Diabetes & Metabolism Journal

Soon Hee Lee (Lee SH)

10 Articles

Cloning of Novel Epidermal Growth Factor (EGF) Plasmid for Gene Therapy on Diabetic Foot Ulcer.: Hye Sook Chung, Chang Shin Yoon, Min Jeong Kwon, Mi Kyung Kim, Soon Hee Lee, Kyung Soo Ko, Byung Doo Rhee, Jeong Hyun Park; Korean Diabetes J. 2008;32(2):131-140. Published online April 1, 2008; DOI: https://doi.org/10.4093/kdj.2008.32.2.131

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BACKGROUND
Epidermal Growth Factor (EGF) is one of the important growth factors involved in the epithelialization during cutaneous wound healing. Peptide EGF has been used for the treatment of diabetic foot ulcer. But the inferiority of cost-effectiveness and the inconvenience of daily application might have restricted its wide clinical usage. EGF gene therapy could dramatically improve the efficacy and inconvenience through long-term expression and bypassing the EGF degradation by hostile non-specific proteinases expressed in the wound bed. METHODS: EGF DNAs were amplified via PCR. For the more effective secretion from the transfected cell, we inserted furin cleavage site into EGF plasmids. The efficacy of novel plasmid pbeta-EGF was verified by transfection into the various animal cell lines, and the biologic potency of expressed EGF was confirmed via phosphorylation of PI3K and GSK3beta by Western blotting. RESULTS: We tested various kinds of human EGFs. One of the human EGF isoforms, EGF(828) including a membrane-anchoring domain was successfully released as the mature EGF protein in the cell culture media. Also EGF plasmid including furin cleavage site showed more than 2-fold increased EGF expression compared with the sequence without furin cleavage site. CONCLUSION: In conclusion, these findings suggest that mature EGF could be released easily out of cells by modifying EGF DNA sequence. Our novel EGF plasmid DNA could markedly increase the efficiency of non-viral gene therapy for diabetic foot ulcer.

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Effective healing of diabetic skin wounds by using nonviral gene therapy based on minicircle vascular endothelial growth factor DNA and a cationic dendrimer
Min J. Kwon, Songhie An, Sunghyun Choi, Kihoon Nam, Hye S. Jung, Chang S. Yoon, Jung H. Ko, Hye J. Jun, Tae K. Kim, Soo J. Jung, Jeong H. Park, Yan Lee, Jong‐Sang Park
The Journal of Gene Medicine.2012; 14(4): 272. CrossRef

Cytoprotective Effect by Antioxidant Activity of Quercetin in INS-1 Cell Line.: Min Jeong Kwon, Hye Sook Jung, Mi Kyung Kim, Seong Hoon Kang, Gwang Wook Seo, Jae Kwang Song, Tae Yeon Yoon, Min Kyeong Jeon, Tae Hwan Ha, Chang Shin Yoon, Mi Kyung Kim, Woo Je Lee, Jeong Hyun Noh, Soo Kyung Kwon, Dong Joon Kim, Kyung Soo Koh, Byung Doo Rhee, Kyung Ho Lim, Soon Hee Lee, Jeong Hyun Park; Korean Diabetes J. 2007;31(5):383-390. Published online September 1, 2007; DOI: https://doi.org/10.4093/jkda.2007.31.5.383

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BACKGROUND
Oxidative stress is induced under diabetic conditions and causes various forms of tissue damages in the patients with diabetes. Recently, pancreatic beta cells are regarded as a putative target of oxidative stress-induced tissue damage, and this seems to explain in part the progressive deterioration of beta cell function in type 2 diabetes. The aim of this study was to examine the potential of Quercetin (QE) to protect INS-1 cells from the H2O2-induced oxidative stress and the effects of QE on the glucose-stimulated insulin secretion in INS-1 cells. METHODS: To study the cell viability, cells were incubated with H2O2 and/or QE at the various concentrations. To confirm the protective effect by QE in response to H2O2, the levels of antioxidant enzymes were assessed by RT-PCR and Western blot, and glutathione peroxidase activities were quantified by spectrophotometrical method. Glucose-stimulated insulin secretion (GSIS) was measured by ELISA. RESULTS: Cell incubations were performed with 80 microM of H2O2 for 5 hours to induce 40 - 50% of cell death. QE gradually showed protective effect (IC50 = 50 microM) in dose-dependent manner. Superoxide dismutase (SOD) mRNA level in H2O2 + QE group was increased as compared to H2O2 group, but catalase did not changed. And the QE recruited glutathione peroxidase activity against H2O2-induced oxidative injuries in INS-1 cells. CONCLUSION: In conclusion, these findings suggest that QE might have protective effect on beta cells by ameliorating oxidative stress and preserving insulin secretory function.

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Anti-diabetic effects of Allium tuberosum rottler extracts and lactic acid bacteria fermented extracts in type 2 diabetic mice model
Bae Jin Kim, Seung Kyeung Jo, Yoo Seok Jeong, Hee Kyoung Jung
Korean Journal of Food Preservation.2015; 22(1): 134. CrossRef
Protective Effects of Sasa Borealis Leaves Extract on High Glucose-Induced Oxidative Stress in Human Umbilical Vein Endothelial Cells
Ji-Young Hwang, Ji-Sook Han
Journal of the Korean Society of Food Science and Nutrition.2010; 39(12): 1753. CrossRef

Serum Adiponectin, TNF-alpha, IL-6 and Insulin Resistance in Women with Polycystic Ovary Syndrome.: Young A Kim, Jung Hyun Noh, Dong Jun Kim, Tae Hyun Um, Chong Rae Cho, Na young Jang, Soo Kyung Kwon, Soon Hee Lee, Jeong Hyun Park, Kyung Soo Ko, Byoung Doo Rhee, Kyung Ho Lim; Korean Diabetes J. 2006;30(2):104-111. Published online March 1, 2006; DOI: https://doi.org/10.4093/jkda.2006.30.2.104

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BACKGROUND
To determine plasma adipokines such as adiponectin, IL-6 and TNF-alpha concentrations in women with and without polycystic ovary syndrome (PCOS) and to assess possible correlations of adipocytokines to the hormonal and metabolic parameters, including measures of insulin resistance (IR). METHODS: Forty-four selected women were classified as follows: 13 obese (body mass index [BMI] > or = 25 kg/m(2)) with PCOS; 15 non-obese (BMI < 25 kg/m(2)) with PCOS; 8 obese without PCOS, and 8 non-obese without PCOS. Blood samples were collected from all women with or without PCOS after an overnight fast. Serum levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH), total testosterone, 17-alpha-hydroxyprogesterone, dehydroepiandrosterone sulfate (DHEA-S), sex hormone-binding globulin (SHBG), insulin, glucose, adiponectin, TNF-alpha and IL-6 were measured. Measures of IR included HOMA-IR and QUICKI. RESULTS: In non-obese group, fasting insulin levels and HOMA-IR in PCOS were significantly higher compared to control. However, Adiponectin, TNF-alpha and IL-6 concentrations were found not to be different in obese women with PCOS as compared with obese women without PCOS and in non-obese women with PCOS as compared with non-obese women without PCOS. Adiponectin concentrations correlated inversely with BMI, waist circumference (WC), total fat mass, serum insulin, and HOMA-IR in PCOS group. However, multiple regression analysis showed that BMI was the only independent determinant of adiponectin concentration. CONCLUSION: Our results suggest that insulin sensitivity per se probably does not play any role in the control of adipokines levels such as adiponectin, TNF-alpha and IL-6 in PCOS women

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Adiponectin in Women with Polycystic Ovary Syndrome
Hyun-Young Shin, Duk-Chul Lee, Ji-Won Lee
Korean Journal of Family Medicine.2011; 32(4): 243. CrossRef

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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Abstract PDF: 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.

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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Abstract PDF: 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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Abstract PDF: 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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Abstract PDF: 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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Abstract PDF: 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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Abstract PDF: 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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Abstract PDF: 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.

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