences were noted in systolic blood pressure, and total and LDL-cholesterol. Also mean fibrinogen level was more elevated significantly in diabetic patients with microvascular complications than those without microvascular complications. 2) Univariate analysis shows significant correlations between fibrinogen and the other variables such as duration of diabetes, total cholesterol level and systolic blood pressure. 3) However, fibrinogen concentration was higher in NIDDM patients with microvascuiar complications regardless of duration of diabetes, hypertension and HbA1c in multivariate logisric regression analysis (P=0.010). Conclusions: These results indicated that hyperfibrinogenemia were observed in NIDDM patient with microvascular complications regardless of duration of diabetes, systolic BP, and total cholesterol. Therefore our study suggests that hyperfibrogenemia may be one of the important missing links in the pathogenesis of diabetic microvascular diseases.

Serum Fasting Proinsulin Level as a Predictor for Development of NIDDM in Korean Subjects.: Geon Sang Park, Chan Soo Shin, Kyong Soo park, Seong Yeon Kim, Hong Kyu Lee, Sun Ja Kwon, Yong Soo Park; Korean Diabetes J. 1997;21(4):365-371. Published online January 1, 2001

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Abstract PDF: BACKGROUND
Proinsulin is raised in people with NIDDM. Hyperproinsulinemia is thought to be a predictor for the subsequent development of NIDDM. We studied to investigate whether hyperproinsulinemia can predict the development of NIDDM in Korean subjects. METHOD: This study was performed as a nested case-control study. The case group was 67 newly developed diabetic patients out of 1193 initially non-diabetic cohott in Yonchon county. We have also selected 66 age-sex-B541-WHR matched control group who remain non-diabetic for 2 years. We compared baseline insulin, proinsulin and proinsulin/insulin ratio between two groups, RESULTS: There was no significant difference in baseline fasting insulin levels[46,77+/-17.3 vs 42.87+/- 11.6(pmol/L)] between converters to diabetes and non-converters. However, the baseline proinsulin levels in converters to diabetes were higher than those in non-converters.[16.07+/-14.3 vs 8.72+/-5.2(pmol/L)) The baseline proinsulin/imulin ratio in converters was also higher than those in non-converters. [0.30+/-0.17 vs 0.20+/-0.10] CONCLUSION: The results suggest that fasting hyper-proinsulinemia may be a predictor for subsequent development of NIDDM in Korean subjects.

Increased Serum 8-hydroxy-Guanine Levels in Diabetic Patients.: Byung Sool Moon, Yun Yong Lee, Chan Soo Shin, Kyong Soo Park, Seong Yeon Kim, Hong Kyu Lee, Su Jin Park, Myung Hee Chung; Korean Diabetes J. 1997;21(3):300-307. Published online January 1, 2001

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Abstract PDF: BACKGROUND
Production of reactive oxygen species(ROS) increased in diabetic patients and oxidative damage may contribute to the development of diabetic complications. 8-OH-deoxyGuanosine (oh8dG) and 8-OH-Guanine(ohSGua) are known as excellent markers of the oxidative darnage to DNA. This study was performed to investigate whether serum 8-OH-guanine increased in diabetic patients and whether the glycemic control(HbAlc) is related to the levels of serum 8-OH-guanine. METHOD: In this study, 28 patients with diabetes mellitus was studied, We also included 27 nondiabetic healthy controls whose age, sex, and BMI were matehed to the diabetic patients. Serum 8-OH-Guanine was assayed by high performance liquid chromatography after antibody-based purification with monoclonal antibodies to S-OH-Guanine. RESULTS: The levels of serum 8-OH-Guanine was significantly higher in diabetic patients than in normal controls(4.02+/-3.77 pmol/mL vs. 0.89+/-0.63 pmol/ mL, p<0.01). Serum 8-OH-Guanine concentration was not related to age, HbAlc, duration of diabetes, creatinine clearance, total cholesterol, triglyceride, and HDL-cholesterol. Conclusions: We found a significant increase in serum 8-OH-guanine levels from diabetic patients compared with their respective controls. These results suggest that diabetic patients have significantly increased oxidatively damaged DNA. The factors regulating the oxidative damage to DNA should be further investigated.

Effect of Troglitazone on Glycogen synthase Activity in Human skeletal Muscle Culture from Obese Non-Diabetic and Obese Non-insulin Dependent Diabetes Mellitus.: Leslie Abrams Carter, Theodore Ciaraldi, Robert R Henry, Kyong Soo Park, Hong Kyu Lee; Korean Diabetes J. 1997;21(3):254-261. Published online January 1, 2001

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Abstract PDF: BACKGROUND
Skeletal muscle is the principal tissue of insulin resistance in obese and non-insulin dependent diabetic(NIDDM) subjects. Troglitazone, a member of thiazolidinedione class of compounds, has been shown to improve glucose tolerance in insulin resistant state. At the cellular level, troglitazone has been shown to improve insulin action in skeletal muscle, liver and adipose tissue. However, there has been no direct assessment of mechanism of this drug in insulin resistant human skeletal muscle from obese and obese NIDDM subjects. METHODS: To determine the effect of troglitzone on skeletal muscle glycogen synthase(GS) activity in insulin resistant human skeletal muscle, muscle cultures from 7 obese non-diabetic and 8 obese NIDDM subjects were grown for 4 weeks and then fused for 4 days either with or without troglitzone(0~5ug/mL) and harvested for GS activity and protein measurement. GS activity was measured by enzymatic method and protein expression was measured by Western blot using polyclonal antibody specific for C-terminal end of GS protein, RESULTS: Troglitzone increased GS activity(GS activity at 0.1 mM G6P and fractional velocity) dose-dependently in both obese non-diabetic and type II diabetes and the increased GS activity by troglitzone was mostly basal rather than insulin-stimulated. Basal fractional velocity of GS increased 2.8+/-0.7 and 3.7 +/-1.2 fold in obese non-diabetic and type II diabetes respectively. There was no changes in GS total activity and GS protein expression in either group with troglitzone treatment.. CONCLUSION: Troglitazone has effects to improve glycogen synthase activity in skeletal tnuscle of obese and obese NIDDM subjects.

Mechanism of Insulin Resistance : Time Dependence of the Development of Insulin Resistance in High Fat Fed Rats.: Kyong Soo Park, Ki Up Lee, Sung Woo Park, Hong Kyu Lee, Hun Ki Min; Korean Diabetes J. 1997;21(2):168-175. Published online January 1, 2001

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Abstract PDF: BACKGROUND
Increased FFA availability is known to induce insulin resistance by decrease in peripheral glucose utilization and increase in hepatic glucose procluction. However, there are conflicting results about the time dependence of the developrnent of insulin resistance with increased availability of FFA. METHODS: To elucidate the time dependence of the development of insulin resistance associated with increased availability of FFA, peripheral glucose utilization rate and hepatic glucose production rate were measured by euglycemic hyperinsulinemic clamp with 3-3H glucose infusion in rats fed high fat diet (1 week or 3 weeks) or control diet(ordinary chow diet). RESULTS: Basal plasrna FFA levels and steady state plasma insulin levels increased after high fat diet. After 1 week of high fat diet, suppressibility of hepatic glucose production rate by insulin was impaired(p<0.05 vs control). Insulin sensitivity index(glucose utilization rates/steady state plasma insulin concentrmtions X100) was decreased only after 3 weeks of high fat diet(p<0.05 vs control) which was accompanied by decreased glycogen synthase activity. CONCLUSION: High fat diet induces hepatic insulin resistance before peripheral insulin resistance and decreased glycogen synthase activity may contribute to the development of peripheral insulin resistance in rats fed high fat diet.

Mitochondrial DNA point mutations in Korean NIDDM patients.: Suk Kyeong Kim, Kyong Soo Park, Chan Soo Shin, Seong Yeon Kim, Bo Youn Cho, Hong Kyu Lee, Chang Soon Koh; Korean Diabetes J. 1997;21(2):147-155. Published online January 1, 2001

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Abstract PDF: BACKGROUND
There are a few genes with proven potential for causing some form of NIDDM, These include the insulin gene, the insulin receptor gene, a gene linked to the adenosine deaminase gene on chrornosome 20, and the glucokinase gene. Recently, an A to G transition at position 3243 in transfer ribonucleic acid ""' ' was reported in maternally inherited NIDDM patients in Japan, it was reported that approximately 1% of diabetes patients have the 3243 bp point mutation. In this study we examined the positive rate and clinical characteristics of Korean NIDDM patients with mitochondrial DNA point mutation. METHODS: We screened randomly selected 433 NIDDM patients (rnale 221, female 212) from the diabetes clinic of Seoul National University Hospital regardless of age of onset, family history of diabetes, mode of' therapy, or any other clinical characteristics. Genomic DNA was extracted from pheripheral lymphocytes. To detect the 3243 bp mutation, PCR was carried out using mtDNA primers(2928-2947, 3558-3539) and then, PCR products were electro-phoresed on a 2%: agarose gel after digestion with the restriction endonuclease Apa-I. When electrophoretic results showed two or three bands, we confirmed mtl)NA 3243 bp point rnutation by DNA sequencing. RESULTS: Of the 433 Korean NIDDM patients, 5 patiients had mtDNA point mutation digested by restriction endonuclease Apa I. Only two patients (OA6%) had heteroplasmic point mutation at nucleo-tide 3243. The remaining three patients(0.69%) with homoplasmic point mutation at nt 3426 were inciden-tally discovered during procedure in detecting 3243 bp point mutation. This 3426 point rnutation had the same adenine to guanine point mutation as 3243 point mutation digested by Apa I and therefore was confused with 3243 point mutation by RFLP method. Two patients with 3243 points mutation, aged 39 and 32 years, BMI 17.0 and 14.4(kg/m), had neither hearing impairrnent nor family history of diabetes. They required insulin for the control of their hyperglycemia and their C-peptide levels less than 1.Ong/mL showed insulin dependent tendency. On the contrary, three patients with 3426 bp point mutation, aged 71, 70, and 62 years, BMI 28.0, 23.0, and 22.6 (kg/m2 ), showed their C-peptide levels 5.4ng/mL and 3.%g/mL and insulin resistant diabetes mellitus. CONCLUSION: Two kinds of point mutation were found in the mtDNA at position nt 3243 and nt 3426, and their incidence were 0.46%(2/433) and 0.69% (3/433) respectively. 3243 point mutation was associated with insulin deficient diabetes mellitus whereas 3426 point mutation insulin resistant diabetes mellitus. 3426 point mutation has the same adenine to guanine transition as 3243 point mutation restricted by Apa I and so, DNA sequencing is warranted to differentiate with 3426 from 3243 point mutation.

Effect of cisapride on diabetic gastroparesis.: Min Seon Kim, Jae Hoon Chung, Yong Soo Park, Kyong Soo Park, Seong Yeun Kim, Myung Chul Lee, Bo Youn Cho, Hong Kyu Lee, Chang Soon Koh, Hun Ki Min; Korean Diabetes J. 1993;17(4):395-402. Published online January 1, 2001

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Abstract 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

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Lowering of plasma free fatty acids by acipimox increases insulin sensitivity in rats.: Ki Up Lee, Kyo Il Suh, Sung Woo Park, Kyung Soo Park, Hong Kyu Lee, Hun Ki Min; Korean Diabetes J. 1993;17(1):73-78. Published online January 1, 2001

821 View
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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

914 View
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Low frequencies of human cytomegalovirus(hCMV) genome in diabetic patients.: Seco In Lee, Kyung Soo Ko, Kyong Soo Park, Seong Kwan Hong, Seong Yeon Kim, Bo Youn Cho, Hong Kyu Lee, Chang Soon Hoh, Hun Ki Min; Korean Diabetes J. 1993;17(1):45-50. Published online January 1, 2001

955 View
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Clinical study of cilostazol in diabetic patients with peripheralvascular disease.: Tai Hee Lee, Young Kil Choi, Kap Bum Huh, Soon Hyun Shin, Hong Kyu Lee, Ho Young Son, Young Seol Kim, Hyun Chul Lee, Min Young Chung; Korean Diabetes J. 1992;16(4):325-334. Published online January 1, 2001

1,177 View
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Increased membrane lipid peroxidation of erythrocytes in NIDDM.: Hak Chul Jang, Young Ki Min, In Kwon Han, Hong Kyu Lee, Hun Ki Min; Korean Diabetes J. 1992;16(4):309-316. Published online January 1, 2001

796 View
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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

937 View
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The frequencies of HLA DQAI, DQBI alleles in Korean adult onset IDDM .: Sung Kwan Hong, Jong Ho Ahn, Kyung Soo Ko, Kyong Soo Park, Seong Yeon Kim, Bo Youn Cho, Hong Kyu Lee, Chang Soon Koh, Hun Ki Min, Yeon Bok Jang; Korean Diabetes J. 1992;16(2):121-127. Published online January 1, 2001

965 View
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Fatty acid composition and delta 6 desaturase activities in strepto-zotocin induced diabetic rats following omega-3 fatty acid supple-mentation.: Chan Soo Shin, Eun Kyung Han, Jong Ho Ahn, Kyong Soo Park, Moon Kyu Lee, Seong Yeon Kim, Bo Youn Cho, Hong Kyu Lee, Chang Soon Koh, Hun Ki Min, Hyung Joon Yoo, Yeung Hwan Chung; Korean Diabetes J. 1992;16(2):111-119. Published online January 1, 2001

1,099 View
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A clinical study on the complications of non-insulin-dependent diabetes mellitus in Korea.: Kyung Soo Ko, Tae Gun Oh, Chul Hee Kim, Kyong Soo Park, Moon Kyu Lee, Seong Yeon Kim, Bo Yeon Cho, Hong Kyu Lee, Chang Soon Koh, Hun Ki Min; Korean Diabetes J. 1991;15(2):257-262. Published online January 1, 2001

927 View
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Effect of Glipizide(Digrin@) in non-insulin-dependent diabetes mellitus.: Kyong Soo Park, Jae Hoon Jung, Kyung Soo Ko, Sung Kwan Hong, Seong Yeon Kim, Hong Kyu Lee, Chang Soon Koh, Hun Ki Min; Korean Diabetes J. 1991;15(1):103-107. Published online January 1, 2001

1,215 View
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