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Volume 29(4); July 2005
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Review
Disturbed Shear Stress Induces Inflammation and Atherosclerosis-Role of BMP4 as a Mechanosensitive and Inflammatory Cytokine.
Hanjoong Jo, Hannah Song
Korean Diabetes J. 2005;29(4):271-281.   Published online July 1, 2005
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AbstractAbstract PDF
Atherosclerosis is an inflammatory disease occurring preferentially in arterial regions exposed to disturbed flow conditions including oscillatory shear stress(OS). In contrast, the arterial regions exposed to laminar shear(LS) are relatively lesion-free. The opposite effects of LS(atheroprotective) and OS(atherogenic) are likely to be determined by differential expression of genes and proteins. Therefore, numerous investigators including us carried out transcript profiling studies to identify mechanosensitive genes that are turned on or off in response to different shear conditions. Through this and subsequent verification approaches using both cultured endothelial cells and human coronary arteries containing atherosclerotic lesions, we discovered that BMP4 expression is a highly regulated by different shear conditions. More importantly, we discovered a novel role of BMP4 as a mechanosensitive pro-inflammatory cytokine. Exposing endothelial cells to OS increased BMP4 protein expression while LS decreased it. Also, we found BMP4 expression only in the selective patches of endothelial cells overlying foam cell lesions in human coronary arteries. Chronic exposure of endothelial cells to OS stimulates inflammatory responses in endothelial cells such as production of intercellular adhesion molecule 1(ICAM-1) leading to monocyte adhesion to endothelium. A series of studies have revealed that exposure to OS induces inflammatory responses by producing BMP4 in endothelial cells. BMP4 then stimulates ICAM-1 expression and monocyte adhesion by the reactive oxygen species(ROS) and NF kappa B-dependent mechanisms. ROS produced in response to OS and BMP4 are derived from NADPH oxidase involving nox1 and p47phox components. These findings strongly suggest that BMP4 is a mechanosensitive, inflammatory factor playing a critical role in early steps of atherogenesis in atheroprone areas. This review is written to summarize this emerging field of shear stress, inflammation and atherosclerosis.
Original Articles
Effective Glycemic Control Achieved by the Transplantation of VEGF-Transfected Islets in STZ-induced Diabetic Mice.
Byung Wan Lee, Hee Young Chae, You Ran Ahn, Seung Hoon Oh, Ji Youn Kim, Yun Jae Chung, Sang Young Kim, Kyun Yung Cho, Jae Hoon Chung, Yong Ki Min, Myung Shik Lee, Moon Kyu Lee, Kwang Won Kim
Korean Diabetes J. 2005;29(4):282-294.   Published online July 1, 2005
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AbstractAbstract PDF
BACKGROUND
Hypoxic damage is one of the major causes of early islet graft failure, and VEGF is known to play a crucial role in revascularization. We tried to evaluate whether the VEGF transgene in an islet graft can increase islet revascularization and; therefore, increase the survival rate of transplanted islets in order to achieve effective glycemic control in diabetic mice models using a non-viral cationic lipid reagent for gene delivery into non- dividing islet cells. METHODS: Human VEGF165 cDNA was transfected into Balb/c mice islets using Effectene, and the vascular neogenesis and glucose levels examined in the recipient syngeneic Balb/c mice. A minimal number of VEGF-transfected islets(100 IEQ/animal) were transplanted into STZ-induced diabetic mice. The recipient mice were classified into three groups: islet transplantation(IT) without intervention(IT-alone group, n=8), IT with an islets transduced rhoJDK-control vector(IT-rhoJDK group, n=8), and IT with an islets transduced rhoJDK-VEGF vector(IT-rhoJDK-VEGF group, n=8). RESULTS: The transfection efficiency was highest with 4microgram/microliter cDNA and 25microliter Effectene(1: 6 weight ratio), with satisfactory cell viability under these conditions. The overproductions of VEGF mRNA and proteins from the conditioned cells were confirmed. A minimal number of the VEGF-transfected islets(100 IEQ/animal) were transplanted into STZ-induced diabetic mice. The control of hyperglycemia in the IT-alone(0/8) and IT-rhoJDK groups(0/8) failed. However, complete abrogation of hyperglycemia and viable islets, and an increased vascularization of the VEGF-transfected grafts were identified in the renal capsules of the IT-rhoJDK-VEGF group(8/8). CONCLUSION: These studies support the utility of VEGF-transfected islet delivery using a cationic lipid reagent to achieve euglycemia with minimal islets via neovascularization.
The Role of cAMP/PKA Activation on Exendin-4-Induced Cyclin D1 Expression in INS-1 Cell.
Gyeong Ryul Ryu, Jung Hoon Kang, Hwa In Jang, Seung Hyun Ko, In Kyung Jeong, Duck Joo Rhie, Shin Hee Yoon, Sang June Hahn, Yang Hyeok Jo, Myung Suk Kim, Myung Jun Kim
Korean Diabetes J. 2005;29(4):295-303.   Published online July 1, 2005
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AbstractAbstract PDF
BACKGROUND
Glucagon-like peptide-1(GLP-1) and exendin-4(EX-4) have been known to induce pancreatic islet proliferation and increases in the betacell mass. Cyclin D1 is a key protein responsible for the entry of the G into the S phase, thereby contributing to cell proliferation. Therefore, the effect of EX-4 on the expression of cyclin D1 in INS-1 cells, a rat pancreatic betacell line, was investigated. The involvement of either mitogen-activated protein kinases(MAPKs) or cyclic adenosine 5'-monophosphate/protein kinase A(cAMP/ PKA) in the EX-4-induced cyclin D1 expression was also examined. METHODS: INS-1 cells were treated with EX-4 (10 nM), and the cyclin D1 protein levels then determined by Western blot. To investigate the involvement of MAPKs in the EX-4- induced cyclin D1 expression, either a combined treatment of MAPKs inhibitors or transient transfection of extracellular signal-regulated kinase-1 (ERK1) was performed. The effect of cAMP on the EX-4-induced cyclin D1 expression was also examined by treatments with forskolin, an adenylyl cyclase activator, and H-89, a PKA inhibitor. RESULTS: EX-4 increased the expression of cyclin D1 protein in a dose-dependent manner. Although EX-4 induced phosphorylation of ERK1/2, the treatment with PD 98059 or the overexpression of ERK1 had no effect on the EX-4-induced cyclin D1 expression. However, forskolin significantly induced the expression of cyclin D1, whereas the pretreatment of H-89 inhibited the EX-4-induced cyclin D1 expression. CONCLUSION: These results suggest that EX-4 induce cyclin D1 expression in INS-1 cells via cAMP/PKA pathway, but this is not due to ERK activation.
Pancreatic Stellate Cell Activation by High Glucose and Its Effect on Angiotensin II.
Seung Hyun Ko, Oak Kee Hong, Min Kyung Lee, Eun He Park, Sung Soo Lee, Yu Bai Ahn, Ki Ho Song, Bong Yun Cha, Ho Young Son, Myung Jun Kim, In Kyung Jung, Kun Ho Yoon
Korean Diabetes J. 2005;29(4):304-314.   Published online July 1, 2005
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AbstractAbstract PDF
BACKGROUND
Pancreatic stellate cells (PSCs) are known to be related to pancreatic inflammation and fibrosis, and are the result of extracellular matrix(ECM) protein synthesis. Recent studies have shown that blockade of the renin-angiotensin system (RAS) attenuated pancreatic inflammation and fibrosis. However, there is little data relating to high glucose (HG) and its effects on PSCs. We investigated the effects of HG on ECM protein and angiotensin II(AT II) in PSCs. METHODS: Isolated PSCs were cultured in HG(D-glucose 5.5(LG), 27.8 mM(HG)) medium. The levels of AT II and TGF-beta were measured using radioimmunoassay, and the AT II-stained cells counted. RT-PCR for the AT II receptor subtypes and Western blot analyses for the expressions of ECM proteins, such as connective tissue growth factor(CTGF) and collagen type IV, were performed. The AT II receptor antagonist, candesartan(10micrometer), and angiotensin converting enzyme inhibitor, ramiprilat(100nM) treatedments were also used. RESULTS: The thymidine uptake of the PSCs increased 4 times in the HG culture. The AT II levels(LG vs. HG, 17.1+/-4.9 vs. 36.0+/-.2pg/mL, P<0.05) and AT II-stained PSCs (LG vs. HG, 22.5+/-2.0 vs. 39.3+/-11.0%, P<0.05) were significantly increased after 6 hrs under HG conditions. The TGF-beta concentration was also significantly higher under HG conditions(LG vs. HG, 436.3+/-69.0 vs. 1115.1+/-434.0pg/mL, P<0.05) after 72 hrs. After 72 hrs, the protein expressions of CTGF and collagen type IV under HG conditions were significantly increased and effectively attenuated by the candesartan and ramiprilat treatments. CONCLUSION: A high glucose concentration could significantly increased PSCs proliferation, which also correlated with the AT II production. Consequently, PSCs proliferation was caused by HG induced ECM protein synthesis, and was attenuated by the AT II receptor antagonist. Therefore, pancreatic inflammation and fibrosis could be aggravated by hyperglycemia, and AT II might play an important role in the pathogenesis.
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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AbstractAbstract 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.
Protective Effects of Lithospermate B on Diabetic Nephropathy in OLETF Rat.
Hyun Joo Lee, Geun Taek Lee, Eun Seok Kang, Kyu Yeon Hur, Zheng Shan Zhao, Chul Woo Ahn, Hun Joo Ha, Man Kil Jung, Bong Soo Cha, Hyun Chul Lee
Korean Diabetes J. 2005;29(4):322-332.   Published online July 1, 2005
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AbstractAbstract PDF
BACKGROUND
Magnesium lithospermate B(LAB), an active component isolated from Salvia milltiorrhizae, has been reported to have renoprotective effects in type 1 diabetic animal model. The purpose of this study was to examine the effects of LAB on the prevention of diabetic nephropathy in Otsuka Long-Evans Tokushima Fatty(OLETF) rat which is regarded as an animal model of type 2 diabetes. METHODS: Ten microgram of LAB/kg or Vehicle(PBS) was given orally once daily to 10-week-old male OLETF rats and LETO rats for 40 weeks. Intra-peritoneal glucose tolerance test was performed at 50 weeks. 24 hr urinary protein excretion amounts were measured. Lipid peroxidation, TGF-beta1 and ED-1 of renal cortex were measured. RESULTS: The mean body weight of LAB+OLETF was not significantly different from that of OLETF rats. LAB treatment decreased proteinuria, lipid peroxidation, and free fatty acid in OLETF rats without decrease in the plasma glucose concentration. Also, LAB inhibited the progression of glomerular hypertrophy and mesangial expansion. LAB effectively decreased ED-1 positive cells, ECM expansion, and TGF-beta1 level in the renal cortex of OLETF rats. CONCLUSIONS: These results suggest that the beneficial effects of LAB on the diabetic renal damage in the OLETF rats may depend on a mechanism of decreasing oxidative stress. LAB might be a new therapeutic agent for the prevention of nephropathy in type 2 diabetes as well as type 1 diabetes.
Relationship of LDL Particle Size to IMT and Insulin Resistance in Non-Diabetic Adult.
Jina Park, Chul Sik Kim, Jong Suk Park, Dol Mi Kim, Min Ho Cho, Jee Hyun Kong, Hai Jin Kim, Jeong Ho Kim, Chul Woo Ahn, Kyung Rae Kim, Bong Soo Cha, Sung Kil Lim, Hyun Chul Lee
Korean Diabetes J. 2005;29(4):333-343.   Published online July 1, 2005
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AbstractAbstract PDF
BACKGROUND
The aims of this study were to investigate the predictor of the low density lipoprotein(LDL) particle size and the relationship of the LDL particle size to the levels of insulin resistance and the carotid intima-media thickness (IMT) in healthy Koreans. METHODS: The subjects were 47 and 89 clinically healthy males and females, aged between 32 and 70years, without medications that could potentially alter glucose and lipid metabolisms. The mean LDL particle size was determined by polyacrylamide tube gel electrophoresis(Lipoprint(r) LDL, Quantimetrix), the insulin resistance using a short insulin tolerance test kit, and the subclinical atherosclerosis from the carotid intima-media thickness. RESULTS: The LDL particle size was found to be significantly correlated with insulin resistance using a simple Pearson's correlation(r=0.233, P<0.01), but the independent predictors of the LDL particle size, as determined by a multiple stepwise regression analysis, were serum triglyceride(TG), high density lipoprotein(HDL) cholesterol level and age(beta=-0.403, P=< 0.001; beta=0.309, P=0.003; beta=-0.219, P=0.016, respectively). Significant relationships were found between an increasing IMT and the traditional risk factors of atherosclerosis: age, LDL cholesterol, HDL cholesterol, systolic and diastolic blood pressure(r=0.490, P<0.001; r=-0.251, P<0.01; r=0.211, P<0.05; r=0.298, P<0.01; r=0.263, P<0.01, respectively). However, no significant correlation was found between an increasing IMT and the LDL particle size (r=-0.172, P=0.075). CONCLUSION: The best predictors for the LDL particle size were the serum TG level, HDL cholesterol level and age. Insulin resistance was not found to be an independent predictor of the LDL particle size. Small dense LDL was not found to be a predictor of the IMT in healthy Koreans.
Effect of Pinitol on Glucose Metabolism and Adipocytokines in Uncontrolled Type 2 Diabetes Mellitus.
Mi Jin Kim, Kwang Ha Yoo, Hyung Suk Park, Sang Man Chung, Choon Jo Chin, Young Sook Choi, Choon Hee Chung
Korean Diabetes J. 2005;29(4):344-351.   Published online July 1, 2005
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AbstractAbstract PDF
BACKGROUND
Pinitol(3-O-methyl-D-chiro-inositol) has been identified in putative insulin mediator fractions possessing hypoglycemic activity, and appears to act downstream in the insulin-signaling pathway to mimic the effects of insulin. We evaluated the effect of pinitol therapy in type 2 diabetic patients who were poorly controlled with hypoglycemic drugs such as sulfonylurea, metformin and/or insulin. METHODS: Twenty type 2 diabetic patients were enrolled in this our study. The fasting glucose and c-peptide, total cholesterol, triglyceride, HDL-and LDL-cholesterols were checked before and after treatment with 20mg.kg(-1).day(-1) pinitol for twelve weeks. All subjects continued their current medications during the study. Adipocytokines, such as adiponectin, leptin, free fatty acid and CRP, were checked before and after the pinitol treatment. RESULTS: After the pinitol treatment, the fasting and post-prandial glucose levels and hemoglobin A1c were significantly decreased(P<0.05). The fasting serum adiponectin, leptin, free fatty acid and CRP levels remained unchanged after the pinitol treatment. In the non-responder groups, the serum c-peptide levels were higher than those in the responder groups. CONCLUSION: Twelve weeks of pinitol treatment altered glucose metabolism, but not the lipid profiles or adipocytokine levels. Additional research will be required are needed to define the physiological and potential therapeutic effects of pinitol.
Randomized Controlled Trial
Relationship between Carotid Atherosclerosis and Chlamydia Pneumoniae Seropositivity in Type 2 Diabetes.
Su Jin Jung, Ji Hye Kim, Ji Hyun Park, Tae Sun Park, Hong Sun Baek
Korean Diabetes J. 2005;29(4):352-357.   Published online July 1, 2005
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AbstractAbstract PDF
BACKGROUND
The major causes of death in diabetic patients are atherosclerosis-related diseases. Infection with Chlamydia pneumoniae(C. pneumoniae) has been reported to play a pathogenic role in atherosclerosis. However, data relating to C. pneumoniae exposure are rare in type 2 diabetes that are more susceptible to infection. The aim of this study was to see whether C. pneumoniae seropositivity was associated with carotid atherosclerosis in type 2 diabetic patients. METHODS: The subjects of this study were 135 type 2 diabetic patients. Serum samples from the subjects were assayed for risk factors, including lipid profiles, HbA1c, fibrinogen and CRP. Serum titers of antibodies to C. pneumoniae(IgG, IgM) were measured using microimmunofluorescence(MIF). tests Carotid ultrasound examination was used to measure the intima-media thickness(IMT), plaques and the presence of stenosis in each segment of both carotid arteries. RESULTS: C. pneumoniae seropositivity was detected in 17.8%(n=24), but without any difference between the sexes, in the 135 type 2 diabetic patients. The CRP level was increased in the seropositive group(P=0.041). The presence of carotid stenosis and IMT were significantly from a associated with C. pneumoniae seropositivity from a univariate analysis(IMTmean: IgG(+), 0.93mm vs. IgG(-), 0.85mm, P = 0.038, IMTmax: IgG(+), 1.29mm vs. IgG(-), 1.17mm, P = 0.025, stenosis: IgG (+), 25% vs. IgG(-) 7.2%, P = 0.020). No association was found for the plaque count or score. After controlling for cardiovascular risk factors, including age, sex, hypertension, cholesterol, and CRP, the association of C. pneumonia seropositivity with the IMTmean or carotid stenosis remained significant(IMTmean: P = 0.027, stenosis: P = 0.026). CONCLUSIONS: Serologic evidence of C. pneumoniae infection was detected in 17.8% randomly-assigned type 2 diabetic patients. C. pneumoniae seropositivity may be a risk factor for carotid atherosclerosis in type 2 diabetic patients.
Original Articles
Clinical Characteristics and Analysis of Risk Factor for Gastroesophageal Reflux Disease in Diabetic Patient.
Kwang Hyuk Park, Seong Bo Yoon, Min Ho Jo, Eon Kyung Hong, Seong Jin Lee, In Kyung Jeong, Chul Young Park, Ki Won Oh, Hyun Kyu Kim, Jac Myoung Yu, Doo Man Kim, Sung Hee Lim, Moon Ki Choi, Hyung Jun Yoo, Sung Woo Park, Heung Young Oh, Jin Bae Kim, Il Hyun Baek, Myung Seok Lee
Korean Diabetes J. 2005;29(4):358-366.   Published online July 1, 2005
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AbstractAbstract PDF
BACKGROUND
A high prevalence of gastroesophageal reflux disease(GERD) has been reported in diabetic patient. However, the exact mechanisms of GERD in diabetic patient have not been described. In several studies, diabetic neuropathy and dysfunction of the autonomic nervous system have been suggested as risk factors of GERD. However, there have been no studies on the exact prevalence or risk factors of GERD in Korean diabetic patients. Therefore, the prevalence of GERD in Korean diabetics patients was examined, and the risk factors for GERD, the differences in symptoms between GERD and non-GERD patients, and the degree of symptom relief after treatment were also analyzed. METHODS: A total of 310 diabetic patients, who underwent an upper gastroendoscopy due to diverse gastrointestinal symptoms, between April 2001 and November 2003, were enrolled. The diagnostic criteria or GERD included the upper gastroendoscopic view, which was analyzed using the scale of 'The Los Angeles Classification of Esophagus' from grades A to D. The prevalence and symptoms of GERD patients and the variable risk factors, such as blood glucose level, smoking and diabetic neuropathy, were examined. RESULTS: 1) There was an 18.4% prevalence of GERD in diabetic patients. 2) The clinical characteristics, including sex, age and serum lipid level, of the GERD group were not significantly different to those of the control group. However, the duration of smoking, the fasting and postprandial 2-hour serum glucose levels, and the diabetic neuropathy significantly affected GERD, 3) The main symptoms of the GERD group were dyspepsia(47.4%) and heart burn(26.3%). 4) The degree of subjective symptom relief in the GERD group after treatment with the proton pump inhibitor, pantoprazole(40mg), was remarkably lower than in the control group for approximately 1 month. CONCLUSION: In this study, the prevalence of GERD in diabetic patient was higher than that found in the general population which suggests that GERD in diabetic patient was due to a poorly controlled serum glucose level and diabetic neuropathy. The chief complaints pertaining to gastrointestinal symptoms in both study groups were non-specific. However, the recovery from symptoms in the GERD group was lower than the control group following drug therapy. The causes of the lower response rate in the GERD group will need to be examined in further studies.
Clinical Meaning of Postprandial Insulin Secretory Function in Korean Type 2 Diabetes Mellitus.
Wan Sub Shim, Soo Kyung Kim, Hae Jin Kim, Se Eun Park, Eun Seok Kang, Yu Mie Rhee, Chul Woo Ahn, Sung Kil Lim, Kyung Rae Kim, Hyun Chul Lee, Bong Soo Cha
Korean Diabetes J. 2005;29(4):367-377.   Published online July 1, 2005
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AbstractAbstract PDF
BACKGROUND
Impaired pancreatic beta-cell responsiveness is associated with type 2 diabetes mellitus. Postprandial insulin deficiency is closely related with fasting plasma glucose, HbA1c and insulin responses to meals, but most studies examining postprandial beta-cell responsiveness have been limited by the small number of type 2 diabetic patients examined. The aim of this study was to evaluate fasting and postprandial insulin secretions in relation to the duration of diabetes, BMI and glycemic control in a large number of patients with variable disease durations. METHODS: We evaluated the fasting plasma glucose, insulin, C-peptide, HbA1c, BMI, postprandial 2 hour glucose, insulin and C-peptide in 1,170(male 662, female 508, age 54.6+/-1.6 years, duration of diabetes 5.2+/-6.3 years, BMI 25.4+/-3.3kg/m(2)) type 2 diabetic patients. The delta C-peptide, delta insulin, fasting(M0) and postprandial(M1) pancreatic beta-cell responsiveness were also calculated. The subjects were divided into three groups according to their duration of diabetes, BMI, and fasting and postprandial C-peptide levels. After adjusting for age, sex and BMI, the correlation of diabetes and HbA1c were correlated parameters. RESULTS: In the group of patients whose duration of diabetes was longer than 10 years, the BMI, fasting, postprandial and delta C-peptide, and M0 and M1 were significantly lower, but age, fasting and postprandial glucose, as well as HbA1c were significantly higher than those in the other groups. There were no significant differences in the fasting and postprandial glucose and HbA1c according to their fasting C-peptide tertiles. However, in the group of patients with the highest postprandial C-peptide tertile, the fasting and postprandial glucose and HbA1c were significantly lower than those in the other groups. The duration of diabetes, after adjustment of age, sex and BMI, was negatively correlated with the fasting, postprandial and delta C-peptide, M0 and M1, but was positively correlated with the fasting and postprandial 2 hour glucose and HbA1c. The HbA1c after adjustment of age, sex and BMI, was positively correlated with duration of diabetes, and fasting and postprandial glucose, but was negatively correlated with fasting postprandial and delta C-peptide, M0 and M1. CONCLUSION: Although the fasting and postprandial insulin secretions were decreased with duration of diabetes, the decrease in the postprandial insulin secretion was more prominent. The postprandial pancreatic responsiveness may be a more important factor in predicting glycemic control in Korean type 2 diabetic patients than the fasting pancreatic responsiveness.
Case Report
Two Cases of Fulminant Type 1 Diabetes.
Yu Min Lee, Kyoung Hee Kweon, Seoung Hoon Baek, Ha Young Kim, Byoung Hyun Park, Chung Gu Cho
Korean Diabetes J. 2005;29(4):378-382.   Published online July 1, 2005
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AbstractAbstract PDF
Type 1 diabetes is characterized by insulin deficiency due to destruction of pancreatic beta-cells. Patients with type 1 diabetes, with no islet autoantibodies, but with acute onset, are classified as having idiopathic of type 1B diabetes. In 2000, this diabetes subtype was described and named "fulminant type 1 diabetes". The clinical characteristics of this subtype of type 1 diabetes are: a remarkably abrupt onset of disease, very short(<1 week) duration of diabetic symptoms, acidosis at diagnosis, negative status of islet-related autoantibodies, virtually no C-peptide secretion(<10 microgram/day in urine), a near normal HbA1c level and an elevated serum pancreatic enzyme level. Since 1988, several cases showing the clinical characteristics of fulminant type diabetes have been reported, with this subtype accounting for approximately 20% of Japanese type 1 diabetes. There have been few cases of fulminant type 1 diabetes in Korea. Herein, our experience of two cases of fulminant type 1 diabetes is reported, with a review of the literature.

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