Kwan Jae Lee

Seoul National University Hospital, Seoul, Seoul, South Korea

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Publications (3)5.42 Total impact

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    ABSTRACT: In epidemiological studies, there is growing concern regarding the association between human exposure to bisphenol A (BPA) and an increased risk for cardiovascular disease. Therefore, we investigated whether BPA accelerates atherosclerosis in mouse model. Apolipoprotein E knockout (ApoE(-/-)) mice were fed a high-fat and high-cholesterol diet with or without 50 μg/kg body weight/day BPA for 12 weeks. Atherosclerotic lesions of the aorta and aortic sinus were evaluated by Oil red O staining. After the 12-week BPA treatment, BPA significantly increased atherosclerotic lesions in the aortas of ApoE(-/-) mice by 1.7-fold (p = 0.03). Non-high-density lipoprotein (HDL) cholesterol levels in the BPA group were significantly higher compared to those in the control group (1,035 ± 70 vs. 484 ± 48 mg/dL, p = 0.02) although body weight and blood glucose levels were not different between groups. Human umbilical vein endothelial cells (HUVECs) were treated with 0.1-10 nM BPA but BPA did not affect HUVEC proliferation or migration. BPA could accelerate atherosclerosis in ApoE(-/-) mice, which may have resulted from an increase in non-HDL cholesterol levels.
    Cardiovascular toxicology 11/2013; 14(2). · 2.56 Impact Factor
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    ABSTRACT: Small heterodimer partner (SHP) is involved in bile, lipid, and glucose metabolism. The aim of this study was to investigate the effect of SHP on the development of atherosclerosis. Apolipoprotein E knockout (ApoE(-/-)) mice were crossed with SHP knockout (SHP(-/-)) mice to generate double knockout (ApoE(-/-)SHP(-/-)) mice. ApoE(-/-) and ApoE(-/-)SHP(-/-) male mice were fed a western diet for 20 weeks. Body weight in ApoE(-/-)SHP(-/-) mice was significantly lower than that in ApoE(-/-) mice (37 ± 4 g vs. 42 ± 5 g, p < 0.01). Loss of SHP in ApoE(-/-) mice decreased the size of adipocytes in white adipose tissue and reduced lipid accumulation in the liver. Glucose intolerance was improved in ApoE(-/-)SHP(-/-) mice as compared with ApoE(-/-) mice (p < 0.01). There was no statistical difference in non-high density lipoprotein cholesterol levels between ApoE(-/-)SHP(-/-) mice and ApoE(-/-) mice despite an increase of cholesterol 7α-hydroxylase expression in the liver. The proportion of atherosclerotic lesions in the aorta was significantly lower in ApoE(-/-)SHP(-/-) mice than in ApoE(-/-) mice (2.8 ± 2.0% vs. 9.1 ± 1.9%, p < 0.01). In conclusion, loss of SHP function can prevent atherosclerosis, and resistance to diet-induced obesity is the primary factor contributing to this protective effect.
    Endocrine Journal 08/2013; · 2.02 Impact Factor
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    ABSTRACT: Bisphenol A (BPA) has been reported to possess hepatic toxicity. We investigated the hypothesis that BPA, below the no observed adverse effect level (NOAEL), can induce hepatic damage and mitochondrial dysfunction by increasing oxidative stress in the liver. Two doses of BPA, 0.05 and 1.2 mg/kg body weight/day, were administered intraperitoneally for 5 days to mice. Both treatments impaired the structure of the hepatic mitochondria, although oxygen consumption rate and expression of the respiratory complex decreased only at the higher dose. The hepatic levels of malondialdehyde (MDA), a naturally occurring product of lipid peroxidation, increased, while the expression of glutathione peroxidase 3 (GPx3) decreased, after BPA treatment. The expression levels of proinflammatory cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) also increased. In HepG2 cells, 10 or 100 nM of BPA also decreased the oxygen consumption rate, ATP production, and the mitochondrial membrane potential. In conclusion, doses of BPA below the NOAEL induce mitochondrial dysfunction in the liver, and this is associated with an increase in oxidative stress and inflammation.
    Journal of Korean medical science 06/2012; 27(6):644-52. · 0.84 Impact Factor