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Letter
Letter: Higher Glycated Hemoglobin Level Is Associated with Increased Risk of Ischemic Stroke in Non-Diabetic Korean Male Adults (Diabetes Metab J 2011;35:551-7)
Seok Hong Lee, Jihyun Ahn, Jaetaek Kim
Diabetes Metab J. 2012;36(1):79-80.   Published online February 17, 2012
DOI: https://doi.org/10.4093/dmj.2012.36.1.79
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  • 23 Download
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Case Report
A Case of Diabetic Ketoacidosis in a GAD Antibody-positive Diabetes Patients who Recently Experienced Hyperglycemic Hyperosmolar State.
Jang Won Son, Seok Hong Lee, Jung Ahn Lee, Jaetaek Kim, Yeon Sahng Oh, Soon Hyun Shinn
Korean Diabetes J. 2005;29(3):267-270.   Published online May 1, 2005
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  • 19 Download
AbstractAbstract PDF
The term latent autoimmune diabetes in adults(LADA) was introduced to define adult diabetic patients who initially do not require insulin, but they have the immune markers of type 1 diabetes and in a number of cases, these patients progress to insulin dependency. LADA patients have several features of classic type 1 diabetes in addition to islet cell antibody positivity, including high rates of HLA-DR3 and DR4. We describe here a case of a patient with a diagnosis of LADA who, having been diagnosed with type 2 diabetes, was affected with diabetic ketoacidosis. In April 2000, a 65-year-old man was admitted to Chung-Ang University Hospital due to his decreased cognitive ability. The patient was diagnosed with type 2 diabetes 30-years ago and he was diagnosed 6-month ago as being in a hyperglycemic hyperosmolar state. He was positive for antibodies against GAD(anti-GAD, 31U/mL). His weight was 70kg, height 167cm, BMI 25 kg/m2 and the blood pressure was 86/52mmHg. No abnormalities on the physical examination were found. His acid-base balance was pH 6.937, serum bicarbonate 2.2mmol/L and the anion gap 38; he also had a strong positive reaction for ketones in his urine and serum. During half a year, the fasting C-peptide level decreased from 0.65nmol/L to 0.13nmol/L, which means the rapid progression of beta-cell destruction. Intensive treatment of LADA with insulin may improve this type of patients' quality of life, and so potentially save the beta-cell function and perhaps lessening the risk of a hyperglycemic crisis
Original Article
Study on the Methylglyoxal-induced Apoptosis in Bovine Retinal Pericytes.
Jaetaek Kim, Seok Hong Lee, Jang Won Son, Jeong An Lee, Yeon Sahng Oh, Soon Hyun Shinn
Korean Diabetes J. 2004;28(3):199-207.   Published online June 1, 2004
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AbstractAbstract PDF
BACKGROUND
One of the histopathological hallmarks of early diabetic retinopathy is the loss of pericytes. Evidences suggest that this pericyte loss in vivo is mediated by apoptosis. However, the underlying cause of pericyte apoptosis is not fully understood. This study investigated the influence of methylglyoxal(MGO), a reactive alpha-dicarbonyl compound of glucose metabolism, on the apoptotic cell death in retinal pericytes. METHODS: Primary cultures of retinal pericytes were prepared from isolated bovine retinal microvessels. The cells were incubated under normoglycemic conditions after treatment with 200-800muM methylglyoxal for 6 hours. The cell viability was assessed using the MTT assay. The apoptosis and intracellular reactive oxygen species(ROS) generation were measured using an ELISA kit and flow cytometry, respectively. The NF-kappaB activation was detected by immunocytochemistry. RESULTS: MGO produced a progressive cytotoxic effect on the retinal pericytes. An analysis of the internucleosomal DNA fragmentation by ELISA showed that MGO(200 to 800muM) induced apoptosis in a concentration-dependent manner. ROS were generated earlier and the antioxidant, N-acetyl cysteine, inhibited the MGO-induced apoptosis. The NF-kappaB activation and increased caspase-3 activity were detected. The apoptosis was also inhibited by the caspase-3 inhibitor, Z-DEVD-fmk, or the NF-kappaB inhibitor, pyrrolidine dithiocarbamate. CONCLUSION: These results suggest that the elevated MGO levels observed in diabetes may cause apoptosis in the retinal pericytes through an oxidative stress mechanism, and suggests that the nuclear activation of NF-kappaB is involved in the apoptotic process.

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