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Chang Beom Lee  (Lee CB) 4 Articles
Effects of Adding omega-3 Fatty Acids to Simvastatin on Lipids, Lipoprotein Size and Subspecies in Type 2 Diabetes Mellitus with Hypertriglyceridemia.
Won Jun Kim, Chang Beom Lee, Cheol Young Park, Se Eun Park, Eun Jung Rhee, Won Young Lee, Ki Won Oh, Sung Woo Park, Dae Jung Kim, Hae Jin Kim, Seung Jin Han, Hong Keum Cho
Korean Diabetes J. 2009;33(6):494-502.   Published online December 1, 2009
DOI: https://doi.org/10.4093/kdj.2009.33.6.494
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AbstractAbstract PDF
BACKGROUND
omega-3 fatty acids are known to improve lipid profiles, the distribution of lipoprotein subclasses, and secondary prevention against post-myocardial infarction. Rare reports have emerged of synergistic results of omega-3 fatty acids with simvastatin in cases of type 2 diabetes mellitus with hypertriglyceridemia. The purpose of this study was to determine the combined relationship of omega-3 fatty acids plus simvastatin on lipid, lipoprotein size and the types of subspecies. METHODS: This randomized, multi-center, comparison study evaluated eight weeks of combination therapy (omega-3 fatty acids (Omacor) 4 g/day plus simvastatin 20 mg/day) or monotherapy (simvastatin 20 mg/day) for at least six weeks in 62 diabetic patients. Subjects with a triglyceride concentration of more than 200 mg/dL were eligible for inclusion. RESULTS: No significant differences for omega-3 fatty acids + simvastatin versus simvastatin alone were observed for triglycerides (-22.7% vs. -14.3%, P = 0.292), HDL peak particle size (+2.8% vs. -0.4%, P = 0.076), LDL mean particle size (+0.4% vs -0.1%, P = 0.376) or LDL subspecies types, although the combination therapy showed a tendency toward lower triglycerides, larger HDL, and LDL particle sizes than did the monotherapy. There were no significant differences between the two groups in regard to HDL-C, LDL-C, or HbA1c levels. There were no serious adverse events and no abnormalities in the laboratory values associated with this study. CONCLUSION: omega-3 fatty acids were a safeform of treatment in hypertriglyceridemic patients with type 2 diabetes mellitus. But, regarding efficacy, a much larger sample size and longer-term follow-up may be needed to distinguish between the effects of combination therapy and monotherapy.
Fetal Organogenesis in a Pregestational Diabetic Mother Who has Taking an Oral Hypoglycemic Agent in Early Pregnancy.
Chang Beom Lee, Seung Yong Kim
Korean Diabetes J. 2004;28(6):530-537.   Published online December 1, 2004
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AbstractAbstract PDF
BACKGROUND
Women with diabetes mellitus are not treated with oral hypoglycemic agents because of the concerns about teratogenicity and neonate complication. There is not enough information about the safety of these drugs and especially during the first trimester of pregnancy. METHODS: Eight type 2 diabetic pregnant women with accidental exposure to an oral hypoglycemic agent during embryogenesis and twenty type 2 diabetic pregnant women who were matched for age, weight, and glycemic control, but they were not exposed to an oral hypoglycemic agent, were compared retrospectively. RESULTS: 1) Three out of the eight neonates (38%) in the oral hypoglycemic agent group had congenital malformations and stillbirth compared with five out of twenty (25%) in the control group (Odds ratio 1.8; range: 0.2~13.8, P >0.05). 2) In the control group, the mean HbA1c of the 5 mothers with anomalistic neonates and stillbirths was higher than that of 15 mothers with normal neonates (8.8% vs. 6.2 %, P = 0.1). The anomalies included three congenital heart diseases (1 ventricular septal defect, 2 patent ductus arteriosus) and one renal agenesis. 3) In the oral hypoglycemic agent group, the mean HbA1c of the 3 mothers with anomalistic neonates and stillbirth was higher than that of the 5 mothers with normal neonates (9.0% vs. 6.3%, P = 0.4). The anomalies included one urachal sinus and one facial palsy that have not been commonly described for diabetic embryopathy. 4) In both groups, the mean HbA1c of 8 mothers with complicated neonates and the 20 mothers with normal neonates was 8.1% and 6.8%, respectively, (P =0.09). CONCLUSION: We found no obvious indication for therapeutic abortions in patients who have accidentally been treated with an oral hypoglycemic agent during embryogenesis. On the contrary, it seems reasonable to reassure these women with respect to their risk of having a malformed baby, and then to stop treatment with an oral hypoglycemic agent and initiate insulin treatment.
The Role of Chromium as an Insulin Sensitizer in Rats Receivieng Corticosteroid.
Dong Sun Kim, Chang Beom Lee, Yong Soo Park, You Hern Ahn, Tae Wha Kim, Ho Soon Choi, Il Kyu Park, Hyun Jin Shin, Ju Seop Kang
Korean Diabetes J. 2001;25(3):211-217.   Published online June 1, 2001
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AbstractAbstract PDF
BACKGROUND
Chromium (Cr) has been known to be essential for the regulation of insulin action. Recently it has been reported that corticosteroid increases urinary loss of Cr, and that Cr supplementation recovers steroid induced diabetes mellitus. METHODS: Rats were daily treated with dexamethasone (0.2 mg/kg, ip) for first 7 days and were further treated daily with dexamethasone plus either chromium picolinate (30 mg/kg) or a placebo for a period of 14 days. RESULTS: At the end of experiment (Day 21), the control rats treated only with dexamethasone weighed 320 gram (80% of initial weight) in average, but the Cr treated rats weighed 364 gram (91% of initial weight. p<0.05). An insulin sensitivity test [subcutaneous injection of insulin (5 U/kg) plus intraperitoneal injection of glucose (30 minutes after insulin injection)] were conducted. During the insulin sensitivity tests, the area under curves (AUC(0->120 min)) of the time-glucose concentrations curves in the Cr-treated group were decreased compared to those in the control group (5250 vs 15883 mg-min/dL, p<0.01). Fasting serum insulin levels in the Cr-treated rats were clearly decreased by 46.9% compared to those in the control group (2.98 vs 5.60 ng/mL, p<0.05). CONCLUSIONS: We conclude that chromium supplementation reverse a catabolic state, and increase insulin sensitivity in dexamethasone treated rats.
The Effect of Cyclosporine on Insulin Sensitivity in Streptozotocin Induced Diabetic Rats.
Ju Seop Kang, Dong Sun Kim, Chang Beom Lee, Yong Soo Park, Woong Hwan Choi, Tae Wha Kim, Mok Hyun Kim
Korean Diabetes J. 1999;23(2):142-146.   Published online January 1, 2001
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AbstractAbstract PDF
BACKGROUND
Cyclosporine (CsA), being used as a immunosuppressant is known to have deleterious effects on the liver and kidney, but the harmful effect on glucose tolerance has not been clearly elucidated. This study was undertaken to determine whether the CsA affected peripheral insulin sensitivity in streptozotocin (STZ)-induced diabetic Sprague-Dawley rats. METHODS: After the daily treatment of CsA (10mg/kg, i.p.) for 2 weeks, glucose tolerance tests were carried out by the intraperitoneal administration of glucose alone or in conjunction with insulin (5 U/kg, s.c.). The glucose tolerance and peripheral insulin sensitivity were determined by measuring the deremental area under the time-lasma glucose concentration curve (AUC; mg-min/mL) according to the trapezoidal rule. The plasma glucose levels (mg/dL) were measured by a glucose analyzer at 0, 10, 30, 60, 90 and 120min after glucose load (2 g/kg). The STZ-diabetic rats were divided into thre groups (GLU- as control, INS+GLU- and CsA+INS+GLU-treated group, n 7 in each groups). RESULTS: In STZ-diabetic rats, the AUC 0-120 of the CsA+INS+GLU-treated group was significantly (p<0.01) lower than those of the control group (48.6% of control), but significantly (p<0.03) higher thain those of the INS+GLUtreated group (28.1% of control). CONCLUSIONS: These results suggest that intraperitoneal injection of CsA gives rise to a deterioration of glucose etabolism which is probably due to a decrease of insulin sensitivity of peripheral tissue in STZ-diabetic rats.

Diabetes Metab J : Diabetes & Metabolism Journal