• Animal Bioscience
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• v.34 no.2
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• pp.276-284
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• 2021

Objective: The objective of this study was to determine whether a dietary vitamin E (VE) supplement could alleviate any detrimental effects of aged corn on lipid metabolism and antioxidant status in laying hens. Methods: The experiment consisted of a 2×3 factorial design with two corn types (normal corn and aged corn (stored for 4 yr) and three concentrations of VE (0, 20, and 100 IU/kg). A total of 216 Lohmann laying hens (50 wk of age) were randomly allocated into six treatment diets for 12 wk. Each treatment had 6 replicates of 6 hens per replicate. Results: The results show that aged corn significantly decreased the content of low-density lipoprotein cholesterol (p<0.05), and reduced chemokine-like receptor 1 (CMKLR1) mRNA expression (p<0.05) in the liver compared to controls. Diet with VE did not alter the content of crude fat and cholesterol (p>0.05), or acetyl-CoA carboxylase, lipoprotein lipase, fatty acid synthase or CMKLR1 mRNA expression (p>0.05) in the liver among treatment groups. Aged corn significantly increased the content of malondialdehyde (MDA) (p<0.05) and decreased superoxide dismutase (SOD) activity (p<0.05) in the liver. The VE increased the content of MDA (p<0.05) but decreased glutathione peroxidase (GSH-Px) activity in serum (p<0.01) and in the ovaries (p<0.05). Adding VE at 20 and 100 IU/kg significantly increased GSH-Px activity (p<0.05) in liver and in serum (p<0.01), 100 IU/kg VE significantly increased SOD activity (p<0.05) in serum. Aged corn had no significant effects on GSH-Px mRNA or SOD mRNA expression (p<0.01) in the liver and ovaries. Addition of 100 IU/kg VE could significantly increase SOD mRNA expression (p<0.01) in the liver and ovary. Conclusion: Aged corn affected lipid metabolism and decreased the antioxidant function of laying hens. Dietary VE supplementation was unable to counteract the negative effects of aged corn on lipid metabolism. However, addition of 100 IU/kg VE prevented aged corninduced lipid peroxidation in the organs of laying hens.

• Korean Journal of Poultry Science
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• v.43 no.1
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• pp.47-54
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• 2016

The aim of this study was to investigate the expression patterns of key genes involved in lipid metabolism in response to dietary Coenzyme Q10 (CoQ10) in hens. A total of 36 forty week-old Lohmann Brown were randomly allocated into 3 groups consisting of 4 replicates of 3 birds. Laying hens were subjected to one of following treatments: Control (BD, basal diet), T1 (BD+ CoQ10 100 mg/kg diet) and T2 (BD+ micellar of CoQ10 100 mg/kg diet). Birds were fed ad libitum a basal diet or the basal diet supplemented with CoQ10 for 5 weeks. Total RNA was extracted from the liver for quantitative RT-PCR. The mRNA levels of HMG-CoA reductase(HMGCR) and sterol regulatory element-binding proteins(SREBP)2 were decreased more than 30~50% in the liver of birds fed a basal diet supplemented with CoQ10 (p<0.05). These findings suggest that dietary CoQ10 can reduce cholesterol levels by the suppression of the hepatic HMGCR and SREBP2 genes. The gene expressions of liver X receptor (LXR) and SREBP1 were down regulated due to the addition of CoQ10 to the feed (p<0.05). The homeostasis of cholesterol can be regulated by LXR and SREBP1 in cholesterol-low-conditions. The supplement of CoQ10 caused a decreased expression of lipid metabolism-related genes including $PPAR{\gamma}$, XBP1, FASN, and GLUTs in the liver of birds (p<0.05). These data suggest that CoQ10 might be used as a dietary supplement to reduce cholesterol levels and to regulate lipid homeostasis in laying hens.

• Nutrition Research and Practice
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• v.10 no.5
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• pp.501-506
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• 2016

BACKGROUNG/OBJECTIVES: Corn silk (CS) extract contains large amounts of maysin, which is a major flavonoid in CS. However, studies regarding the effect of CS extract on cholesterol metabolism is limited. Therefore, the purpose of this study was to determine the effect of CS extract on cholesterol metabolism in C57BL/6J mouse fed high-fat diets. MATERIALS/METHODS: Normal-fat group fed 7% fat diet, high-fat (HF) group fed 25% fat diet, and high-fat with corn silk (HFCS) group were orally administered CS extract (100 mg/kg body weight) daily. Serum and hepatic levels of total lipids, triglycerides, and total cholesterol as well as serum free fatty acid, glucose, and insulin levels were determined. The mRNA expression levels of acyl-CoA: cholesterol acyltransferase (ACAT), cholesterol 7-alpha hydroxylase (CYP7A1), farnesoid X receptor (FXR), lecithin cholesterol acyltransferase (LCAT), low-density lipoprotein receptor, 3-hyroxy-3-methylglutaryl-coenzyme A reductase (HMG-CoA reductase), adiponectin, leptin, and tumor necrosis factor ${\alpha}$ were determined. RESULTS: Oral administration of CS extract with HF improved serum glucose and insulin levels as well as attenuated HF-induced fatty liver. CS extracts significantly elevated mRNA expression levels of adipocytokines and reduced mRNA expression levels of HMG-CoA reductase, ACAT, and FXR. The mRNA expression levels of CYP7A1 and LCAT between the HF group and HFCS group were not statistically different. CONCLUSIONS: CS extract supplementation with a high-fat diet improves levels of adipocytokine secretion and glucose homeostasis. CS extract is also effective in decreasing the regulatory pool of hepatic cholesterol, in line with decreased blood and hepatic levels of cholesterol though modulation of mRNA expression levels of HMG-CoA reductase, ACAT, and FXR.

• Journal of Physiology & Pathology in Korean Medicine
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• v.28 no.3
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• pp.288-295
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• 2014

Bojungchiseub-tang (BJCST) has been used in symptoms and signs of edema, dampness-phlegm, kidney failure, and so on. BJCST is also expected to have strong anti-obesity activities. However, little is known about the mechanisms of its inhibitory effects on adipocyte differentiation and adipogenesis. In the present study, we examined the effects and mechanism of BJCST on transcription factors and adipogenic genes of 3T3-L1 preadipocytes to understand its inhibitory effects on adipocyte differentiation and adipogenesis. Our results showed that BJCST significantly inhibited differentiation and adipogenesis of 3T3-L1 preadipocytes in a dose-dependent manner. To elucidate the mechanism of the effects of BJCST on lowering lipid content in 3T3-L1 adipocytes, we examined whether BJCST modulate the expressions of transcription factors to induce adipogenesis and adipogenic genes related to regulate accumulation of lipids. As a result, the expression of steroid regulatory element-binding protein (SREBP)1, cytidine-cytidine-adenosine-adenosine-thymidine (CCAAT)/enhancer binding proteins ${\alpha}$ ($C/EBP{\alpha}$), $C/EBP{\beta}$, $C/EBP{\delta}$, and peroxisome proliferator-activated receptor ${\gamma}$ ($PPAR{\gamma}$) genes, which induce the adipose differentiation, liver X receptor $(LXR){\alpha}$ and fatty acid synthase (FAS) genes, which induce lipogenesis and adipose-specific aP2, Adipsin, lipoprotein lipase (LPL), CD36, TGF-${\beta}$, leptin and adiponectin genes, which compose fat formation were decreased. BJCST also reduced the expression of acyl CoA oxidase (ACO) and uncoupling protein (UCP) genes related to lipid oxidation. In conclusion, BJCST could regulate transcript factor related to induction of adipose differentiation and inhibited the accumulation of lipids and expression of adipogenic genes.

• Korean Journal of Acupuncture
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• v.31 no.4
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• pp.168-178
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• 2014

Objectives : Mahuang-Chuanwu(Mahwang-Cheonoh) Pharmacopuncture(MCP) has been used to treat obesity in Clinical Korean Medicine. MCP solution(MCPS) is also expected to have strong anti-obesity activities. However, little is known about the mechanisms of its inhibitory effects on adipocyte differentiation and lipogenesis. Methods : In the present study, we examined the effects of MCPS on differentiation and lipogenesis of 3T3-L1 adipocytes. To elucidate the mechanism of the effects of MCPS on lowering lipid content in 3T3-L1 adipocytes, we examined whether MCPS modulates the expressions of transcription factors to induce lipogenesis and adipogenic genes related to regulate the accumulation of lipids. Results : Our results showed that MCPS significantly inhibited differentiation and lipogenesis of 3T3-L1 adipocytes in a dose-dependent manner. MCPS suppressed the mRNA expressions of cytidine-cytidine-adenosine-adenosine-thymidine(CCAAT)/enhancer binding proteins ${\alpha}$($C/EBP{\alpha}$), C/EBP ${\beta}$, $C/EBP{\delta}$, and peroxisome proliferator-activated receptor ${\gamma}$($PPAR{\gamma}$) genes related to the induction of adipose differentiation. MCPS inhibited the mRNA expressions of adipose-specific aP2, adipsin, lipoprotein lipase(LPL), CD36, TGF-${\beta}$, and leptin genes related to the fat formation. MCPS downregulated the mRNA expressions of liver X receptor(LXR) ${\alpha}$ and fatty acid synthase(FAS) genes related to the induction of lipogenesis. In addition, MCPS reduced the production of adipocyte-induced pro-inflammatory cytokines. Conclusions : MCPS could regulate the accumulation of lipids and expression of adipogenic genes via inhibition of transcript factors related to induction of adipose differentiation.

• BMB Reports
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• v.57 no.2
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• pp.92-97
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• 2024

Elevated blood glucose is associated with an increased risk of atherosclerosis. Data from the current study showed that glucosamine (GlcN), a normal glucose metabolite of the hexosamine biosynthetic pathway (HBP), promoted lipid accumulation in RAW264.7 macrophage cells. Oleic acid- and lipopolysaccharide (LPS)-induced lipid accumulation was further enhanced by GlcN in RAW264.7 cells, although there was no a significant change in the rate of fatty acid uptake. GlcN increased acetyl CoA carboxylase (ACC), fatty acid synthase (FAS), scavenger receptor class A, liver X receptor, and sterol regulatory element-binding protein-1c (SREBP-1c) mRNA expression, and; conversely, suppressed ATP-binding cassette transporter A1 (ABCA-1) and ABCG-1 expression. Additionally, GlcN promoted O-GlcNAcylation of nuclear SREBP-1 but did not affect its DNA binding activity. GlcN stimulated phosphorylation of mammalian target of rapamycin (mTOR) and S6 kinase. Rapamycin, a mTOR-specific inhibitor, suppressed GlcN-induced lipid accumulation in RAW264.7 cells. The GlcN-mediated increase in ACC and FAS mRNA was suppressed, while the decrease in ABCA-1 and ABCG-1 by GlcN was not significantly altered by rapamycin. Together, our results highlight the importance of the mTOR signaling pathway in GlcN-induced macrophage lipid accumulation and further support a potential link between mTOR and HBP signaling in lipogenesis.

• The Journal of Internal Korean Medicine
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• v.35 no.2
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• pp.175-183
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• 2014

Objectives : We tried to uncover the anti-lipogenic effect and underlying mechanism of Laminaria japonica on an experimental cellular model of non-alcoholic fatty liver disease. Methods : Ethanol extract of Laminaria japonica (LJ) was prepared. Intracellular lipid content of palmitate-treated HepG2 cells was evaluated with or without LJ treatment. We measured the effects of LJ on liver X receptor ${\alpha}$ ($LXR{\alpha}$) and sterol regulatory element-binding transcription factor-1c (SREBP-1c) expression, transcription level of lipogenic genes, including acetyl-CoA carboxylase (ACC), fatty acid synthase (FAS), stearoyl-CoA desaturase-1 (SCD-1), and nuclear factor erythroid 2-related factor 2 (Nrf2) activation in HepG2 cells. Results : LJ markedly attenuated palmitate-induced intracellular lipid accumulation in HepG2 cells. LJ suppressed $LXR{\alpha}$-dependent SREBP-1c activation, and SREBP-1c mediated induction of ACC, FAS, and SCD-1. Furthermore, LJ activated Nrf2, which plays an important cytoprotective role in non-alcoholic fatty liver disease. Conclusions : Our study suggests that LJ has the potential to alleviate hepatic lipid accumulation, and this effect was mediated by inhibiting the $LXR{\alpha}$-SREBP-1c pathway that leads to hepatic steatosis. In addition, the anti-lipogenic potential may, at least in part, be associated with activation of Nrf2.

• Animal Bioscience
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• v.34 no.10
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• pp.1590-1599
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• 2021

Objective: This study investigates the expression patterns of toll-like receptors (TLRs) and intracellular mediators in horse muscle cells after exercise, and the relationship between TLRS expression in stressed horse muscle cells and immune cell migration toward them. Methods: The expression patterns of the TLRs (TLR2, TLR4, and TLR8) and downstream signaling pathway-related genes (myeloid differentiation primary response 88 [MYD88]; activating transcription factor 3 [ATF3]) are examined in horse tissues, and horse peripheral blood mononuclear cells (PBMCs), polymorphonuclear cells (PMNs) and muscles in response to exercise, using the quantitative reverse transcription-polymerase chain reaction (qPCR). Expressions of chemokine receptor genes, i.e., C-X-C motif chemokine receptor 2 (CXCR2) and C-C motif chemokine receptor 5 (CCR5), are studied in PBMCs and PMNs. A horse muscle cell line is developed by transfecting SV-T antigen into fetal muscle cells, followed by examination of muscle-specific genes. Horse muscle cells are treated with stressors, i.e., cortisol, hydrogen peroxide (H₂O₂), and heat, to mimic stress conditions in vitro, and the expression of TLR4 and TLR8 are examined in stressed muscle cells, in addition to migration activity of PBMCs toward stressed muscle cells. Results: The qPCR revealed that TLR4 message was expressed in cerebrum, cerebellum, thymus, lung, liver, kidney, and muscle, whereas TLR8 expressed in thymus, lung, and kidney, while TLR2 expressed in thymus, lung, and kidney. Expressions of TLRs, i.e., TLR4 and TLR8, and mediators, i.e., MYD88 and ATF3, were upregulated in muscle, PBMCs and PMNs in response to exercise. Expressions of CXCR2 and CCR5 were also upregulated in PBMCs and PMNs after exercise. In the muscle cell line, TLR4 and TLR8 expressions were upregulated when cells were treated with stressors such as cortisol, H₂O₂, and heat. Migration of PBMCs toward stressed muscle cells was increased by exercise and oxidative stresses, and combinations of these. Treatment with methylsulfonylmethane (MSM), an antioxidant on stressed muscle cells, reduced migration of PBMCs toward stressed muscle cells. Conclusion: In this study, we have successfully cultured horse skeletal muscle cells, isolated horse PBMCs, and established an in vitro system for studying stress-related gene expressions and function. Expression of TLR4, TLR8, CXCR2, and CCR5 in horse muscle cells was higher in response to stressors such as cortisol, H₂O₂, and heat, or combinations of these. In addition, migration of PBMCs toward muscle cells was increased when muscle cells were under stress, but inhibition of reactive oxygen species by MSM modulated migratory activity of PBMCs to stressed muscle cells. Further study is necessary to investigate the biological function(s) of the TLR gene family in horse muscle cells.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.8
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• pp.3741-3745
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• 2012

Background: Hepatocellular carcinoma (HCC) is the sixth most common cancer worldwide and the most common form of liver cancer. However, while it is associated frequently with hepatitis C virus (HCV) there is only an elementary understanding of its molecular pathogenesis. Methods: To gain insight into the molecular mechanisms of HCV-induced hepatocarcinogenesis, we performed microarray analysis on 75 surgical liver samples from 48 HCV-infected patients. Results: There were 395 differentially expressed geness between cirrhotic samples and HCC samples. Of these, 125 genes were up-regulated and 270 genes were down-regulated. We performed pathway enrichment analysis and screened as described previously. Conclusions: The differentially expressed genes might be involved in hepatocarcinogenesis through upregulating the pathways of ECM-receptor interaction, focal adhesion, cell adhesion molecules and other cancer-related pathways, and downregulating the pathways of "complement and coagulation cascades". We hope our results could aid in seeking of therapeutic targets for HCV-induced hepatocellular carcinoma.

• Asian-Australasian Journal of Animal Sciences
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• v.18 no.5
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• pp.601-605
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• 2005

Three lines of White Leghorn (WL) chickens (IWJ, IWG and IWC) maintained at Central Avian Research Institute, Izatnagar (UP), were used for chorioallantoic membrane (CAM) and liver tumour (LT) assay. Eleven-day-old embryos of each line were partitioned into three groups and inoculated with 0.2 ml of subgroup A, subgroup C and an equal mixture of subgroup A and C Rous sarcoma virus (RSV). Subgroup virus receptor on the cell surface membrane for subgroup A is coded for by tumour virus a (tva) locus and for subgroup C by tumour virus c (tvc) locus. The random association of the genes at the tva and tvc loci in IWJ and IWC line was assessed and the $x^2$-values for phenotypic classes were found to be significant, indicating the linkage between the tva and tvc loci. The linkage value was estimated to be 0.09 on pooled sex and pooled line basis. On the basis of four subclass tumour phenotypes a 4-allele model was proposed for tva locus having $a^{s1}$, $a^{s2}$, $a^{r1}$ and $a^{r2}$ alleles and the frequencies were calculated as 0.47, 0.13, 0.13 and 0.27 for IWJ line, 0.31, 0.33, 0.14 and 0.22 for IWG line and 0.44, 0.11, 0.21 and 0.24 for IWC line, respectively. Similarly, for tvc locus the frequencies of four alleles i.e. $c^{s1}$, $c^{s2}$, $c^{r1}$ and $c^{r2}$ were calculated as 0.42, 0.20, 0.21 and 0.17 for IWJ line, 0.42, 0.17, 0.27 and 0.14 for IWG line and 0.30, 0.21, 0.16 and 0.33 for IWC line, respectively. The $x^2$-values for all classes of observations were not significant (p>0.05), indicating a good fit to the 4-allele model for the occurrence of 4-subclass tumour phenotypes for tva and tvc loci. On the basis of the 2-allele model both tva and tvc locus carries three genotypes each. But, on the basis of the 4-allele model tva and tvc locus carries 10 genotypes each. The interaction between A-resistance and C-resistance (both CAM and LT death) was ascertained by taking the 10 genotypes of tva locus and 3 genotypes of tvc locus by pooling the lines and partitioning the observations into 3 classes. The $x^2$-values for the genotypic classes of CAM (-) LT (+) and CAM (-) LT (-) phenotypes to mixed virus (A+C) infection were found to be highly significant (p<0.01), indicating increased resistance, which indicates the joint segregation of $a^r$ and $c^r$ genes, suggesting the existence of close linkage between the tva and tvc loci. Therefore, an indirect selection approach using subgroup C viruses can be employed to generate stocks resistant to subgroup A LLV, obviating contamination with the most common agent causing LL in field condition.