• Journal of Nutrition and Health
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• v.36 no.8
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• pp.801-810
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• 2003

Chronic alcoholism is considered a common cause of malnutrition. Especially, micronutrient deficiency may playa critical role in the incidence of alcoholic liver diseases. This study was conducted to investigate the effect of folate deficiency and ethanol consumption on cholesterol metabolism and the antioxidative system in rats. Plasma concentration of total cholesterol was increased by ethanol administration in folate-fed rats. HDL-cholesterol tended to be higher in the folate-fed group, but it was not significant. The plasma and hepatic levels of malondialdehyde were increased after chronic ethanol feeding, but dietary folate depressed the plasma malondialdehyde content of rats. Ethanol or folate feeding did not significantly change alcohol dehydrogenase activity. But folate feeding increased catalase activity in ethanol-fed rats. There was no significant change in superoxide dismutase activity among the experimental groups. Glutathione peroxidase activity tended to decrease by chronic ethanol feeding, but dietary folate did not affectthe glutathione peroxidase activity of chronic ethanol-fed rats. Glutathionine-S-transferase activity was not affected by ethanol feeding or folate deficiency. The plasma and hepatic levels of retinol decreased after chronic ethanol feeding. The hepatic level of retinol significantly decreased in ethanol-fed rats by folate deficiency. The plasma level of $\alpha$-tocopherol tended to be low in the folate deficient group with ethanol feeding, but there was no difference among the experimental groups in the hepatic level of $\alpha$-tocopherol. These results demonstrate that chronic ethanol consumption changes the plasma cholesterol metabolism and antioxidative system of rats, and optimal folate feeding in ethanol-fed rats exerts protective effects to some extent.

• Journal of the Korean Society of Food Science and Nutrition
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• v.32 no.2
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• pp.278-286
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• 2003

Alcohol is well known agent which can damage the human tissues such as liver via stimulating lipid peroxidation. On the other hand, carotenoids in addition to vitamins A, C and I play important roles in protecting these oxidative damages as well as preventing the production of free radicals. This study was carried out to investigate the effect of dietary vitamin A on lipid peroxidation and antioxidants status in ethanol-treated rats. In the experiment, male Sprague-Dawley rats weighing 160~180 g were given a liquid diet containing 36% of total calories as ethanol for 7 weeks. The pair-fed control rats received an isocaloric amount of diet containing sucrose instead of ethanol on the following day Additionally, the liquid diet contained adequate amount of $\beta$-carotene, retinyl acetate or 13-sis-reinoic acid except vitamin A-deficient diet. The results obtained are as follows. The levels of plasma and hepatic lipid peroxide were increased after chronic ethanol feeding in rats. Retinyl acetate supplementation significantly reduced lipid peroxidation induced by ethanol feeding Glucose 6-phosphatase activity was significantly reduced in rats fed vitamin A-deficient diet with ethanol and alkaline phosphatase activity was significantly induced in rats fed 13-cis-reinoic acid diet with ethanol. Catalase and alcohol dehydrogenase activities did not show a consistent tendency in experiment groups. The hepatic antioxidant enzyme activities did not significantly changed by chronic ethanol feeding groups. The striking decrease in conversion of $\beta$-carotene to retinol was observed in rats fed a $\beta$-carotene diet with ethanol feeding The level of retinol and retinoic acid in plasma and liver was decreased after chronic ethanol administration Based on this result, these data suggest that ethanol feeding enhances oxidative stress especially in those fed a vitamin A-deficient diet, and vitamin A supplementation, especially, retinyl acetate intake can prevent enhanced lipid peroxidation and related damage to some extent.

• Journal of the Korean Society of Food Science and Nutrition
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• v.27 no.4
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• pp.731-738
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• 1998

The present study was aimed to investigate the effect of dietary supplementation of $\beta$-carotene on vitamin A metabolism in ethanol-fed rats. Sprague-Dawley rats weighing 190~210g were fed a liquid diet containing 36% of total calories as ethanol for 6 weeks. The pair-fed control rats(1BP group, 2BP group) were given an isocaloric amount of diet containing sucrose instead of ethanol on the following day. Additionally, the liquid diet, contained different levels of $\beta$-carotene(1BE group: 2.1, 2BE group: 21mg/L liquid diet). Body weight gains and food efficiency ratios of ethanol groups were lower than those of pair-fed groups. This effect did not change with dietary supplementation of $\beta$-carotene. The levels of plasma and hepatic retionl were decreased after chronic ethanol feeding, but the values in 2BE group were higher than in 1BE group. The content of hepatic retinoic acid tended to increase in proportion to $\beta$-carotene supplementation. There results suggest that ethanol consumption may affect the vatamin A methabolism and reduce the conversion of $\beta$-carotene to retinol in rats.

• Journal of Nutrition and Health
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• v.26 no.6
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• pp.680-691
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• 1993

Rats were fed for an 8-week period a low riboflavin diet(5ug riboflavin/day) or a control diet(30ug/day) supplied either ad libitum or by pair feeding in order to study the effect of riboflavin on the metabolism of lipids and neurotransmitters. Erythrocyte glutathione reductase (EGR) and monomine oxidase(MAO) activity in the liver and brain were assayed. EGR activity coefficient in riboflavin deficient rats was significantly higher than in ad libitum controls whereas MAO activity was decreased in the deficient rats. Fatty acid composition showed a different trend in the serum, liver and brain. In the serum, the concentrations of essential fatty acids and $\omega$-3 fatty acids(eicosapentaenoic acid, docosahexaenoic acid)were decreased about 20-40% in the deficient and pair-fed than in the ad libitum controls. Brain serotonin and 5-HIAA(5-hydroxyindole acetic acid) concentrations were decreased in the riboflavin deficient rats. Learning ability measured by a water maze and exploratory activity using the open field test were not impaired in the deficient rats. These results indicate that brain lipid metabolism was protected in subclinical riboflavin deficiency, however, riboflavin deficiency affected brain serotonin content.

• Journal of Nutrition and Health
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• v.30 no.2
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• pp.123-131
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• 1997

The influence of (-0-Hydroxycitrate(HCA), shown to be a competitive inhibitor of adenosine 5-triphosphate(ATP) citrate lyase, on food intake and body weight, serum triglyceride and cholosterol level, in vivo rates of fatty acid and cholesterol synthesis, and fat cell number and size was investigated. 3 groups of female, 5 weeks old Sprague Dawley rats, 8 animals each, were ad libitum meal-fed or pair-fed(3 hours from 10 : 00 to 13 : 00) AIN based high glucose diet for a total period of 8 weeks. Providing normolipidemic rats orally with 400mg of HCA formula containing approximately 20mg of HCA 1 hour prior to daily feeding schedule significantly depressed in vivo hepatic rates of fatty acid and cholesterol synthesis in the liver and adipose tissue. Serum triglyceride and cholesterol levels were significantly reduced by HCA. At the end of treatment period, the rats administered with HCA resulted in a significantly reduction in body weight gain. The reduction in weights was attributable to a significant decrease in fat cell size with a smaller extent, but not significant, reduction in fat cell number. Rats receiving HCA demonstrated less food intake than the controls ; however, this decreased caloric intake was not fully responsible for the HCA induced depression of hepatic and adipocytic lipogenesis, since experiment using pair-fed cojntrol rats showed, less magnitude but similar results. Both a anorectic and an antilipogenic properties of HCA seem to be responsible for this weight reduction activity of HCA. The outcome of this study suggest that metabolic regulation may be a feasible approach to the control of obesity and hyperlipidemia.

• Food Science and Biotechnology
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• v.15 no.1
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• pp.51-56
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• 2006

We investigated the effects of fructooligosaccharides and chicory inulin on the profiles of cecal and fecal short-chain fatty acids (SCFAs) and fecal bile acids in rats. Thirty-six Sprague Dawley male rats weighing about 190 g were randomly divided among four treatments; control diet, control diet +6%(w/w) fructooligosaccharide (POS), control diet +6% chicory inulin oligosaccharide(CIOS), and control diet +6% chicory inulin(CI). The rats were pair-fed and experimental diets were maintained for 5 weeks. Cecal and fecal pH was significantly decreased in rats that were fed fructooligosaccharides and chicory inulin. Cecal propionate was significantly elevated in rats fed CIOS diets, and butyrate was lower in rats fed FOS and CI than control values. Cecal lactate was significantly higher in the FOS group than in the control group. The fecal excretions of acetate and total SCFA were 200-300% higher in rats that were fed fructooligosaccharides and chicory inulin than in the control group. Lactate excretion was highest in rats that were fed FOS, followed by those fed CIOS and CI. The cholic acid and total bile acid concentrations in feces were significantly lower in the rats that were fed fructooligosaccharides and chicory inulin. The deoxycholic acid concentrations in wet feces were significantly lower in the groups of rats that ate CIOS (0.186 mM), FOS (0.274 mM), and CI (0.362 mM) than in the control group (0.595 mM). Among the fructans, short-chain fructooligosaccharide was more effective at decreasing colonic pH and lactate production, but medium-chain chicory inulin oligosaccharide was more effective at increasing fecal butyrate and lowering the fecal secondary bile acid concentration.

• Journal of the Korean Society of Food Science and Nutrition
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• v.24 no.6
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• pp.848-858
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• 1995

The present study was conducted to investigate the effect of dietary vitamin A on the antioxidant status in ethanol-treated rats. Weaning rats were fed a basal diet until they reached about 160-180g body weight. Thereafter, four experimental groups were fed a liquid diet containing 36% ethanol of total calorie and four pair-fed groups were fed isocaloric sucorse instead of ethanol. Additionally, the liquid diet contained adequate amount of ${\beta}-carotene$, retinyl acetate, or 13-cis-retinoic acid except vitamin A deficient diet. The rats were sacrificed after 7 weeks of feedng periods. Significant decrease in hepatic vitamin E content was found in rats treated with chronic ethanol. However, dietary supplementation of retinyl acetate modified the change to some extent. Total vitamin C content of liver increased in vitamin A-deficient or ${\beta}-carotene$ groups with ethanol feeding. The ratio of reduced/oxidized vitamin C increased in the plasma and liver of ${\beta}-carotene$ group with ethanol feeding. Chronic ethanol intake did not change the total glutathione content of rat liver, but increased reduced glutathione(GSH)/oxidized glutathione(GSSG) ratio. This increase in hepatic GSH after chronic ethanol treatment. The changes of Se content in plasma and liver was not consistant. Fe content of liver increased by ethanol treatment, but this increase reduced in rats fed dietary retinyl acetate or 13-cis-retinoic acid. Fe content of plasma increased in vitamin A-deficient and ${\beta}-carotene$ supplemented groups with ethanol intake.

• Journal of Life Science
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• v.5 no.2
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• pp.57-62
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• 1995

Casein or soybean protein was subjected to there action with caffeic acidtyrosinase system at 30-35$\circ$C, pH 6.8 with aeration for 5hr. The resulting brown proteins were washed with acetone until the washings were on longer colored. However, modified protein still retained a light brown. The effects of the modified proteins and brown compounds on male Wistar strain rats were studied by pair-feeding of a cholesterol-free diet for 14days. Significant decrease in protein digestibility for the rats fed with the modified proteins were observed. Weight gain and protein digestibility were not influenced by feeding brown compounds, but the feeding of brown compound from casein caused an enlargement of caecum. The concentrations of serum cholesterol and triglyceride in the rats fed with modified proteins and brown compounds were mostly unchanged against the rats fed with untreated proteins. These results suggest that the decrease in protein digestibility induced by enzymic browning-reaction did not cause the decrease in concentration of serum cholesterol.

• Journal of the Korean Society of Food Science and Nutrition
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• v.32 no.3
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• pp.469-473
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• 2003

This study was conducted to determine the effect of a mixture of two water-soluble dietary fibers, psyllium husk and glucomannan, on serum lipids, fecal fat excretion and body fat. Twenty one female Sprague-Dawley rats were randomly assigned into three groups (control, pair-fed control and test group) and fed a high saturated fat (20% lard) diet (control diet) or a test diet (psyllium husk and glucomannan added to the control diet at the level of 0.9% and 0.68%, respectively) for 8 weeks. Pair-fed control rats were allowed to eat the amount of diet consumed by test group the preceding day. The body weight gain and food efficiency ratio of test group were significantly lower compared with these of control group. The mean values of body weight gain and food efficiency ratio were lower in test group than in pair-fed control group, but the difference was not significant. There were no differences in food intake. The dry weight and water content of feces and fecal fat excretion were markedly greater in test group than in control groups. Serum total cholesterol and triacylglycerol levels were significantly lower in test group than in two control groups.1'he rats of two control groups had higher body fat contents than that of test group. These results indicate that the combination of the two water-soluble dietary fibers, psyllium husk and glucomannan, can be used as a potent lipid-lowering agent in individuals consuming high saturated fat diet.

• Preventive Nutrition and Food Science
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• v.16 no.2
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• pp.95-103
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• 2011

This study was performed to investigate the antioxidant mechanism of tomato wine with varying lycopene content in rats fed a high fat diet (HFD). Male Sprague-Dawley rats were randomly divided into five groups (n=10 per group) and fed an HFD (35% of total energy from fat) plus ethanol (7.2% of total energy from alcohol), tomato wine with varying lycopene content (0.425 mg%, 1.140 mg% or 2.045 mg% lycopene) or an isocaloric control diet for 6 weeks. Mice fed HFD plus ethanol significantly increased erythrocyte hydrogen peroxide and thiobarbituric acid reactive substances (TBARS) levels with increases in activities of erythrocyte antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and glutathione reductase (GR) compared to pair-fed rats. Supplementation of tomato wine with varying lycopene content decreased ethanol-mediated increases of erythrocyte lipid peroxidation and antioxidant enzyme activities in HFD-fed rats, and tomato wine with higher lycopene appeared to be more effective. Tomato wine also dose-dependently lowered TBARS levels with decreased pro-oxidant enzyme, xanthine oxidase (XOD) activity in plasma of HFD-fed rats. In contrast to erythrocytes, the inhibitory effects of tomato wine on hepatic lipid peroxidation were linked to increased hepatic antioxidant enzymes (SOD and CAT) and alcohol metabolizing enzyme (alcohol dehydrogenase and aldehyde dehydrogenase) activities. There were no significant differences in hepatic XOD and cytochrome P450-2E1 activities among the groups. Together, our data suggest that tomato wine fortified with lycopene has the potential to protect against ethanol-induced oxidative stress via regulation of antioxidant or pro-oxidant enzymes and alcohol metabolizing enzyme activities in plasma, erythrocyte and liver.