Background: Hepatitis C virus (HCV) causes acute and chronic human hepatitis infection and as such is an important global health problem. The virus was discovered in the USA in 1989 and it is now known that three to four million people are infected every year, WHO estimating that 3 percent of the 7 billion people worldwide being chronically infected. Humans are the natural hosts of HCV and this virus can eventually lead to permanent liver damage and carcinoma. HCV is a member of the Flaviviridae family and Hepacivirus genus. The diameter of the virus is about 50-60 nm and the virion contains a single-stranded positive RNA approximately 10,000 nucleotides in length and consisting of one ORF which is encapsulated by an external lipid envelope and icosahedral capsid. HCV is a heterogeneous virus, classified into 6 genotypes and more than 50 subtypes. Because of the genome variability, nucleotide sequences of genotypes differ by approximately 31-34%, and by 20-23% among subtypes. Quasi-species of mixed virus populations provide a survival advantage for the virus to create multiple variant genomes and a high rate of generation of variants to allow rapid selection of mutants for new environmental conditions. Direct contact with infected blood and blood products, sexual relationships and availability of injectable drugs have had remarkable effects on HCV epidemiology. Hundreds of thousands of people die each year from hepatitis and liver cancer caused by HCV virus infection. Approximately 80% of patients with acute hepatitis C progress into a chronic disease state leading to serious hepatic disorders, 10-20% of which develop chronic liver cirrhosis and hepatocellular carcinoma. The incubation period of HCV is 6-8 weeks and the infection is often asymptomatic so it is very hard to detect at early stages, making early treatment very difficult. Therefore, hepatitis C is called a "silent disease". Neutralizing antibodies are produced against several HCV proteins during infection but the virus mutates to escape from antibodies. Some patients with chronic hepatitis C may have some symptoms such as fatigue, muscle aches, nausea and pain. Autoimmune and immunecomplex-mediated diseases have also been reported with chronic HCV infection.
Seo, Kyoung-Chun;Kim, Mi-Jin;Hong, Sun-Hee;Cha, So-Yeon;Noh, Jeong-Sook;Kim, Mi-Jeong;Song, Yeong-Ok
Preventive Nutrition and Food Science
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v.15
no.2
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pp.83-87
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2010
The cholesterol-lowering effects of soymilk fermented with Bacillus subtilis KCCM42923 were studied in apolipoprotein E knockout (ApoE KO) mice and compared to the cholesterol-lowering effects of soymilk to which cheonggukjang powder had been added. ApoE KO mice were divided into 3 groups (n=7/group). Animals were fed either an atherogenic diet only (AD, control group), an AD supplemented with fermented soymilk containing Corni fructus (FSM group), or an AD supplemented with soymik to which cheonggukjang (CGJ) powder had been added at 5% (w/v) (CPS group) for 8 weeks. The amount of FSM or CPS supplementing the AD was 20.8 mL/kg BW. There were no differences in either body weight gain or organ weights among three groups. In the FSM group, the concentration of plasma total cholesterol (TC) and LDL cholesterol (LDLC) were significantly decreased by 26.2% and 30.3% compared with the values of the control group (p<0.05). However, the triglyceride (TG) and HDL-cholesterol (HDLC) levels were not affected. These beneficial effects of FSM on suppressing the increase in plasma cholesterol level by AD were greater than those of CPS, which revealed 15.4% and 16.4% inhibition for TC and LDLC, respectively. However, these differences between FSM and CPS groups were not significantly different. A preventative effect of FSM or CPS on the accumulation of hepatic TC, but not on TG, was observed. FSM and CPS did not demonstrate any effects on fecal lipid excretion. In conclusion, the cholesterol-lowering effects of the soymilk fermented with Bacillus subtilis KCCM42923 were comparable to CGJ powder-added soymilk. These results suggest that drinking FSM might provide beneficial effects on controlling plasma cholesterol levels.
This study was to compare the effects of dietary n-6 and n-3 fatty acids and fat unsaturation on plasma lipids and chemical composition of VLDL and LDL fraction and lipogenic enzymes activity in rat liver under the conditions providing 1) a similar amount of n-6, n-3 fatty acids(LA, ALA, EPA+DHA) in diets and 2) the various degree of fat unsaturation. Male Sprague-Dawley rats weighing 420g were treated for 6-n with six experimental diets providing 25% of energy as fat and which were different only in fatty acid composition. The fats used for a source of each fatty acid were beet tallow for saturated fatty acid corn oil for n-6 linoleic acid(LA) perilla oil for n-3 $\alpha$-linolenic acid(ALA) and fish oil n-3 eicosapentaenoic acid (EPA) and n-3 docosahexaenoic acid(DHA). Plasma cholesterol level was increased by corn oil to compare with beef tallow but was decreased by perilla oil or fish oil. Plasma TG level was significantly decreased by perilla oil or fish oil. Fish oil significantly reduced the level of HDL-Chol and the proportion of Chol in LDL fraction and that of TG in vVLDL fraction. Overall there was a singificant negative correlation between the level of each plasma lipid(Chol TG, VLDL-TG, LDL-C) and the degree of fat unsaturation. However this rerlationship is not always true when compared the hypolipidemic effect of each fatty acid at a similar level of fat unsaturation. There was a trend such taht glucose 6-P dehydrogenase 6-phosphogluconate dehydrogenase and malic enzyme activites were reduced by n-3 fatty acids. Perilla oil significantly increased the incorporation of c20:5 and c22:5 into liver tissue and fish oil suignificantly increased the incorporation of c20:5, c22:6 into liver tissue and the effect of long chain n-3 fatty acid incorporation was greater by fish oil. therefore the hypotriglyceridemic effect of n-3 fatty acid could be resulted from the interference of hepatic lipogenesis by long-chain n-3 fatty acids and the reduced proportion of TG in VLDL fraction and its effect was greater by n-3 EPA+DHA than n-3 ALA even though plasma Chol and TG levels were also influenced by the degree of dietary fat unsaturation.
Li, Y.;Ma, Q.G.;Zhao, L.H.;Guo, Y.Q.;Duan, G.X.;Zhang, J.Y.;Ji, C.
Asian-Australasian Journal of Animal Sciences
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v.27
no.6
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pp.907-915
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2014
Alpha-lipoic acid (${\alpha}$-LA) is not only involved in energy metabolism, but is also a powerful antioxidant that can protect against hepatic oxidative stress induced by some drugs, toxins, or under various physiological and pathophysiological conditions. Here, we investigated the effect of ${\alpha}$-LA against liver oxidative damage in broilers exposed to aflatoxin $B_1$ ($AFB_1$). Birds were randomly divided into four groups and assigned different diets: basal diet, 300 mg/kg ${\alpha}$-LA supplementation in basal diet, diet containing 74 ${\mu}g/kg$$AFB_1$, and 300 mg/kg ${\alpha}$-LA supplementation in diet containing 74 ${\mu}g/kg$$AFB_1$, for 3 weeks. The results revealed that the addition of 300 mg/kg ${\alpha}$-LA protected against the liver function damage of broilers induced by chronic low dose of $AFB_1$ as estimated by a significant (p<0.05) change in levels of plasma total protein, albumin, alkaline phosphatase and the activities of liver glutamic-oxalacetic transaminase and glutamic-pyruvic transaminase. The histopathological analysis also showed that liver tissues were injured in the $AFB_1$ diet, but this effect was alleviated by the addition of 300 mg/kg ${\alpha}$-LA. Additionally, $AFB_1$ induced a profound elevation of oxidative stress in birds, as indicated by an increase in malondialdehyde level, a decrease in glutathione peroxidase activity and a depletion of the glutathione content in the liver. All of these negative effects were inhibited by treatment with ${\alpha}$-LA. Our results suggest that the inhibition of $AFB_1$-induced excess production of lipid peroxides and the maintenance of intracellular antioxidant status may play important roles in the protective effects of ${\alpha}$-LA against $AFB_1$-induced oxidative damage in the liver.
Objectives : This study was undertaken to verify the modulation mechanism of Gyeongshingangjeehwan18 (GGEx18) in ob/ob male mice. Methods : Eight-week old mice (wild-type C57BL/6J and ob/ob) were used for all experiments. Wild-type C57BL/6J mice were used as lean control and obese ob/ob mice were randomly divided into 5 groups : obese control, GGEx15 (Ephedra sinica Stapf + Rheum palmatum L.), GGEx16 (Ephedra sinica Stapf + Laminaria japonica Aresch), GGEx17 (Rheum palmatum L. + Laminaria japonica Aresch), and GGEx18 (Ephedra sinica Stapf + Laminaria japonica Aresch + Rheum palmatum L.). After mice were treated with several kinds of GGEx for 11 weeks, the mRNA expression of peroxisome proliferator-activated receptor (PPAR) target genes and uncoupling protein (UCP) were measured. In addition, $PPAR{\alpha}$ and $PPAR{\beta}$ transactivation was examined in NMu2Li hepatocytes, C2C12 myocytes, and 3T3-L1 preadipocytes using transient transfection assays. Results : 1. Hepatic $PPAR{\alpha}$ target genes, such as ACOX and VLCAD mRNA levels were significantly increased by GGEx18 compared with obese controls. In skeletal muscle, LCAD mRNA expression was stimulated by GGEx16, GGEx17, and GGEx18, whereas MCAD mRNA expression by GGEx17 and GGEx18. $PPAR{\beta}$ target LPL mRNA levels were also increased by GGEx16, GGEx17, and GGEx18 in skeletal muscle, but adipose LPL mRNA levels were decreased. In addition, GGEx18 upregulated UCP mRNA expression in skeletal muslce. 2. $PPAR{\alpha}$ reporter gene expression was increased by GGEx18 in NMu2Li cells compared with vehicle. $PPAR{\alpha}$ and $PPAR{\beta}$ reporter activities were also increased by all GGEx treatments in C2C12 and 3T3-L1 cells. Conclusions : These results suggest that GGEx can act as $PPAR{\alpha}$ and $PPAR{\beta}$ activators, and that GGEx may regulate obesity by stimulating $PPAR{\alpha}$, $PPAR{\beta}$, and UCP activity. Of the 4 compositions, GGEx18 seems to be most effective in improving obesity and lipid disorders.
Journal of the Korean Society of Food Science and Nutrition
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v.41
no.6
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pp.774-781
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2012
This study investigated dose-response effects of chlorogenic acid (CA) on glucose metabolism and the antioxidant system in streptozotocin (STZ)-induced diabetic mice with a high-fat diet (HFD). Male ICR mice were fed with a HFD (37% calories from fat) for 4 weeks prior to intraperitoneal injection with STZ (100 mg/kg body weight). Diabetic mice were supplemented with two doses of CA (0.02% and 0.05%, wt/wt) for 6 weeks. Both doses of CA significantly improved fasting blood glucose level, glucose tolerance and insulin tolerance without any changes in plasma insulin and C-peptide levels. Plasma leptin concentration was significantly higher in the CA-supplemented groups than in the diabetic control group. Both doses of CA significantly increased hepatic glucokinase activity and decreased glucose-6-phosphatase activity compared to the diabetic control group. The ratio of glucokinase/glucose-6-phosphatase was dose-independently higher in CA-supplemented mice than in diabetic control mice. CA supplementation dose-independently elevated superoxide dismutase and catalase activities, whereas it lowered lipid peroxide levels compared to the diabetic control mice in the liver and erythrocyte. These results suggest that low-dose CA may be used as a hypoglycemic agent in a high-fat diet and STZ-induced diabetic mice.
To clarify the annual reproductive cycle of the banded catfish, Pseudobagrus fulvidraco (Richardson), the seasonal changes in histological aspect of gonad and liver were examined. The adult fish was raptured from the upper stream of Young-San river, Chunnam in each month from May 1992 to June 1993. Based on the annual changes in GSI (gonadosomatic index), HSI (hepatosomatic index), CF (condition factor) and histological aspects of the gonads, the annual reproductive cycle were classified into 5 periods as follows: 1) Growing phase (from April to early May): The value of GSI increased and the size of oocytes in perinucleolus stage in oocytes increased gradually. Spermatogonia were developed actively from the epithelial tissues of seminiferous tubules. 2) Maturing phase (from Hay to early June): GSI levels increased rapidly in both sex. Oocytes at various developmental stages were observed. Appearance of active spermatogenesis were observed. 3) Mature and spawning phase (from June to August): High values of GSI remained static and oocytes accumulated significant quantitis of yolk globules. 4) Degenerating phase (from September to November): GSI levels decreased and ovaries were filled mostly with oocytes at the perinucleolus stage. Hepatic cells accumulated significant amounts of lipid droplets. 5) Resting period (from December to March) : Low values of GSI were kept and the size of oocytes at the perinucleolus stage did not increase. Spermatogenesis was not observed.
The hypothesis that calcium provoke $O_2^-$ formation by Kupffer cells and may contribute to carbon tetrachloride $(CCl_4)$ induced liver injury was studied in SD rats. In $CCl_4-treated$ animals, hepatic malonaldehyde (nmole/gm liver) and plasma ALT (IU/ml) levels elevated significantly from $119.63{\pm}13.00$ to $268.97{\pm}14.82$ and from $17.3{\pm}0.18$ to $806.08{\pm}37.63$, respectively, compared to those in controls. Activation of Kupffer cells with high dose of retinol (250,000 IU/kg/day, po, for 7 day) significantly enhanced ALT levels, while inactivation of Kupffer cells with gadolinium chloride (7.5 mg/kg/day, ip, for 2 day) attenuated the increase of serum ALT level following $CCl_4$ treatment. Diltiazem (10 mg/kg/day, ip for 2 day) given in combination with retinol led to a marked decrease in ALT levels compare to the level in rats treated only with retinol against $CCl_4$ treatment. In order to determine any alterations in cytochrome P450 activities, the P450 content and the CYP2E1 activity were measured and all $CCl_4-treated$ rats showed significantly lower levels compared to those in controls and vehicle-treated animals. There were significant increases in glutathione peroxidase in all $CCl_4-treated$ rats except diltiazem treated groups. No difference was found among untreated and vehicle-treated rats. It is concluded that Kupffer cells contribute to $CCl_4-induced$ liver injury and that calcium antagonist attenuated the increased $CCl_4-induced$ liver injury due to activation of Kupffer cells.
A total of twenty, 2-wk-old male broiler chickens were allotted into control diet(CON) or a diet supplemented with 1% ground grape seed(GGS). They had free access to feed and water for 3 wk. Growth performance and antioxidant markers in plasma, intestine and liver were determined. Dietary addition of 1% GGS did not affect weight gain, feed intake, feed conversion and organ weight in 35 day-old broiler chickens significantly. There was no difference in plasma levels of glucose, triglyceride, cholesterol, AST, ALT and LDH activity. However, total antioxidant status(TAS) in blood increased(P<0.05) in chickens fed the diet supplemented with 1% GGS compared to those fed the control diet. In addition, the specific activity of intestinal superoxide dismutase(SOD) increased(P<0.05) in birds fed the diet supplemented with GGS. However, the activities of intestinal gluthathione peroxidase(GSHPx) and gluthathione -S- transferase(GST) and hepatic SOD, GSHPx and GST were not affected by the dietary GGS. The levels of reduced glutathione and lipid peroxidation in the small intestine and liver were not different between the two groups. In conclusion, dietary supplementation of 1% GGS did not result in a negative effect on growth performance. In addition, some antioxidant indicators including blood TAS and intestinal SOD were markedly elevated in response to dietary GGS. Therefore, dietary addition of 1% GGS may be beneficial to improve antioxidant capacity in broiler chicken.
Park, Jung-Hyun;Kang, Hee;Ahn, Kwang-Seok;Shim, Bum-Sang;Kim, Sung-Hoon;Choi, Seung-Hoon;Ahn, Kyoo-Seok
Journal of Physiology & Pathology in Korean Medicine
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v.23
no.3
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pp.685-694
/
2009
This experimental study was designed to investigate the inhibitory effects of ethanol extract of modified Yukgunja-tang(mYGJT) on high-fat diet-induced obesity and hyperlipidemia in Sprague-Dawley rats, Animals were divided into normal, control, mYGJT(100 mg/kg and 200 mg/kg) treated groups. Obesity with hyperlipidemia was induced by high fat diet treatment for 6 weeks. mYGJT was given to the amimals by oral gavage for 4 weeks, starting at the high-fat diet regimen, The effect of mYGJT on the differentiation of 3T3 L1 adipocytes in vitro and serological paramamters for obesity and hyperlipidemia in vivo were evaluated, mYGJT significnatly inhibited the differentiation of 3T3 L1 adipocytes in a concentration dependent manner. mYGJT treatment siginficantly reduced body weight, abdominal and epididymal fat weight, and FER(Food Efficiency Ratio) compared with control group in a dose dependent manner. It also signficantly inhibited the levels of serum total lipid, triglyceride, phospholipid, total cholesterol, LDL, AI(Atherosclerosis Index) and returned the serum HDL to normal. Total lipids, triglycerides and cholesterols in the liver, as well as malondialdehyde(MDA) and hydroxy radical in the serum were significantly reduced. However, superoxide dismutase(SOD) activity was significantly increased in mYGJT treated group compared with control group. Finally, mYGJT treatment signficantly decreased the MDA and protein carbonyl concentrations of the hepatic homogenate but signficantly increased the activities of SOD, GSH-Px and Catalase. Taken together, these results suggest that mYGJT can be clinically useful in inhibiting high-fat diet-induced obesity and hyperlipidemia.
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