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Now showing items 1 - 16 of 24

  • Hepatic iron storage is related to body adiposity and hepatic inflammation

    Park, Chan Yoon   Chung, Jayong   Koo, Kyung-Ok   Kim, Min Soo   Han, Sung Nim  

    Background: Obesity has been reported to be associated with iron deficiency. However, few studies have investigated iron status in low adiposity. To investigate whether body adiposity was associated with altered hepatic iron status, we compared liver iron levels and markers involved in inflammation and iron absorption in obese, control, and mildly calorie restricted mice. Methods: Seven week old C57BL/6 mice were fed control (10% kcal fat, Control) or high fat (60% kcal fat, HFD) diets, or reduced amount of control diet to achieve 15% calorie restriction (CR) for 16 weeks. Hepatic non-heme iron content and ferritin protein level, and hematocrit and hemoglobin levels were determined to assess iron status. Hepatic expression of Mcp-1 and Tnf-a were measured as hepatic inflammatory markers. Hepatic hepcidin (Hamp) and Bmp6, and duodenal Dmt1, Dcyt1b, hephaestin (Heph) and ferroportin mRNA levels were measured as factors involved in regulation of iron absorption. Results: Hepatic non-heme iron and ferritin protein levels were significantly higher in the CR group compared with the Control group, and significantly lower in the HFD group. These two iron status markers showed significantly negative correlations with the amount of white adipose tissue (r =3D -0.689 for hepatic non-heme iron and r =3D -0.740 for ferritin). Hepatic Mcp-1 and Tnf-a mRNA levels were significantly lower in the CR compared with the HFD (74 and 47% lower) and showed significantly negative correlations with hepatic non-heme iron levels (Mcp-1: r =3D -0.557, P < 0.05; Tnf-a: r =3D -0.464, P < 0.05). Hepatic Hamp mRNA levels were lower in the HFD and higher in the CR groups compared with the Control group, which could be a response to maintain iron homeostasis. Duodenal Dcyt1b mRNA levels were higher in the CR group compared with the HFD group and duodenal Heph mRNA levels were higher in the CR group than the Control group. Conclusion: We showed that body adiposity was inversely correlated with liver iron status. Low inflammation levels in hepatic milieu and enhanced expression of duodenal oxidoreductases induced by calorie restriction could have contributed to higher iron status.
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  • Quantification of Marker Compounds in Cirsium setidens Nakai by HPLC-DAD

    Jeong, Hyun Cheol   Shim, You-Shin   Rhee, Young Kyoung   Choi, Sang Yoon   Hong, Hee-Do   Chung, Jayong   Han, Myung Joo   Cho, Chang-Won  

    An effective method of high performance liquid chromatography-diode array detector (HPLC-DAD) was developed for the simultaneous quantification of two marker compounds, pectolinarin and pectolinarigenin, in Cirsium setidens Nakai, a Korean wild herb. The two marker compounds of C. setidens were separated on a C18 column with a gradient system. The calibration curves of the two standard compounds exhibited good linearity (R-2 >0.9992). The limits of detection (LOD) values of pectolinarin and pectolinarigenin were 0.52 and 0.41 mu g/mL, respectively, while their limits of quantification (LOQ) values were 1.57 and 1.25 mu g/mL, respectively. The relative standard deviations (RSDs) of the data of the intra- and inter-day experiments were less than 1.65 and 2.78%, respectively. The results of the recovery test were 98.06-105.81% with an RSD value of 1.87-3.50%. In conclusion, the results of validation showed that the proposed BPLC method was useful for the quantification of the two marker compounds in C. setidens.
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  • Diet-induced obesity leads to decreased hepatic iron storage in mice

    Chung, Jayong   Kim, Min Soo  

    An increased risk of iron deficiency has been reported in obese individuals. We investigated hepatic iron status and serum levels of both adipokines and inflammatory markers in obese mice to test the hypothesis that high-fat-diet (HFD)-induced obesity leads to reduced iron storage associated with inflammation. Four-week-old C57BL mice were fed a HFD containing 60% energy from fat for 16 weeks and were compared with mice on a control diet with 10% energy from fat. The HFD group had significantly higher levels of leptin (43.7 ng/mL in control, n = 16 vs 104.3 ng/mL in HFD, n = 17; P < .001) and significantly lower amounts of high-molecular-weight adiponectin (4.80 mu g/mL in control, n = 16 vs 3.67 mu g/mL in FIFD, n = 18; P = .002) compared with the control group. Higher serum amyloid A levels in the FIFD group (60.4 mu g/mL in control, n = 17 vs 117.9 mu g/mL in HFD, n = 18; P < .001) suggest inflammation in the HFD-induced obese animals. The FIFD group had lower hepatic nonheme iron (3.12 mu g/mg protein in control, n = 17 vs 0.869 mu g/mg protein in HFD, n = 16; P < .001). Expression of hepcidin messenger RNA (mRNA) was only 54% of the control levels in HFD mice (P = .016). However, the ratio of hepcidin mRNA expression to nonheme iron was 2.5-fold higher in the HFD compared with the control animals. Hepcidin is a homeostatic regulator of iron metabolism that restricts intestinal iron absorption and is also known as a mediator of inflammation. Increased serum amyloid A levels and a higher ratio of hepatic hepcidin mRNA expression to nonheme iron suggest that lower hepatic iron status in obese animals might be associated with inflammation. (C) 2011 Elsevier Inc. All rights reserved.
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  • Effect of Copper on the Regulation of Ferroportin-1 Gene Expression

    Park, Bo-Yoen   Chung, Jayong  

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  • Ferroportin-1 Is Not Upregulated in Copper-Deficient Mice

    Chung, Jayong   Prohaska, Joseph R.   Wessling-Resnick, Marianne  

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  • Molecular Mechanisms and Regulation of Iron Transport

    Chung, Jayong   Wessling-Resnick, Marianne  

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  • Base-pair interactions in the gas-phase proton-bonded complexes of C(+)G and C(+)GC

    Han, Sang Yun   Lee, Sang Hak   Chung, Jayong   Bin Oh, Han  

    Interactions involved in the formation of gas-phase proton-bonded molecular complexes of cytosine (C) and guanine (G) were theoretically investigated for the case of C(+)G and C(+)GC using B3LYP density functional theory. In this study, particular focus was on the dimeric interaction of proton-bonded C(+)G, where a proton bond and a hydrogen bond are cooperatively involved. The dimer interaction energy in terms of dissociation energy (D(e)) was predicted to be 41.8 kcal/mol. The lowest (frozen) energy structure for the C(+)G dimeric complex was found to be CH(+)center dot G rather than C center dot H(+)G in spite of the lower proton affinity of the cytosine moiety, which was more stable by 3.3 kcal/mol. The predicted harmonic vibrational frequencies and bond lengths suggest that the combined contributions of proton and hydrogen bonding may determine the resultant stability of each complex structure. In contrast to the dimer case, in the case of the isolated C(+)GC triplet, the two minimum energy structures of CH(+)center dot GC and C center dot H(+)GC were predicted to be almost equivalent in total energy. The dissociation energy (D(e)) for the C(+)G pairing in the C(+)GC triplet was 43.7 kcal/mol. Other energetics are also reported. As for the proton-transfer reaction in the proton-bond axis, the forward proton-transfer barriers for the dimer and trimer complexes were also predicted to be very low, 3.6 and 1.5 kcal/mol (Delta E(e)(PT)), respectively. (c) 2007 American Institute of Physics.
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  • Effects of chronic alcohol and excessive iron intake on mitochondrial DNA damage in the rat liver

    Park, Jung-Eun   Lee, Jeong-Ran   Chung, Jayong  

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  • The alteration of zinc transporter gene expression is associated with inflammatory markers in obese women.

    Noh, Hwayoung   Paik, Hee Young   Kim, Jihye   Chung, Jayong  

    Obesity, a chronic inflammatory state, is associated with altered zinc metabolism. ZnT and Zip transporters are involved in the regulation of zinc metabolism. This study examined the relationships among obesity, zinc transporter gene expression, and inflammatory markers in young Korean women. The messenger RNA (mRNA) levels of leukocyte zinc transporters between obese (BMI =3D 28.3 =C2=B1 0.5 kg/m(2), n =3D 35) and nonobese (BMI =3D 20.7 =C2=B1 0.2 kg/m(2), n =3D 20) women aged 18-28 years were examined using quantitative real-time polymerase chain reaction. Inflammatory markers, such as C-reactive protein (CRP), tumor necrosis factor-alpha (TNF-alpha), and interleukin (IL)-6, were measured in serum by enzyme immunoassay. ZnT1 and Zip1 were the most abundantly expressed zinc transporters in leukocytes. The mRNA levels of many zinc transporters (ZnT4, ZnT5, ZnT9, Zip1, Zip4, and Zip6) were significantly lower in obese women, and expression of these genes was inversely correlated with BMI and body fat percentage. In addition, inflammatory markers (CRP and TNF-alpha) were significantly higher in obese women. The mRNA levels of ZnT4, Zip1, and Zip6 were inversely correlated with CRP (P < 0.05), and mRNA levels of ZnT4 and ZnT5 were inversely correlated with TNF-alpha (P < 0.05). In standardized simple regression models, levels of TNF-alpha and CRP were negatively associated with mRNA levels of zinc transporters such as ZnT4, ZnT5, Zip1, and Zip6 (P < 0.05). These results suggest that the expression of zinc transporters may be altered in obese individuals. Changes in zinc transporters may also be related to the inflammatory state associated with obesity.=20
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  • The changes of zinc transporter ZnT gene expression in response to zinc supplementation in obese women.

    Noh, Hwayoung   Paik, Hee Young   Kim, Jihye   Chung, Jayong  

    Obesity is associated with an alteration in zinc metabolism. This alteration may be associated with changes in gene expression of zinc transporters. In this study, we examined the leukocyte expression of zinc transporter ZnTs in response to zinc supplementation in young obese women. Thirty-five young obese women (BMI=E2=89=A525 kg/m(2)), aged 18-28 years, were randomly assigned to two groups: a placebo group or a zinc group (30 mg zinc/day for 8 weeks). Usual dietary zinc intake was estimated from 3-day diet records. Serum zinc and urinary zinc concentrations were measured by atomic absorption spectrometry. Messenger RNA (mRNA) levels of leukocyte ZnT transporters were examined using quantitative real-time PCR. Expression levels of two ZnT transporters, ZnT1 and ZnT5, in obese women, increased significantly after zinc supplementation. At the end of the study, mRNA levels of ZnT1 and ZnT5 showed no correlation with serum zinc or urinary zinc concentration in obese women. In addition, a further study was conducted to identify whether the association between the gene expression levels of leukocyte ZnT1 and ZnT5 and dietary zinc intake remained consistent in 216 healthy young adults aged 20-29 years. A positive correlation between ZnT1 and dietary zinc intake (r=3D0.181, P=3D0.089) was also observed in healthy men although the significance was marginal. Taken together, these results show that the gene expression levels of ZnT1 and ZnT5 may be changed by zinc intake, suggesting that zinc supplementation could potentially restore ZnT transporter expression in obese women with altered zinc metabolism.=20
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  • Association of glutathione-S-transferase polymorphisms with atopic dermatitis risk in preschool age children

    Chung, Jayong   Oh, Se-Young   Shin, You-Kyung  

    Background: Glutathione S-transferase (GST) enzymes are critical for detoxifying reactive oxygen species (ROS) and their products which have been implicated in the pathology of inflammatory diseases such as atopic dermatitis (AD). Methods: We investigated the effects of genetic polymorphisms of GST on the risk of AD in preschool age children. Biomarkers for oxidative stress were also evaluated with respect to GST genotype. Results: The GSTP1 Val105 allele was significantly associated with an increased risk of AD [odds ratio (OR)=1.62, p<0.05]. The combination of the GSTP1 Val105 allele and the GSTT1 null genotype further increased this risk by 2.3-fold (p<0.01). No association was observed for the GSTM1 null or GSTT1 null genotype alone. In children with AD, blood total antioxidant capacity was significantly less (p-0.001), while malondialdehyde was higher (p=0.12). Children with the GSTP1 Val105 allele had significantly lower concentrations of erythrocyte glutathione compared to GSTP1 Ile/Ile homozygotes (p=0.03). Conclusions: Our study suggests that the GSTP1 Val105 allele is an important determinant of susceptibility to AD in preschool age children and increased oxidative stress may play a role in the pathogenesis of AD. Clin Chem Lab Med 2009;47:1475-81.
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  • Effects of various metal ions on the gene expression of iron exporter ferroportin-1 in J774 macrophages

    Park, Bo-Yeon   Chung, Jayong  

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  • Retinoic acid inhibits hepatic Jun N-terminal kinase-dependent signaling pathway in ethanol-fed rats

    Chung, Jayong   Chavez, Pollyanna RG   Russell, Robert M   Wang, Xiang-Dong  

    Retinoic acid (RA) supplementation suppresses ethanol-enhanced hepatocyte hyperproliferation in rats; however, little is known about the mechanism(s). Here, we investigated whether RA affects the protein kinase signaling pathways in the liver tissues of rats fed with a high dose of ethanol for a prolonged period of time (6 months). Results show that there were greater levels of phosphorylated Jun N-terminal kinase (JNK) and phosphorylated c-Jun protein, but not total JNK protein, in livers of ethanol-fed rats vs those of controls. Moreover, ethanol feeding to rats increased the levels of phosphorylated mitogen-activated protein kinase kinase-4 (MKK-4) and decreased the levels of mitogen-activated kinase phosphatase-1 (MKP-1) in liver tissue. However, hepatic levels of phosphorylated-p38 protein and total-p38 protein were not altered by the ethanol treatment. In contrast, all-trans-RA supplementation at two doses in ethanol-fed rats greatly attenuated the ethanol-induced hepatic phosphorylation of MKK-4, phosphorylated-JNK and c-Jun proteins. The level of MKP-1 was increased in ethanol-fed rats supplemented with all-trans-RA. Further, ethanol-induced hepatocyte hyperproliferation, measured by immunostaining for proliferating cell nuclear antigen, were markedly decreased by all-trans-RA supplementation. Interestingly, hepatic apoptosis in the liver of ethanol-fed rats after 6 months of treatment decreased significantly. This decrease of hepatic apoptosis in ethanol-fed rats was prevented by all-trans-RA supplementation in a dose-dependent manner. The results from these studies indicate that restoration of RA homeostasis is critical for the regulation of JNK-dependent signaling pathway and apoptosis in the liver of ethanol-fed rats.
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  • Effects of high-fat diet induced obesity on tissue zinc concentrations and zinc transporter expressions in mice

    Min, Byulchorong   Chung, Jayong  

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  • Relationship of Unbalanced Diet and Eating Behavior between School Age Children and Their Mothers in Wonju Area

    Hong, Jinhee   Oh, Sugyoung   Chung, Jayong  

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  • Effects of developmental iron deficiency and post-weaning iron repletion on the levels of iron transporter proteins in rats

    Oh, Sugyoung   Shin, Pill-Kyung   Chung, Jayong  

    BACKGROUND/OBJECTIVES: Iron deficiency in early life is associated with developmental problems, which may persist until later in life. The question of whether iron repletion after developmental iron deficiency could restore iron homeostasis is not well characterized. In the present study, we investigated the changes of iron transporters after iron depletion during the gestational-neonatal period and iron repletion during the post-weaning period. MATERIALS/METHODS: Pregnant rats were provided iron-deficient (<6 ppm Fe) or control (36 ppm Fe) diets from gestational day 2. At weaning, pups from iron-deficient dams were fed either iron-deficient (ID group) or control (IDR group) diets for 4 week. Pups from control dams were continued to be fed with the control diet throughout the study period (CON). RESULTS: Compared to the CON, ID rats had significantly lower hemoglobin and hematocrits in the blood and significantly lower tissue iron in the liver and spleen. Hepatic hepcidin and BMP6 mRNA levels were also strongly down-regulated in the ID group. Developmental iron deficiency significantly increased iron transporters divalent metal transporter 1 (DMI1) and ferroportin (FPN) in the duodenum, but decreased DMT1 in the liver. Dietary iron repletion restored the levels of hemoglobin and hematocrit to a normal range, but the tissue iron levels and hepatic hepcidin mRNA levels were significantly lower than those in the CON group. Both FPN and DMT1 protein levels in the liver and in the duodenum were not different between the IDR and the CON. By contrast, DMT1 in the spleen was significantly lower in the IDR, compared to the CON. The splenic FPN was also decreased in the IDR more than in the CON, although the difference did not reach statistical significance. CONCLUSIONS: Our findings demonstrate that iron transporter proteins in the duodenum, liver and spleen are differentially regulated during developmental iron deficiency. Also, post-weaning iron repletion efficiently restores iron transporters in the duodenum and the liver but not in the spleen, which suggests that early-life iron deficiency may cause long term abnormalities in iron recycling from the spleen.
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