• Food Science of Animal Resources
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• v.30 no.4
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• pp.582-589
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• 2010

The current study was designed to assess the effects of emulsified sausage supplemented with ginseng saponin on lipid metabolism by applying a rat model. Four groups of 8 rats (5 wk old) were each allocated one of 4 treatments: basal feed (C), and basal feed with 20% sausage powder containing 0% (S0), 2% (S2) and 4% (S4) ginseng saponin. The experiment was conducted for 4 wk. The results did not differ among the treatments with different amounts of sausage (ST), but daily feed intake (p<0.01) and feed conversion (p<0.001) were significantly increased in STs compared to C. Both total serum cholesterol and triglyceride concentrations were significantly (p<0.001) reduced, by 45 and 46%, and 48 and 46%, in S2 and S4, respectively, compared to S0. In the liver, the total cholesterol level was dramatically (p<0.05) decreased according to increasing sausage powder levels. In particular, S4 showed approximately 14% reduction compared to S0 (p<0.05). Liver triglyceride content also showed a similar tendency, where S2 and S4 resulted in 7% and 31% reduction. With regard to fatty acid composition in the liver tissues, palmitic acid (16:0), oleic acid (18:1), eicosanoic acid (20:1), and eicosatrienoic acid (20:3) did not differ among the STs, whereas both linoleic acid (18:2) (p<0.01) and linolenic acid (18:3) (p<0.001) showed significant increases in S2 compared to S0. The current data demonstrated that emulsified sausages supplemented with ginseng saponin effectively reduce total cholesterol and triglyceride concentrations in the serum and liver, and increase unsaturated and essential fatty acid in the liver. These data collectively imply that the sausage improved the overall lipid profile in a rat model, and can be further generalized to the result that emulsified sausage can improve lipid metabolism depending on the products' formula.

• Journal of Nutrition and Health
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• v.32 no.2
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• pp.137-149
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• 1999

This study was performed to investigate the effets of hesperidin extracted from tangerine peel on Cadmium (Cd) and lipid metabolism lipid peroxide formation, and antioxidative enzyme activities in rats. Forty-eight male Sprague-Dawley rats weighing 158.3$\pm$3.5g were blocked into eight groups according to body weight. Rats were raised for three weeks with diets containing 0 or 0.04%(w/w) cadmium chloride and 1%(w/w) extracted hesperidin from tangerine peel, commercial hesperidin or naringin. Food intake, weight gain and food efficiency ratio were significantly lower in the Cd-administered groups. The Cd concentrations in blood and liver and the Cd excretions in urine and feces were significantly higher in the Cd-administered groups. Among the Cd groups, blood Cd concentrations were decreased, fecal Cd excretions were increased, and Cd retenition ratios were decreased by feeding flavonoid diets. Plasma total lipid concentrations were significantly lower in the extracted hesperidin group, plasma triglyceride concentrations were significantly lower in the extracted hesperidin and naringin groups. Plasma HDL-cholesterol concentrations and HDL : total cholesterol ratios were increased by feeding flavonoids. Among the Cd groups, liver total lipid concentratons were decreased by feeding flavonoids. Fecal total lipid, fecal cholesterol, and fecal triglyceride excretions were significantly higher in the naringin group, and they were increased by feeding flavonoids among Cd groups. Thiobarbituric acid reactive substance concentrations in plasma and liver were higher in Cd groups, and were significantly decreased by feeding flavonoids. The activities of erythrocyte catalase, superoxide dismutase and glutathione peroxidase showed a tendency to increase by feeding. The activities of liver catalase, superoxide dismutase and glutathione peroxidase were not significantly affected by administering Cd or flavonoids. In conclusion, all flavonoids that were used in this experiment inhibited lipid peroxide formation in plasma and liver, but this effect was not caused by the increased in the activities of antioxidative enzymes.

• Animal Bioscience
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• v.35 no.8
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• pp.1184-1194
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• 2022

Objective: High concentrate diets are widely used to satisfy high-yielding dairy cows; however, long-term feeding of high concentrate diets can cause subacute ruminal acidosis (SARA). The endocrine disturbance is one of the important reasons for metabolic disorders caused by SARA. However, there is no current report about thyroid hormones involved in liver metabolic disorders induced by a high concentrate diet. Methods: In this study, 12 mid-lactating dairy cows were randomly assigned to HC (high concentrate) group (60% concentrate of dry matter, n = 6) and LC (low concentrate) group (40% concentrate of dry matter, n = 6). All cows were slaughtered on the 21st day, and the samples of blood and liver were collected to analyze the blood biochemistry, histological changes, thyroid hormones, and the expression of genes and proteins. Results: Compared with LC group, HC group showed decreased serum triglyceride, free fatty acid, total cholesterol, low-density lipoprotein cholesterol, increased hepatic glycogen, and glucose. For glucose metabolism, the gene and protein expression of glucose-6-phosphatase and phosphoenolpyruvate carboxykinase 1 in the liver were significantly up-regulated in HC group. For lipid metabolism, the expression of sterol regulatory element-binding protein 1, long-chain acyl-CoA synthetase 1, and fatty acid synthase in the liver was decreased in HC group, whereas carnitine palmitoyltransferase 1α and peroxisome proliferator activated receptor α were increased. Serum triiodothyronine, thyroxin, free triiodothyronine (FT3), and hepatic FT3 increased in HC group, accompanied by increased expression of thyroid hormone receptor (THR) in the liver. Conclusion: Taken together, thyroid hormones may increase hepatic gluconeogenesis, β-oxidation and reduce fatty acid synthesis through the THR pathway to participate in the metabolic disorders caused by a high concentrate diet.

• Journal of the Korean Home Economics Association
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• v.23 no.2
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• pp.45-53
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• 1985

The influence of fat level and dietary fiber on serum and liver lipid concentration of the rat was investigated. Groups of rats were fed respectively 3%, 5%, 20% fat containing and free fiber diet until 5th week. From 5th week to 9th week high fat diet groups of rates were devided high fat diet group, high fat pectin supplemented diet group and high fat celulose supplemented diet group. Pectin and cellulose at 10% was supplemented to high fat diets. After rats were fed for 9 weeks, all rats were sacrificed to collect the liver and blood samples by heart puncture. Serum and liver lipids were determined on all rats and compared the histochemical lipid staining method with the biochemical analysis of serum and liver lipids. A high fat diet caused increased level of the total lipids, total cholesterol and free cholesterol contents in the liver and the serum. Rats fed pectin reduced body weight, werum lipid and liver lipid but cellulose had no effect to reduce serum and liver lipid concentration. These results indicate that dietary fat level led to changes in the lipid metabolism of rats and that pectin was more effective in lowering serum and liver lipid than cellulose.

• Toxicological Research
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• v.22 no.1
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• pp.1-8
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• 2006

The primary metabolism of pyribenzoxim was studied in rat liver microsomes in order to identify the cytochrome P450 (CYP) isoform(s) and esterases involved in the metabolism of pyribenzoxim. Chemical inhibition using CYP isoform-selective inhibitors such as ${\alpha}$-naphthoflavone, tolbutamide, quinine, chlorzoxazone, troleandomycin, and undecynoic acid indicated that CYP1A and CYP2D are responsible for the oxidative metabolism of pyribenzoxim. And inhibitory studies using eserine, bis-nitrophenol phosphate, dibucaine, and mercuric chloride indicated pyribenzoxim hydrolysis involved in microsomal carboxylesterases containing an SH group (cysteine) at the active center.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1997.04a
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• pp.97-97
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• 1997

It was reported that ATP depletion occurs and accelerates cell damage during ischemia and reperfusion. To determine the mechanism of cell damage, the change of energy metabolism in liver was studied during ischemia/reperfusion. The groups were divided into four categories : sham-operated group, ischemia/reperfusion group, and two types of ATP-MgCl$_2$ treatment groups(one was treated during ischemia and the another during reperfusion). Rats were administered intravenously saline or ATP-MgCl$_2$. Rats were anesthetized and blood vessels in the left and median lobes of the liver were occluded. After 60min of ischemia, the clamp at those vessels were removed. After ischemia, one and five hours after reflow, energy metabolites(ATP, ADP, AMP, inosine, adenosine, hypoxanthine, xanthine) in liver were measured with HPLC. To observe mitochondrial function, aterial keton body ratio in blood and mitochondrial glutamate dehydrogenase activity in liver were measured. And lipid peroxidation was measured to evalutate the involvement of free radicals. In this study, ATP and ADP were catabolized to their metabolites(AMP, inosine, adenosine, hypoxanthine, xanthine) during ischemia and they resynthesized ATP and ADP during reperfusion. But total purine base were not restored to level of normal rat. The main source of resynthesizing ATP and ADP was AMP. In both ATP-MgCl$_2$ treated groups, mitochondrial function was protected and lipid peroxidation was significantly reduced. Our findings suggest that ischemia/reperfusion impairs hepatic energy metabolism.

• YAKHAK HOEJI
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• v.53 no.2
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• pp.74-77
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• 2009

Food deprivation decreases hepatic glutathione (GSH) levels, which is ascribed to alterations in availability of hepatic cysteine, a rate limiting factor for the GSH synthesis. The present study examines the effects of food deprivation on hepatic metabolism of sulfur amino acid in male rats. In rats fasted for 24 or 48 hours, hepatic GSH levels were decreased from $6.70{\pm}0.16{\mu}mol/g$ liver to $4.02{\pm}0.20$ or $4.06{\pm}0.07{\mu}mol/g$ liver, respectively. Hepatic S-adenosylmethionine levels were also decreased in fasted rats, but S-adenosylhomocysteine levels were increased. Hepatic methionine levels were not changed by food deprivation for 48 hours. On the other hand, hepatic cysteine or taurine levels were increased from $106.2{\pm}4.1$ to $130.0{\pm}2.7$ nmol/g liver or from $2.45{\pm}0.43$ to $5.07{\pm}0.78{\mu}mol/g$ liver, respectively, in 48-hour fasted rats. Activity of cystathionine beta-synthase catalyzed homocysteine to cystathionine, was markedly decreased, but activity of betaine homocysteine methyltransferase was increased in fasted rats, indicating that methylation of homocysteine to methionine is activated. Also activity of cysteine dioxygenase, involved in taurine synthesis, was increased. These results suggested that hepatic methionine levels were maintained in rats fasted for 48 hours through increase in homocysteine methylation, and hepatic GSH may serve as a cysteine supplier reservoir in fasting state.

• Biomedical Science Letters
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• v.7 no.3
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• pp.99-102
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• 2001

Toluene is mainly metabolized in liver by oxidative pathway. Oxigen free radicals occur through the process of toluene metabolism Therefore it causes tissue and cell min by the oxygen free radicals from the metabolism of toluene. Melatonin acts as a highly efficient free radical scavenger that protects cells from damage by oxygen free radicals. To test this hypothesis, toluene hepatotoxicity was induced by an abdominal injection of toluene. To see if the melatonin protects the rat's liver, melatonin was administrated orally, at the time of each toluene injection. Aspartate aminotransferase(AST), alanin aminotransferase(ALT), latic dehydrogenase(LDH) and alkaline phosphatase(ALP) levels in serum were measured to estimate hepatic function. Malondialdehyde(MDA), which gives an indirect index of oxidative injury was also measured. Hippuric acid is the last metabolic Production of toluene was measured by HPLC. There were significantly higher in AST, ALT, LDH, MDA and hippuric acid in toluene group, but there were no significant difference in melatonin group except ALT and hippuric acid. There was significantly lower in ALP level in toluene group, but there was no significant difference melatonin group, suggesting a significant hepatotoxicity due to oxygen free radicals through the process of toluene metabolism Melatonin treatment significantly protected hepatic function and free radical-mediated injury in the liver against toluene-induced changes. Accordingly, this study shows that melatonin is helpful in protecting liver injury by acute toluene intoxication.

• The Journal of Korean Medicine
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• v.21 no.1
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• pp.68-76
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• 2000

Objectives: This experiment was conducted to verify the effects of Chungganhaeju-tang(Qingganjiejiu-tang) on the alcohol metabolism and liver functions, by measuring the activity levels of ADH and ALDH, as well as glucose, triglyceride, and BUN. Damage of the liver cells caused by alcohol was determined through the examination of serum levels of AST, ALT, ALP, LDH, and uric acid. Methods: Sprague-Dawley rats were used in this experiment and the rats were divided into control and experiment groups. Chungganhaeju-tang(Qingganjiejiu-tang) extract was orally administered in the experiment group for three weeks. Each group was further classified into two sub-groups, and control group's blood was taken without oral ingestion of alcohol, while the experiment group' s blood was withdrawn after ingestion of alcohol. Evaluation of damage level was done considering the presence of extract and alcohol. Results: In this experiment, Chungganhaeju-tang(Qingganjiejiu-tang) significantly suppressed the activity of ADH which is a precursor enzyme of acetaldehyde, but didn't cause significant changes in the activity of ALDH which is a catabolic enzyme. Decreased glucose level due to alcohol consumption was recovered back to the normal level and increased levels of triglyceride, BUN, AST, ALT, ALP, LDH, and uric acid were significantly reduced. Conclusions: These experiment results suggest that Chungganhaeju-tang(Qingganjiejiu-tang) inhibits the formation of acetaldehyde in the metabolism of alcohol, and affects the recovery of weakened liver functions due to alcohol.

• Korean Journal of Acupuncture
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• v.22 no.4
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• pp.83-90
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• 2005

Objectives : To investigate the effects of acupuncture at Gansoo (B-18) and Chungwan (CV-12) on lipid metabolism in rats fed peroxidized lipid diet. Methods : Effects of acupuncture at Gansoo and Chungwan on plasma and liver lipid composition and antioxidative capacity were investigated in rats fed peroxidized lipids. Results : Although the level of plasma total cholesterol and triglyceride showed a tendency to decrease in the acupuncture group, the plasma HDL-cholesterol concentration showed no significant difference. The level of liver total cholesterol and triglyceride showed no significant difference in all treatment groups. Thiobarbituric acid( TBARS ) values in plasma and liver showed a tendency to decrease in the acupuncture groups. The plasma GOT and GPT activities showed low values in the acupuncture groups. The liver glutathione peroxidase, superoxide dismutase and catalase activity showed high values in the acupuncture groups. Conclusions : The results suggest that acupuncture at Gansoo (B-18) and Chungwan (CV-12) may have an influence on lipid metabolism via enhancing antioxidative capacity.