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Sung Woo Ha  (Ha SW) 15 Articles
The Effect of High Glucose and TGF-beta on the Cellular Injury in Cultured Glomerular Epithelial Cells.
Gui Hwa Jeong, Sung Chang Chung, Eui Dal Jung, Yun Jeong Doh, Hee Kyoung Kim, Soon Hong Park, In Hae Park, Jung Guk Kim, Sung Woo Ha, Bo Wan Kim, In Kyu Lee, Cheol Woo Ko
Korean Diabetes J. 2006;30(4):254-263.   Published online July 1, 2006
DOI: https://doi.org/10.4093/jkda.2006.30.4.254
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BACKGROUND
The glomerulus is a complex physiological structure, as well as selective filtration barrier in the control of renal blood flow and blood pressure. Glomerular epithelial cells may play an important role in development of diabetic nephropathy. Apoptosis of the glomerular epithelial cells are characterized by disappearance of a selective filtration barrier. TGF-beta is a key factor in the development of diabetic nephropathy because of its effects on the accumulation of extracellular matrix and mesangial cell proliferation. We examined whether the high glucose and TGF-beta induce the apoptosis in cultured rat glomerular epithelial cells. METHODS: Glomerular epithelial cells were cultured from rat glomeruli and conditioned with different concentration of TGF-beta or high-glucose. We measured apoptosis of cultured rat glomerular epithelial cell conditioning with different concentration of TGF-beta or high-glucose by using DNA electrophoresis. RESULTS: High glucose (25 mM) induced apoptosis of cultured rat glomerular epithelial cells compared to controls. TGF-beta also induced cell death of cultured rat glomerular epithelial cells in dose dependent manner. CONCLUSION: These results suggest that high glucose and TGF-beta-induced cell death of glomerular epithelial cell may play an important role in diabetic nephropathy and proteinuria. Pathway of apoptosis or cell death by high glucose and TGF-beta must be investigated in the glomerular epithelial cells.
Effect and Mechanism of High Glucose Level on the Expression of an Adhesion Protein, beta ig-h3, and Cellular Function in Endothelial Cells.
Sung Woo Ha, Hye Jin Yeo, Jong Sup Bae, Sung Chang Chung, Jung Guk Kim, In San Kim, In Kyu Lee, Bo Wan Kim
Korean Diabetes J. 2003;27(4):323-331.   Published online August 1, 2003
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BACKGROUND
Diabetes mellitus is a high risk condition for the development of atherosclerotic and thromboembolic macroangiopathy. There are many factors which are involved in development of these processes. Given the central pathogenic role of endotheliopathy in atherosclerosis, it is likely that this vascular monolayer is the ultimate target of injury in response to many cytokines and growth factors. A dysfunctional endothelium may contribute to the proatherogenic environment. Transforming growth factor (TGF-beta) is a key factor in the development of diabetic angiopathy and atherosclerosis because of its effect on the accumulation of extracellular matrix proteins and endothelial function. The adhesive molecule betaig-h3 is an extracellular matrix protein whose expression is induced by TGF-beta. Considering that TGF-beta plays an important role in diabetic complications and that betaig-h3 is a downstream target gene of TGF-beta, we hypothesized that betaig-h3 may also play a role in the development of diabetic angiopathy through its effect on the endothelial function. Therefore, we examined the effects of high glucose level on the expression of betaig-h3 and endothelial function in human umbilical vein endothelial cells (HUVECs). We also studied the mechanisms of this high glucose-induced betaig-h3 expression. METHODS: Endothelial cells were isolated from human umbilical cord and conditioned with different concentrations of TGF-beta or glucose. We measured TGF-beta and betaig-h3 protein presence/concentration/expression in cell supernatant by ELISA and examined whether TGF-beta is involved in high glucose-induced betaig-h3 expression. Finally, we investigated the biologic function of betaig-h3 in endothelial cells by using adhesion assay. RESULTS: Our study demonstrated that both high glucose level and TGF-beta induced betaig-h3 protein expression in HUVECs. High glucose level also induced TGF-beta protein expression in cells. Anti-TGF-beta antibody almost completely blocked high glucose-induced betaig-h3 expression. betaig-h3 was found to support the adhesion of endothelial cells. CONCLUSION: These results suggest that high glucose level upregulates betaig-h3 protein levels through the induction of TGF-beta and that betaig-h3 may play an important role in diabetic angiopathy by regulating adhesive function of endothelial cells.
Effect of Heat Shock on the Vascular Reactivity and Expression of Heat Shock Protein in an Animal Model of Type 2 Diabetes Mellitus (OLETF rat).
Soon Hee Lee, Sung Woo Ha, Bo Wan Kim
Korean Diabetes J. 2003;27(3):199-212.   Published online June 1, 2003
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BACKGROUND
Heat shock proteins (HSPs) are highly expressed in cardiovascular tissues, with heat shock possibly modulating the vascular reactivity to vasoactive agents. An abnormal vascular reactivity has been shown in diabetes, and may be closely associated to diabetic vascular complications. The aim of this study was to investigate the effects of heat shock on the vascular reactivity and the expression of HSP70 in the isolated aortae of OLETF rats, a commonly used animal model for type 2 diabetes mellitus, and LETO rats, as age matched controls. METHODS: In 4 ring segments of the thoracic aorta isolated from each rat, the endothelium was denuded in 2 (EC-) and reserved in the other 2 (EC+). To induce heat shock, the aortic rings were exposed to 42 degrees C for 45 minutes. The vascular reactivity responses to various vasoactive agents were measured by organ chamber studies, and by changes in the HSP expression, using Western blotting of the aortic rings in the OLETF rats and controls. RESULTS: The contractile responses to KCl became apparent 4 hours after the end of the heat shock induction. After heat shock, the phenylnephrine-induced contractile responses were similarly increased in the OLETF rats and the controls, but the increase was more significant in the EC(-) than the EC(+) rings, in both the OLETF rats and the controls. The relaxative responses to either acetylcholine (ACh) in the EC(+) aortic rings, or to sodium nitroprusside in the EC(-) rings, were not significantly affected by the heat shock treatment in either the OLETF rats or the controls, although the maximal relaxative response to ACh before the induction of the heat shock was lower in the aortic rings of the OLETF rats than in the controls. The HSP70 levels before the heat shock were higher in the aortic rings of the OLETF rats than in the controls, whereas those after heat shock were higher than those before in both the OLETF rats and the controls. The increase in the expression of HSP70 following the heat shock was higher in rings of the controls than in those of the OLETF rats. The HSP70 levels following the heat shock were increased to a greater extent in the EC(+) than the EC(-) rings of both the OLETF rats and the controls. CONCLUSION: These results suggest that the vascular reactivity to heat shock was decreased to a greater extent in the aortae of OLETF rats than in those of the controls, and that HSP70 seems to play an important role in the vascular response to heat shock through interaction of the endothelium and the smooth muscle.
Changes in Cutaneous Blood Flow in Type 2 Diabetics with or without Neuropathy and Retinopathy.
Chang Hoon Choi, Ju Young Lee, Sin Won Lee, Gui Hwa Jung, Jung Guk Kim, Sung Woo Ha, Bo Wan Kim
Korean Diabetes J. 2003;27(1):18-25.   Published online February 1, 2003
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BACKGROUND
Although diabetic microangiopathy has its greatest clinical effects in the retina, kidneys and nerves there is much evidence that the process is generalized, and that these lesions involve most capillary beds. However, the potential relationship between the presence of diabetic neuropathy, and/or retinopathy, and skin blood flow has not been fully evaluated. Therefore we measured the cutaneous blood flow in diabetics, both with and without microangiopathy, to determine the relationship between microangiopathy and the cutaneous blood flow. METHODS: One hundred-and nineteen type 2 diabetic patients were classified into four categories, based on the presence of polyneuropathy or retinopathy. The skin blood flow was measured in the diabetic patients with or without neuropathy and retinopathy, before, during and after exposure to cold. Before, during and 1 min after the application of a cold-pack, skin blood flow measurements were performed using a laser Doppler techniques at the following right-sided locations: (1) the dorsum of the wrist and ankle, as nutritive microvasculatures, and (2) the pulp of tip of the index finger and big toe, as themoregulatory ones. RESULTS: During the 1-min cold applications, the percentage changes in the decrement of the skin blood flow, at the 4 skin sites, showed decreasing trends in the neuropathy group. However, the differences in the diabetics with neuropathy were not significantly greater than in those without neuropathy. The changes at the same sites in the group with retinopathy were similar to those with neuropathy. The percentage changes in the increment of the skin blood flow were measured at the 4 skin sites 1 min after exposure to cold, and also showed a blunted tendency in both the diabetic neuropathy and retinopathy groups. The percentage changes in the flow increment at the pulp of the big toe were greater in the diabetics without neuropathy or retinopathy, compared to those with these complications (p<0.05). CONCLUSION: These results suggest that changes in the cutaneous blood flow would be more predominant at the thermoregulatory vasculature sites in the type 2 diabetics with neuropathy or retinopathy, and seems to be related to diabetic microangiopathy.
Differences in Dynamic Plantar Pressure in Type 2 Diabetics with or without Peripheral Neuropathy.
Gui Hwa Jeong, Ju Young Lee, Shin Won Lee, Chang Hoon Choi, Soon Hee Lee, Jung Guk Kim, Sung Woo Ha, Bo Wan Kim
Korean Diabetes J. 2002;26(6):481-489.   Published online December 1, 2002
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BACKGROUND
Foot ulcers, and lower-extremity amputations, are relatively common complications of diabetes mellitus and their clinical management is very important. High plantar pressure is known to be a major risk factor of foot ulceration in diabetic patients. The EMED-system is used for the assessment of pressure distribution for the identification of focal areas at high risk of ulceration that merit protection from preventive footwear. However, a potential relationship between diabetic neuropathy and the plantar pressure has not been fully evaluated. Changes in the plantar pressure were measured in diabetic patients, both with and without peripheral polyneuropathy, using the EMED - AT system to clarify if diabetic neuropathy increases the plantar pressure. METHODS: Ninety seven patients with type 2 diabetes were divided into two groups on the basis of their peripheral polyneuropathy. No patient had a past history of foot ulceration. The clinical characteristics of 2 groups were analyzed, and their plantar pressures was measured using the EMED - AT system. These results were analyzed, with the EMED software program, after their division into ten masks for a so-called "regional analysis". The pressure time (PTI) and force- time (FTI) integrals were analyzed for each mask on both feet. RESULTS: The diabetic neuropathy (DN) group showed significantly higher FTI levels in both masks 05 (area of the 1st metatarsal head) and masks 08 (area of the hallux) than the diabetic control (DC) group. The PTI was also higher in right the mask 08 of the DN group than in the DC group. CONCLUSION: These results suggest that peripheral neuropathy to be an important risk factor, and predictor of diabetic foot ulcers, due to the increasing plantar pressure in some areas of the foot. Measurement of the plantar pressure may be a useful method for the diagnosis and monitoring of foot disorders in diabetic patients with peripheral neuropathy.
Effect and Mechanism of Vascular Endothelial Growth Factor on Endothelial Nitric Oxide Synthase Expression in Aortic Endothelial Cells.
Soon Hee Lee, Jung Guk Kim, Joong Yeol Park, Sung Woo Ha, Bo Wan Kim
Korean Diabetes J. 2002;26(5):396-404.   Published online October 1, 2002
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BACKGROUND
Vascular endothelial growth factor (VEGF), a soluble angiogenic factor produced by many tumor and normal cells, is a potent angiogenic and vascular permeability factor. VEGF plays a key role in both pathological and physiological angiogenesis. There are many recent findings regarding the role of VEGF in diabetic microvascular and macrovascular diseases. Many approaches with VEGF-related therapies begin to treat and prevent these complications and have been used for the treatment of microvascular complications such as diabetic retinopathy, whereas VEGF agonists have been used to treat macrovascular complications such as myocardial infarction and peripheral limb ischemia. Nitric oxide (NO) is known to mediate many physiological and pathological functions, including modulation of vascular tone, permeability, and capillary growth. Recent reports indicate that NO may play an intimate role in VEGF signaling. Therefore, we hypothesized that the expression of eNOS may be regulated by VEGF. The objectives of the present study were to determine whether VEGF up-regulates the expression of endothelial NO synthase (eNOS) in endothelial cells and to elucidate the mechanism that mediate this response. METHODS: Endothelial cells were isolated from bovine aortae. The expression of eNOS was assessed by Northern blotting analysis. To evaluate the mechanism of VEGF-induced eNOS expression, endothelial cells were conditioned with VEGF and pretreated with phorbol-12-myristate acetate (PMA), a protein kinase C (PKC) activator, or GF109203X (GFX), a PKC inhibitor. The changes of eNOS gene expression. RESULTS: VEGF significantly increased the expression of eNOS mRNA in bovine aortic endothelial cells (BAEC) in time and dose dependent manners. PMA increased the expression of eNOS mRNA, as well as the VEGF-induced expression of eNOS mRNA in endothelial cells, while inhibition of the PKC activity, with the GFX blocked the upregulation of the VEGF-induced eNOS mRNA. CONCLUSION: The results suggest that VEGF upregulates eNOS gene expression in aortic endothelial cells, by a PKC dependent pathway and, eNOS may be important in the development of VEGF-induced angiopathy.
Effect of Transforming Growth Factor-Induced Gene Product, beta ig-h3 on Proliferation, Migration, and Adhesion of Aortic Smooth Muscle Cells Cultured in High Glucose.
Sung Woo Ha, Gui Hwa Jung, He Jin Yeo, Jong Sup Bae, Soon Hee Lee, Jung Guk Kim, Rang Woon Park, In San Kim, Bo Wan Kim
Korean Diabetes J. 2002;26(4):286-295.   Published online August 1, 2002
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BACKGROUND
Diabetes mellitus is associated with a substantial increase in the prevalence of atherosclerotic disease. There are many factors which are involved in development of these processes. Transforming growth factor (TGF-beta) is known to be an important factor in the pathogenesis of diabetic vascular complications. TGF-beta-induced gene-h3 (beta ig-h3) is an adhesive molecule whose expression is induced by TGF-beta. Considering that TGF-beta plays an important role in diabetic complications and that beta ig-h3 is induced by TGF-beta, we hypothesized that beta ig-h3 may also play a role in the development of diabetic angiopathy. Then, we examined the effects of beta ig-h3 on biologic function of vascular smooth muscle cells (VSMCs) and potential roles of beta ig-h3 in the pathognesis of diabetic angiopathy. METHODS: VSMCs were isolated from rat thoracic aorta. We conditioned cells with different concentration of TGF-beta or glucose. We measured TGF-beta and beta ig-h3 protein in cell supernatant by ELISA. We also examined whether TGF-beta involves in high glucose-induced beta ig-h3 expression. Finally, we did proliferation, migration, and adhesion assay to investigate biologic function of beta ig-h3 in VSMCs. RESULTS: Our results demonstrated that TGF-beta induced beta ig-h3 expression in VSMCs in dose dependent manners. High glucose induced TGF expression as well as beta ig-h3 protein. Finally, beta ig-h3 was found to support the proliferation, migration, and adhesion of rat VSMCs. CONCLUSION: These results suggest that high glucose-and TGF-beta-induced beta ig-h3 may play an important role in diabetic angiopathy by regulating proliferation, migration, and adhesion of VSMCs.
Effect of Heat Shock on the Vascular Reactivity in Diabetic Rat Aorta.
Seong Mo Koo, Soon Hee Lee, Jung Hun Han, Gi Young Jeong, In Kyum Kim, Jung Guk Kim, Sung Woo Ha, Bo Wan Kim
Korean Diabetes J. 2001;25(5):343-353.   Published online October 1, 2001
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BACKGROUND
Heat shock has been known to change cellular response to noxious stimuli by inducing heat shock proteins (HSP). HSP are expressed in many tissues, and increased expression of some HSP enhances the survival of cells exposed to oxidative stress. Recently, Some HSP are known to associate with vascular reactivity. Under diabetic conditions, there is abnormal vascular reactivity to relaxing or contracting factors. Abnormal vascular response to some stimuli is an important role in the development of diabetic complications. However, the effects of heat shock on the vascular reactivity in diabetic condition is unclear. Therefore, we investigated effects of heat shock on the vascular reactivity in isolated aorta of streptozotocin-induced diabetic rats. METHODS: After mounced in organ bath, aortic ring preparations were exposed to 42 for 45 minutes followed by being subjected to contraction and relaxation in 4 hours. Tissues were frozen for measurement of HSP 70 and phosphorylation of myosin light chain after functional study. RESULTS: Heat shock not only increased expression of HSP70 in rat aorta but also augmented contraction to KCl and phenylephrine in the aorta of control and diabetic rats (p<0.05). Relaxation responses to acetylcholine (ACh) were not changed in the aorta of control rats with and without heat shock for 45 minutes. However, heat shock for 45 minutes decreased relaxative responses to ACh in the aorta of diabetic rats compared to those in the aorta of control rats. CONCLUSION: This result suggests that heat shock increases vascular contractility in the aorta of diabetic and control rats through the induction of HSP70 while heat shock seems to decrease relaxative response in the aorta of diabetic ratscompared to control rats (p<0.05). Whether heat shock impaired relaxative response in the aorta of diabetic rats deserves additional studies.
The Prevalence of Chronic Complications in Non-Insulin Dependent Diabetic Patients.
Jick Hwa Nam, Soon Hee Lee, Hyun Jeong Lee, Jeung Hun Han, Jung Guk Kim, Sung Woo Ha, Bo Wan Kim
Korean Diabetes J. 1999;23(5):702-714.   Published online January 1, 2001
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BACKGROUND
The chronic complications of diabetes mellitus are important prognostic factors of diabetics. The pathogenic mechanisms have not been known exactly and the prevalence is different according to the race and the reporter. In general, the development of diabetic microangiopathy depends on the duration and the severity of disease, while that of macroangiopathy does not. This study was undertaken to investigate the prevalence of diabetic chronic complications according to age and duration of diabetes and to elucidate associated factors and correlation of chronic complications. METHODS: We studied 1,270 patients with non- insulin dependent diabetes mellitus (NIDDM) who visited the Endocrine-metabolism clinic at Kyungpook National University during the period from February 1992 to September 1996. We investigated prevalence, severity, associated factors and correlation of chronic vascular complications, including micro- and macroangiopathy. RESULT: 1) The ratio of male to female was similar and the average duration was 7.8 years. Diabetes mellitus was most prevalent in the 6th decade and the 1-5 years of diabetes duration. 2) The prevalences of retinopathy, nephropathy and peripheral polyneuropathy were 47.8%, 31.9% and 41.0%, respectively. Macrovascular complications were found in 6.2% of patients and the prevalences of coronary artery disease, cerebrovas-cular disease and peripheral artery disease were 2.4%, 3.4%, 0.4%, respectively. Prevalence of diabetic foot was 4.4%. 3) The prevalence and severity of microvascular complications increased as the age and diabetic duration of patients increased. In the group of same age, the prevalence of microvascular complications increased as the duration of diabetes increased. However, prevalence of macrovascular complica-tions especially coronary artery disease depended on the age, but not the duration of diabetes (p<0.05). 4) In the group over 10 years of diabetes, the fasting blood glucose, age and serum creatinine levels were increased, while hemoglobin and total protein levels were decreased than other groups (p<0.05). 5) The development of diabetic retinopathy was related to the duration, fasting blood glucose, albumine excretion rate and serum creatinine. The nephropathy was related to the duration and systolic blood pressure. The peripheral polyneuropathy was related to the duration, fasting blood glucose and body mass index. Macrovascular complications-particularly, coronary artery disease-were related to the age of diabeties (p<0.05). 6) There was significant relation between development of retinopathy, nephropathy and neuropathy but no relation between development of micro and macrovascular complications (p<0.05). CONCLUSION : The prevalence of microvascular complications in non-insulin dependent diabetics increased as the duration and the age of diabetics increased. The development of microvascular complications was related to the duration of disease and the glycemic control. There was relation between development of retinopathy, nephropathy and neuropathy. The development of macrovascular complications, however, was related to the age of diabetics but not to the microvascular complications. Our results suggest that different pathogenic mechanisms may be involved in the development of micro- and macrovaseular complications of diabetes mellitus.
Clinical Manifestation and Prognostic Factors in Nonketotic Hyperosmolar Coma.
Bo Wan Kim, Jung Guk Kim, Sung Woo Ha, Hyun Jeong Lee, Jeung Hun Han, Sang Won Jung, Jick Hwa Nam, Si Hyung Park, Soon Hee Lee
Korean Diabetes J. 1999;23(4):575-584.   Published online January 1, 2001
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BACKGROUND
Nonketotic hyperosmolar coma is usually a complication of non-insuli#n dependent diabetes and a syndrome of profound dehydration, hyperglycemia and hyperosmolarity. Therefore the patients present a progressive mental change. We evaluated the clinical manifestations of nonketotic hyperosmolar coma to assess the correlation between initial clinical manifestations and responses to treatment in patients with nonketotic hyperosmolar coma. METHODS: We studied 31 patients who had experienced proven nonketotic hyperosmolar coma at Kyungpook National University Hospital from March 1987 to February 1998. We divided nonketotic hyperosmolar coma patients into two groups, tbe complete recovery group and the incomplete recovery group, and compared clinical features and laboratory findings between these two groups. RESULTS: l) A total of 31 patients were studied. Eighteen patients were in the complete recovery group and thirteen patients were in the incomplete recovery group. 2) Mean age was 63.1+10.1 years old, initial blood glucose was 781.8+314.3 mg/dL, effective osmolarity was 342.6+34.9 mosm/L, arterial pH was 7.34. Serum creatinine level was 241.7+130.0 uol/L and BUN was 23.1+12.5 mmol/L. 3) Among clinical features of both groups (complete recovery and incomplete recovery groups), initial systolic blood pressure was 131.4+26.1 mmHg and 104.1+28.6 mmHg, diastolic blood pressure was 90.6+16.5 mmHg and 63.2+17.4 mmHg, and mean arterial blood pressure was 104.2 +18.2 mmHg and 76.8+19.7 mmHg. They revealed a significant difference statistically. 4) Arterial blood pH was 7.40 and 7.25, BUN was 18.4+11.7 mmol/L and 29.5+11.1mmol/L, and WBC count was 13850+4122/ mm and 19823+ 5946/mm. They revealed a significant difference statistically. 5) We also analyzed the significant factors together using multivariate logistic regression analysis. The only significant independent factor responsible for prognosis of nonketotic hyperosmolar coma was initial mean arterial blood pressure. CONCLUSION: Nonketotic hyperosmolar coma occurred more frequently in patients who were older and had abnormal renal function. The prognosis of patients was related with mean arterial blood pressure independently. Mean arterial blood pressure thought to be related to intravascular volume and arterial hypotension seems to reflect dehydration state. In conclusion, prevention and rapid correction of hypotension due to dehydration in older diabetics is the most important treatment to improve the prognosis.
Effect of Transforming Growth Factor-B1 and Platelet Derived Growth Factor on Synthesis and Gene Expression of Collagen and Non-Collagen Protein in Aortic Smooth Muscle Cells Cultured in Different Concentrations of Insulin and Glucose.
Kun Young Sohn, In San Kim, Bo Wan Kim, Jung Guk Kim, Sung Woo Ha, Jick Hwa Nam, Seong Mo Koo, Rang Woon Park, Sam Kweon
Korean Diabetes J. 1999;23(4):518-529.   Published online January 1, 2001
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BACKGROUND
The mechanism for accelerated atberosclerosis in diabetes mellitus is unclear although diabetes mellitus is associated with substantial increase in prevalence of atherosclerotic disease. Extracellular matrix formation by vascular smooth muscle cells has been accepted as playing important roles during development of atherosclerosis. High glucose condition has been reported to increase the synthesis of extracellular matrix such as collagen and fibronectin in cultured mesangial cells. Insulin and some cytokines such as TGF-B and PGF have also been reported to stimulate the synthesis of collagen in mesangial cells. So we studied the effect of high glucose, insulin, TGF-Band PDGF on vascular smooth muscle cells. METHODS: To determine the effect of bigh glucose condition on collagen synthesis in vascular smooth muscle cells, cells were grown in the culture medium containing either normal (5.5 mM) or high (25 mM) glucose. And we used several concentrations of TGF-B1PDGF-BB and insulin in order to determine the synergistic effects of collagen synthesis and type I collagen mRNA expression. RESULTS: We observed that cells cultured in high glucose media synthesized more collagen and increased expression of type I collagen mRNA as compared to normoglycemic media. The amount of synthesized collagen and type I collagen mRNA expression increased proportionally to the increase in insulin concentration. There was no relationship of TGF-B1or PDGF-BB with the expression of type I collagen mRNA but these cytokines stimulated the synthesis of collagen and noncollagen protein. There was no synergistic effect of col)agen synthesis and type 1collagen mRNA expression by high glucose, insulin, and cytokines. CONCLUSION: These results suggest that TGF-Band PDGF may not influence type I collagen mRNA expression under hyperglycemia or hyperinsulinemia in vascular smooth muscle cells. Further studies about the other types of collagen expressions such as type IV, and V are needed because TGF-Band PDGF stimulated the synthesis of collagen and noncollagen protein.
Association Between QTc Dispersion and Cardiovascular Autonomic Dysfuction in Non-insulin Dependent Dabetes Mellitus.
Jung Guk Kim, Hun Sik Park, Jick Hwa Nam, Byoung Ho Sin, Seong Mo Koo, Sung Woo Ha, Bo Wan Kim
Korean Diabetes J. 1998;22(2):173-181.   Published online January 1, 2001
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BACKGROUND
Diabetic patients with autonomic dysfunction have worse prognosis, including an increased incidence, of sudden death, than those without autonomic dysfunction. This event may be due to sympathetic imbalance causing disturbances of ventricular repolarization. QT dispersion have recently been demonstrated to reflect dispersion of ventricular refractoriness and is a marker of arrhythmogenic potential. METHODS: Sixty diabetic patients and 31 normal subjects were studied. All patients had clinical test for cardiovascular autonomic dysfunction by Ewings method and defined as normal, early involved, definitely involved, severely involved and atypical group for 5 validated tests. Resting standard 12-lead electrocardiograms were recorded for measurement of QT dispersion, defined as the difference of longest QT interval and shortest QT interval, and corrected for heart rate using Bazetts formula. RESULTS: Twenty-seven dIiabetic patient were abnormal in cardiovascular autonomic function tests. In these patients corrected QT dispersion (QTc) were significantly longer compared to that 33 patients without autonomic dysfunction(47.4+14.7 vs 22.6+ 8.1msec p<0.001). And also there was significant difference of QTc dispersion between normal subject and diabetic patients with autonomic neuropathy group(20.5+9.2 vs 47.4+14.7msec p<0.001). But there was no difference between normal control and diabetic patients without autonomic neuropathy group. And QTc dispersion was not related to the presence ot nephropathy, retinopathy or peripheral polyneuropathy. We also found that there was no relationship between the severity of autonomic neuropathy and degree of Q7c dispersion. CONCLUSION: We concluded that QTc dispersion may be a good method for evaluation of cardiovascular autonomic neuropathy and increased QTc dispersion may be one of the markers of arrhythmia in diabetic patients with autonomic neuropathy.
The Role of NO in Endothelial Cell Function and Insulin Action.
Sung Woo Ha
Korean Diabetes J. 1998;22(2):127-130.   Published online January 1, 2001
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No abstract available.
Relationship between Peripheral Neuropathy and Cardiovascular Autonomic Neuropathy in Non-Insulin Dependent Diabetics.
Sung Woo Ha, Hyun Jeong Lee, Jeung Hun Han, Sang Won Jung, Jick Hwa Nam, Byoung Ho Sin, Seong Mo Koo, Jung Guk Kim, Sam Kwon, Bo Wan Kim
Korean Diabetes J. 1997;21(4):476-483.   Published online January 1, 2001
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BACKGROUND
Autonomic neuropathy was detected in some diabetics with symmetric peripheral neuropathy, a common complication of diabetes mellitus that may be associated with considerable morbidity. There has been known to be similarity of pathogenic mechanism in two neuropathies. Then we examined nerve conduction velocity and cardiovascular autonomic function tests. We studied relationship between peripheral and cardiovascular autonomic neuropathy in non-insulin dependent diabetics. METHODS: We studied 166 patients with or witbout peripheral neuropathy who had been diagnosed as non-insulin dependent diabetes mellitus. We examined nerve conduction tests to assess diabetic peripheral neuropathy and classified them into 4 groups aecording to neuropathic symptoms and results of nerve conduction tests. We examined five cardiovascular autonomic function tests by Ewing's methods. RESULTS: 1. The duration of diabetes mellitus was significantly longer in the group of cliabetics with neuropathic symptoms and abnormal findings in the nerve conduction velocity tests than the other groups. The level of blood glucose was significantly higher in the group of diabetics with neuropathic symptoms and findings than the other groups. 2. In the 5 cardiovascular autonomic function tests, heart rate response to deep breathing and Valsalva maneuver had significant differences between the diabetic group with peripheral neuropathy and the other groups. 3. The frequency and severity of autonomic neuropathy were higher in the group with peripheral neuro-pathic symptoms and findings than the other groups without neuropathic syrnptoms and findings. There was an overall significant relationship between sensorirnotor neural function and autonomic function. 4. There was no association between peripheral neuropathy and nephropathy although peripheral neuropathy was related with retinopathy. CONCLUSION: Diabetic peripheral neuropathy accompanies autonomic neuropathy. Then, this result suggests that there is the relationship between peripheral and cardiovascular autonomic neuropathy.
Lipopolysaccharide-Induced Changes in Vascular Reactivity of Diabetic Rat Aorta.
Ye Kyung Seo, Sang Won Chung, Jik Hwa Nam, Byoung Ho Sin, Dong Hee Kim, Jung Guk Kim, Sung Woo Ha, Bo Wan Kim
Korean Diabetes J. 1997;21(3):280-288.   Published online January 1, 2001
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Backgound: Hemodynamic deteriorations in diabetes mellitus may be mediated by increased contractile response to catecholamines and/or by decreased relaxative response to vasodilators such as acetylcholine(Ach). Decrease in peripheral vascular reactivity to vasoconstrictor was known to be an ominous sign that happens during sepsis or after injection of bacterial lipopolysaccharides(LPS). In this study, we compared the effects of LPS on function of diabetic rat aorta with impaired vascular reactivity with those of control rat aorta. METHODS: Contractile responses to cumulative concentrations(10'M to 3X10'M) of norepinephrine (NE) were measured in aorta isolated ftom the control and 4 to 5-week streptozotocin-induced diabetic rat at 6 hours after LPS treatment to compare with contractile responses of untreated group. We measured relaxative responses to cumulative concentrations(10'M to 10M) of Ach and nitroprusside (NTP) in these aortas contracted submaximally by NE. RESULTS: Diabetic rat aortas showed significantly more impairment in relaxative responses to Ach than control rat aortas before LPS treatment(p0.05 = 0.0l). LPS treatment in those diabetic rat aortas decreased contractile responses to NE by 26.6%(p < 0.01); the changes were sirnilar to those of control (30.9%, p0.01). Relaxative responses to Ach were also significantly decreased by 25.0%(p 0.01) after L.PS treatment; the changes were similar to those of control(34.1%, p0.01). However relaxative responses to NTP were not changed in control and d.iabetic rat aortas by LPS treatment. CONCLUSION: These results suggest that diabetes may induce impairment in endothelium-dependent vascular relaxation and there rnay be no difference of L,P,S-induced effects on hemodynamic deterioration between 4 to 5-week diabetic and control rats.

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