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Chong Ho Lee  (Lee CH) 2 Articles
Oxidative Stress and Antioxidative Defense System in Offspring of Protein-Malnourished Rats.
Eun Young Cho, Hyeong Kyu Park, Hyeon Jeong Jeon, Suk Kyeong Kim, Kyong Soo Park, Chong Ho Lee, Seong Yeon Kim, Hong Kyu Lee
Korean Diabetes J. 2001;25(3):190-199.   Published online June 1, 2001
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AbstractAbstract PDF
BACKGROUND
Free radical-mediated oxidative damage has been implicated in a variety of pathological processes such as diabetes mellitus, aging and atherosclerosis. The susceptibility of a given organism to oxidative damage is influenced by the overall balance between the degree of oxidative stress and antioxidative capabilities. Nutrition plays an important role in determining the cellular antioxidative defense mechanism. Thus, the aim of this study is to investigate the effects of fetal protein malnutrition on oxidative stress and antioxidative capabilities. METHOD: Rats were fed a low-protein (8% casein) diet throughout pregnancy and lactation. Male offspring were weaned onto either a control (18% casein) diet (group 2) or a low-protein diet (group 3). Offspring from rats fed a control diet were weaned onto a control diet (group 1). The activities of superoxide dismutase (SOD), glutathione peroxidase (GPx) and the concentration of thiobarbituric acid- reactive substances (TBARS) were determined at 10 and 15 wk in liver and skeletal muscle from offspring. RESULTS: SOD activities of liver in group 3 were significantly lower than those in group 1 at 10 wk (4.14+/-0.65 U/mg protein, 9.09+/-0.85 U/mg protein) and 15 wk (4.18+/-0.58 U/mg protein, 7.63+/-0.74 U/mg protein), respectively. But SOD activities of skeletal muscle were not different between groups. Whilst GPx activities of liver were not different at 10 wk, GPx activities in group 2 (1.80+/-0.16 U/mg protein) were significant higher than those in group 1 (1.24+/-0.15 U/mg protein) at 15 wk. GPx activities of skeletal muscle were not different between groups. The TBARS concentrations in liver or skeletal muscle were not different between groups at 10 and 15 wk. There was a significant negative correlation between SOD activities and TBARS concentrations in liver (r=-0.359). CONCLUSION: In offspring of rats fed a low-protein diet throughout pregnancy and lactation, the antioxidant enzyme activities were significantly decreased, compared with offspring of rats fed a control diet. These alterations were not fully restored in low-protein offspring even when weaned onto a control diet. These results suggest that fetal protein malnutrition impair the antioxidative defense system.
Limitation of Validity of Homeostasis Model Assessment as a Index of Insulin Resistance.
Yong Seok Yun, Seok Won Park, Young Duk Song, Hyo Kyung Park, Oh Yoen Kim, Chul Woo Ahn, Jae Hyun Nam, Su Youn Nam, Bong Soo Cha, Chong Ho Lee, Sumg Gil Lim, Kyung Rae Kim, Hyun Chul Lee, Kap Bum Huh
Korean Diabetes J. 2000;24(5):541-551.   Published online January 1, 2001
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AbstractAbstract
BACKGROUND
Homeostasis model assessment of insulin resistance (HOMAIR) had been proposed as a simple and inexpensive alternative to other complex procedures measuring insulin resistance. We evaluated the validity of HOMAIR, comparing to total glucose disposal rate measured by euglycemic clamp test in 63 subjects with normal glucose tolerance, 21 with impaired glucose tolerance and 47 with type 2 DM. METHODS: HOMAIR and HOMA cell function (Homeostasis model assessment of cell function) were calculated with formula described by Matthews [HOMAIR: fasting insulin ( U/mL) X fasting glucose (mmol/L) / 22.5, HOMA cell function: 20 X fasting insulin ( U/mL) / (fasting glucose (mmol/L) - 3.5)]. 2-hour euglycemic (5 mmol/L) hyper insulinemic (717 pmol/L) clamp test were carried out. RESULTS: The strong inverse correlation (r=-0.658, <0.001) was shown between log transformed HOMAIR and total glucose disposal rates. The agreement of two methodes in the categorization according to insulin resistance was moderate (weighed kappa=0.45). The magnitude of correlation coefficients were smaller in subjects with lower BMI (BMI < 23.7 kg/m2, r = -0.441 vs BMI > or = 23.7 kg/m2, r = -0.693, p = 0.0183), lower HOMA cell function (HOMA cell function < 57.2, r = -0.514 vs HOMA cell function > or = 57.2, r = -0.773, p = 0.0091) and higher fasting glucose levels (fasting glucose < 102 mg/dL, r = -0.697 vs fasting glucose > or = 102 mg/dL, r = -0.59, p = 0.0735). The results of correlation analysis was not significant in diabetics with lower BMI. CONCLUSION: Limitation of validity of HOMAIR should be carefully considered in subjects with lower BMI and lower fasting insulin to glucose levels, such as lean type 2 diabetes with insulin secretory defects.

Diabetes Metab J : Diabetes & Metabolism Journal