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Volume 27(5); October 2003
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Review
Methods of Research in Diabetic Retinopathy.
Jaetaek Kim
Korean Diabetes J. 2003;27(5):385-390.   Published online October 1, 2003
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AbstractAbstract PDF
No abstract available.
Editorial
Prospective Follow-up of Autoantibody Prevalences in Patients with Type 1 Diabetes.
Yong Soo Park
Korean Diabetes J. 2003;27(5):391-394.   Published online October 1, 2003
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No abstract available.
Original Articles
Five Year Follow-up of ICA and GADA in Childhood onset Type 1 DM.
Si Hyung Lee, Ji Sung Yoon, Mi Jung Eun, Jin Ho Kim, Yong Ho Park, Kyu Chang Won, Ihn Ho Jo, Hyoung Woo Lee
Korean Diabetes J. 2003;27(5):395-404.   Published online October 1, 2003
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AbstractAbstract PDF
BACKGROUND
Type 1 diabetes develops due to the destruction of insulin-secreting beta-cells by an autoimmune process, in which both genetic and environmental factors are involved. In children with newly diagnosed type 1 DM, the prevalence of ICA (Islet cell cytoplasmic antibody) is 60~86% and is highest at the time of onset after which it decreases. But, GADA (glutamic acid decarboxylase anti- bodies) are characterized by substantial fluctuations in the humoral immune response over a long period after clinical manifestation. This study was performed to evaluate the persistence of type 1 DM associated autoantibodies, including ICA and GADA, and their relation to clinical characteristics of the disease after clinical manifestation. METHODS: Eighteen childhood onset type 1 diabetes patients (mean age 13.7 years; duration 3.9 years) were included in this study. ICA was measured by indirect immunofluorescence using conventional ICA-IgG and positive samples were titered by serial dilutions. Also the sera were screened for GADA by radioimmuno-assay. RESULTS: The positivities of ICA and GADA at the time of study were 55.6% and 61%, falling to 44.4% and 41.2% 5 years later, respectively. There was no case of an ICA negative patient becoming positive or whose ICA titer was increased later. One case of a GADA negative patient became positive later. Initial c-peptide levels didn't have any correlation with initial ICA titers or ICA prevalence, but did with initial GADA titer. There were significant correlations between initial GADA titer and ICA prevalence (p<0.001), and between initial GADA titer or ICA titer and later ICA persistence (p<0.05). CONCLUSION: ICA and GADA persisted long after the clinical diagnosis of type 1 diabetes. And the persistence of autoantibody positivity showed a weak relation with endogenous insulin secretion and clinical characteristics, both at and after diagnosis of overt type 1 diabetes.
Insulin Gene Therapy Using HVJ-liposome and Epstein-Barr Virus Plasmid in Murine Streptozotocin Induced Diabetes.
Yong Deuk Kim, Keun Gyu Park, Seong Wook Han, Jong Doek Ahn, Hyo Jung Lee, Mi Jung Kim, Hye Soon Kim, Nam Hee Park, In Kyu Lee
Korean Diabetes J. 2003;27(5):405-413.   Published online October 1, 2003
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AbstractAbstract PDF
BACKGROUND
Despite improvement in insulin preparation and delivery, the use of insulin therapy alone to maintain normal glucose concentration and prevent the development of diabetic complication is not easy. Therefore, there has been considerable interest in developing gene therapy to supply insulin. We investigated that the administration of hemagglutinating virus of Japan (HVJ)- liposome complex, containing human insulin construct into the portal vein to control the blood glucose level in murine streptozotocin (STZ)-induced diabetes. METHODS: Human insulin gene was delivered to STZ-induced diabetic rats through the portal vein using HVJ-liposome containing Epstein-Barr virus (EBV) replicon-based plasmid (pEB). Blood glucose and body weight were measured after insulin gene delivery. The animals were sacrificed 28 days later and the livers were collected for immuno-histochemical staining of insulin. In addition plasma insulin and C-peptide levels were measured. RESULTS: Significant decrease in blood glucose levels and an increase in insulin and C-peptide levels were observed in the insulin gene transfection group as compared to the control group. Immunohistochemical staining of insulin also showed significant differences between these two groups. CONCLUSION: This study demonstrated the possibility of insulin gene therapy through the portal vein using pEB and HVJ-liposome method to produce a sustained improvement of diabetic glucose metabolism.
Insulin Secretory Dysfunction in the Pathogenesis of Type 2 Diabetes in Koreans: A Minimal Model Analysis.
Sung Hoon Kim, Dong Jun Kim, Byung Wan Lee, In Ah Seo, Jae Hoon Chung, Young Ki Min, Myung Shik Lee, Kwang Won Kim, Moon Kyu Lee
Korean Diabetes J. 2003;27(5):414-419.   Published online October 1, 2003
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AbstractAbstract PDF
BACKGROUND
Type 2 diabetes is a complex, heterogeneous disorder, characterized by impairments in both insulin secretion and insulin action. This study was done to examine the significance of alterations in insulin sensitivity and beta-cell function in the pathogenesis of type 2 diabetes in Korean subjects with varying degrees of glucose intolerance. METHODS: Forty Korean subjects were studied, 12 with normal glucose tolerance (NGT), 14 with impaired glucose tolerance (IGT) and 14 with type 2 diabetes. An oral glucose tolerance test (OGTT) was performed on each subject. Insulin sensitivity (SI), glucose effectiveness (Sg), acute insulin response after intravenous glucose (AIRg) and the disposition index (DI= SI x AIRg) were measured by the insulin-modified, frequently sampled intravenous glucose tolerance test (FSIGT). RESULTS: Neither fasting serum insulin level nor SI was significantly different among the NGT, lGT and diabetes groups. Sg was significantly lower in the type 2 diabetes group than in the NGT group. The mean AIRg was blunted in the IGT and diabetes groups when compared with the NGT group. DI was more powerful in differentiating between NGT and IGT, compared to AIRg alone. CONCLUSION: These findings suggest that a defect in the compensatory insulin secretion might be more important than insulin resistance in the development of type 2 diabetes in Korean subjects.
Efficacy of Serum Leptin Level as an Indicator to Predict the Clinical Response of Rosiglitazone in Patients with Type 2 Diabetes Mellitus.
Jae Hyuk Lee, Soo Kyung Kim, Kyu Yeon Hur, Han Seok Choi, Ji Young Jung, Wan Sub Shim, Hyun Joo Lee, Chul Woo Ahn, Sung Kil Lim, Kyung Rae Kim, Hyun Chul Lee, Bong Soo Cha
Korean Diabetes J. 2003;27(5):420-432.   Published online October 1, 2003
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AbstractAbstract PDF
BACKGROUND
Leptin is a protein secreted by adipocytes that regulates food intake by acting on the hypothalamus and is correlated with body fat mass. Insulin resistance is also correlated with body fat mass and obesity. Rosiglitazone (RSG) is known as a highly selective and potent agonist for the peroxisome proliferator-activated receptor-gamma (PPARgamma). It improves glycemic control by improving insulin sensitivity in peripheral tissue. This study was performed to evaluate the antidiabetic and insulin sensitizing effects of RSG combination therapy and the efficacy of serum leptin level as an indicator to predict the clinical response of RSG in type 2 diabetic patients with oral agents such as metformin and/or sulfonylurea. METHODS: The study subjects were 140 type 2 diabetic patients (90 male, 50 female) who received a 12-week course of daily 4 mg RSG, in addition to the previous medications. The glucose level, indices of insulin resistance and metabolic parameters were measured. Serum leptin level was measured by radioimmunoassay before and after RSG treatment. Visceral fat and subcutaneous fat were measured by sonography. RESULTS: After 12 weeks of RSG treatment, FPG (12.6+/-28.1 mg/dL), HOMAIR (0.3+/-0.9), serum fasting insulin (1.9+/-4.7 microU/mL), SBP and DBP had all decreased significantly, whereas body weight, BMI, waist circumference, WHR, body fat mass, and subcutaneous fat had all increased. Serum leptin level also tended to increase after RSG treatment, but without significance. deltaFPG (delta=value after treatment- value before treatent) was inversely correlated with basal serum leptin level (r=-0.202), basal HOMAIR (r=-0.226) and basal FPG (r=-0.565). There was no correlation between deltaFPG and basal BMI or serum insulin level. RSG treatment showed significant inverse correlation between serum leptin level and deltaHOMAIR (r=-0.416), delta insulin (r=-0.365) and deltaHbA1c (r=-0.189). Serum leptin level was positively correlated with the subcutaneous fat amount (r=0.548), basal BMI (r=0.521), and basal HOMAIR (r=0.343). CONCLUSION: These results showed that RSG treatment can improve not only hyperglycemia but also insulin resistance in type 2 diabetic patients. The serum leptin level at baseline can be used as an indicator to predict the clinical response of RSG treatment in type 2 diabetes patients.

Diabetes Metab J : Diabetes & Metabolism Journal