- In vivo Corneal Confocal Microscopy and Nerve Growth Factor in Diabetic Microvascular Complications.
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Ji Sun Nam, Young Jae Cho, Tae Woong Noh, Chul Sik Kim, Jong Suk Park, Min ho Cho, Hai Jin Kim, Ji Eun Yoon, Han Young Jung, Eun Seok Kang, Yu Mie Rhee, Hyung Keun Lee, Chul Woo Ahn, Bong Soo Cha, Eun Jig Lee, Sung Kil Lim, Kyung Rae Kim, Hyun Chul Lee
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Korean Diabetes J. 2007;31(4):351-361. Published online July 1, 2007
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DOI: https://doi.org/10.4093/jkda.2007.31.4.351
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Abstract
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- BACKGROUND
In vivo corneal confocal microscopy (IVCCM) is being recognized as a non-invasive, early diagnostic tool for diabetic neuropathy, for it provides a clear image of corneal subbasal nerve plexus in detail. Nerve growth factors (NGF) are believed to regulate peripheral and central nervous system, neuronal differentiation, and regeneration of damaged nerves, and their role in diabetic neuropathy is being emphasized these days. Moreover, NGFs and receptors are also expressed in retina and renal mesangial cells, suggesting their possible role in the common pathogenesis of diabetic microvascular complications. We plan to examine corneal structures of diabetic patients and compare IVCCM with conventional tools and analyze their serum and tear NGF levels. METHODS: IVCCM, nerve conduction velocity (NCV), and serum, urine, and tear samplings were done to 42 diabetic patients. From IVCCM, we measured corneal nerve density, branch, and tortuosity, total corneal/epithelial thickness, and the number of endothelial/keratocyte cells, and we checked patients' biochemical profiles and serum and tear NGF levels. RESULTS: Patients with more severe neuropathy had less corneal endothelial cells (3105 +/- 218 vs. 2537 +/- 142 vs. 2350 +/- 73/mm3 vs. 1914 +/- 465/mm3, P = 0.02), higher serum NGF (36 +/- 15 vs. 60 +/- 57.66 vs. 80 +/- 57.63 vs. 109 +/- 60.81 pg/mL, P = 0.39) and tear NGF levels (135.00 +/- 11.94 vs. 304.29 +/- 242.44 vs. 538.50 +/- 251.92 vs. 719.50 +/- 92.63 pg/mL, P = 0.01). There was a positive correlation between neuropathy and corneal nerve tortuosity (r2 = 0.479, P = 0.044) and negative correlation between neuropathy and endothelial cell count (r2 = -0.709, P = 0.002). Interestingly, similar changes were seen in other microvascular complications as well. CONCLUSION: Our results provide a possibility of using novel tools, IVCCM and NGF, as common diagnostic tools for diabetic microvascular complications, but it should be followed by a large population study.
- Activation of NF-kappaB and AP-1 in Peripheral Blood Mononuclear Cells Isolated from Patients with Diabetic Nephropathy.
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Jisun Nam, Min Ho Cho, Jong Suk Park, Geun Taek Lee, Hai Jin Kim, Eun Seok Kang, Yu Mie Lee, Chul Woo Ahn, Bong Soo Cha, Eun Jig Lee, Sung Kil Lim, Kyung Rae Kim, Hun Joo Ha, Hyun Chul Lee
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Korean Diabetes J. 2007;31(3):261-273. Published online May 1, 2007
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DOI: https://doi.org/10.4093/jkda.2007.31.3.261
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Abstract
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- BACKGROUND
We evaluated the role of oxidative stress in diabetic nephropathy by measuring intracellular reactive oxygen species (ROS) and redox-sensitive transcription factors in isolated peripheral mononuclear cells (PBMC). METHODS: From 66 diabetic patients with or without diabetic nephropathy (Group III and II, respectively) and 49 normal control subjects (Group I), spontaneous and stimulated ROS levels, activities of nuclear factor-kappa B (NF-kappaB), activator protein-1 (AP-1), and specificity protein1 (Sp1) in PBMC, urinary and PBMC TGF-beta1 (transforming growth factor-beta1), and 24-hour urinary albumin excretion (UAE) were measured. RESULTS: Spontaneous ROS was significantly higher in group III and II than group I (60.7 +/- 3.3 vs. 60.0 +/- 3.0 vs. 41.1 +/- 2.4%, respectively), and stimulated ROS were significantly higher in Group III compared to Group II (Increment of H2O2-induced ROS production: 21.8 +/- 2.2 vs. 11.1 +/- 2.0%, respectively; increment of PMA-induced ROS production 23.5 +/- 4.5 vs. 21.6 +/- 2.2%, respectively). The activities of NF-kappaB and AP-1, but not of Sp1, were significantly higher in Group III than in Group II (2.53 vs. 2.0 vs. 1.43-fold, respectively). Both PBMC- and urinary TGF-beta1 levels were higher in Group III than Group II (3.23 +/- 0.39 vs. 1.99 +/- 0.68 ng/mg in PBMCs, 16.88 +/- 6.84 vs. 5.61 +/- 1.57 ng/mL in urine, both respectively), and they were significantly correlated with activities of NF-kappaB and AP-1 and 24-hour UAE. CONCLUSIONS: Increased intracellular ROS generation in PBMCs of diabetic patients is involved in the pathogenesis of diabetic nephropathy through activation of NF-kappaB and AP-1, but not Sp1, and increased expression of TGF-beta1.
- Thebeta3-adrenergic Receptor Gene Polymorphism in Non-Insulin Dependent Diabetes Mellitus.
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Ji Hyun Lee, Hai Ri Li, Sang Won Lee, Su Youn Nam, Young Jun Won, Bong Soo Cha, Moon Suk Nam, Young Duk Song, Eun Jig Lee, Sung Kil Lim, Kyung Rae Kim, Hyun Chul Lee, Kap Bum Huh
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Korean Diabetes J. 1997;21(2):130-137. Published online January 1, 2001
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Abstract
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The B3-adrenergic receptor, located mainly in adipose tissue, is known to be involved in the regulation of lipolysis and thermogenesis. Recently studies have shown that the B3-adrenergic receptor gene polymorphism is associated with Non-Insulin Dependent Diabetes Mellitus(NIDDM) and insulin resistance. We investigated the relationship between the B3-adrenergic receptor gene polymorphism and the cli!ical and biochemical features of NIDDM patients. METHODS: Anthropometeric and biochemi al characteristics were determined for 134 NIDDM subjects and 30 nondiabetic controls. All subjects were genotyped for the 0-adrenergic receptor gene mutation using restriction fragment length polymorphism assay. RESULTS: The allelic frequency of the mutated allele was similar in NIDDM subjects and nondiabetic controls(11%, 12% respectively). There was no difference in the Arg64 allelic frequency of the B3-adrenergic receptor gene according to the onset age of diabetes. In diabetic group, the clinical and biochemical characteristics were not statistically different between the B3-adrenergic receptor gene mutation and nonmutation group. In control group, also no clinical differences were found between mutation and non-mutation group. When comparing frequency of obesity according to the B3-adrenergic receptor gene mutation in diabetic patients, we did not find the difference between the two groups. CONCLUSION: These results suggest that the b3-adrenergic receptor gene is not a major determinant for the development of obesity and NIDDM in Korea.
- A case of insulinoma localized by endoscopic ultrasonography and intraoperative ultrasonography.
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Jae Sik Cho, Kyeong Mi Lee, Eun Jig Lee, Kyung Rac Kim, Jae Bok Jng, Hyun Chul Le, Kap Bum Huh, Hee Dae Lee, Ki Hwang Kim, Ki Bum Lee
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Korean Diabetes J. 1993;17(3):315-320. Published online January 1, 2001
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- The relationship between renin-aldosterone system and obesity in non-insulin dependent diabetes mellitus(NIDDM).
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Kwang Jin Ahn, Yoon Sok Chung, Choon Hee Chung, Eun Jig Lee, Sung Kil Lim, Kyung Rac Kim, Hyun Chul Lee, Kap Bum Huh
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Korean Diabetes J. 1993;17(3):283-291. Published online January 1, 2001
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- Effects of w3 fatty acid supplementation on serum lipids in patients with non-insulin dependent diabetes mellitus.
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Yoon Sok Chung, Seog Won Park, Jin Ahn Kim, Eun Jig Lee, Sung Kil Lim, Kyung Rac Kim, Hyun Chul Lee, Kap Bum Huh, In Kyoung Paik, Ji Young Yoon, Hee Son Kim, Hyun Jong Chang
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Korean Diabetes J. 1993;17(3):267-274. Published online January 1, 2001
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- No abstract available.
- Is the pancreas of cytomegalovirus genome in type I diabetic Koreans significant?.
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Yoon Sok Chung, Hyun Chul Lee, Kwang Jin Ahn, Eun Jig Lee, Seung Kil Lim, Kap Bum Huh, Dong Soo Kim, Duk Hi Kim, Jeong Im Lee
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Korean Diabetes J. 1991;15(2):213-219. Published online January 1, 2001
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- No abstract available.
- Insulin secretory capacity of human fetal pancreas.
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Hyun Chul Lee, Kwang Jin Ahn, Eun Jig Lee, Sung Kil Lim, Kyung Rae Kim, Kap Bum Huh
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Korean Diabetes J. 1991;15(2):197-203. Published online January 1, 2001
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- No abstract available.
- The effect of interleukin-1 beta on isolated rat pancreatic islets.
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Hyun Chul Lee, Kwang Jin Ahn, Eun Jig Lee, Sung Kil Lim, Kyung Rae Kim, Kap Bum Huh
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Korean Diabetes J. 1991;15(1):73-78. Published online January 1, 2001
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- No abstract available.
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