• 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.

• YAKHAK HOEJI
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• v.50 no.4
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• pp.254-262
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• 2006

This study had been done for the investigation of the effect of Vitis vinifera extract(V), Schisandra chinensis extract (S), Taraxacum officinale extract (T), Gardenia jasminoides extract (G), Angelica acutiloba extract (A) and Paeonia japonica extract (P), and their mixtures on the antioxidant and ethanol oxidation system which was induced by Lieber-DeCarli ethanol liquid diet. Male Sprague-Dawley rats were randomly divided into eight groups: ethanol diet (ED), normal diet (ND), ED+V (100 mg/kg/day), ED+S, ED+T, ED+G, ED+A and ED+P (300 mg/kg/day). We studied the effect on alcohol dehydrogenase (ADH) and acetaldehyde dehydrogenase (ALDH) after herbal extracts administration for 6 weeks in rats induced by Lieber-DeCarli ethanol liquid diet. The differences in ADH and ALDH activity of the rats treated with herbal extracts and ED group were not significant. Phase I enzyme activity was found to be significantly higher in the ED+V than the ED group. Phase II enzymes (glutathione-S-transferase, phenol sulfatransferase) activities were found to be higher in the herbal extracts than the ED group. Herbal extracts not only reduced ethanol-induced elevation of level malondialdehyde but also protected against ethanol-induced decrease of reduced glutathione, gluthione reducatse, glutathione peroxidase, catalase and superoxide dismutase activities. Therefore, they can be utilized as a health functional food or new drug candidate for fatty liver and hepatotoxicity which was induced by chronic alcohol consumption.

• Nutrition Research and Practice
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• v.7 no.2
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• pp.109-114
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• 2013

We compared the preventive capacity of high intakes of vitamin C (VC) and vitamin E (VE) on oxidative stress and liver toxicity in rats fed a low-fat ethanol diet. Thirty-two Wistar rats received the low fat (10% of total calories) Lieber-DeCarli liquid diet as follows: either ethanol alone (Alc group, 36% of total calories) or ethanol in combination with VC (Alc + VC group, 40 mg VC/100 g body weight) or VE (Alc + VE group, 0.8 mg VE/100 g body weight). Control rats were pair-fed a liquid diet with the Alc group. Ethanol administration induced a modest increase in alanine aminotransferase (ALT), aspartate aminotransferase (AST), conjugated dienes (CD), and triglycerides but decreased total radical-trapping antioxidant potential (TRAP) in plasma. VE supplementation to alcohol-fed rats restored the plasma levels of AST, CD, and TRAP to control levels. However, VC supplementation did not significantly influence plasma ALT, AST, or CD. In addition, a significant increase in plasma aminothiols such as homocysteine and cysteine was observed in the Alc group, but cysteinylglycine and glutathione (GSH) did not change by ethanol feeding. Supplementing alcohol-fed rats with VC increased plasma GSH and hepatic S-adenosylmethionine, but plasma levels of aminothiols, except GSH, were not influenced by either VC or VE supplementation in ethanol-fed rats. These results indicate that a low-fat ethanol diet induces oxidative stress and consequent liver toxicity similar to a high-fat ethanol diet and that VE supplementation has a protective effect on ethanol-induced oxidative stress and liver toxicity.

• BMB Reports
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• v.29 no.5
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• pp.393-397
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• 1996

Sprague-Dawley male rats (150 g) were chronically treated with 5 v/v % ethanol admixed with nutritionally complete liquid diet and fed ad libitum for 3 weeks. Controls were pair fed with the isocaloric sucrose liquid diet. One half of each group was exposed to cold stress at $4^{\circ}C$ either for 24 h (for determination of mRNA by in situ hybridization) or for 48 h (for determination of enzyme activity). Chronic ethanol treatment (ethanol) did not affect tyrosine hydroxylase (TH) mRNA level in locus coeruleus (LC) of brain and adrenal medulla (AM) compared to controls. Cold stress showed strong increase of TH mRNA level in LC and AM compared to controls. Pretreated ethanol reduced the increased TH mRNA level by cold stress in LC and AM. Ethanol did not affect TH activity in LC and adrenal glands (adrenals). Cold stress increased TH activity in LC but not in adrenals. Pretreated ethanol did not reduce the increased TH activity by cold stress in LC but this result was not shown in adrenals. It is suggested that ethanol does not affect the message level and enzyme protein level for TH in LC and AM in normal rat. It is also hypothesized that pretreated ethanol reduces the magnitude of acute cold stress response, that is induction of TH mRNA in LC and AM, and does not reduce the increased TH enzyme protein that is also acute cold stress response in LC.

• Journal of the Korean Society of Food Science and Nutrition
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• v.43 no.2
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• pp.187-193
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• 2014

This study investigated whether or not Citrus unshiu peel extract (CPE) affects fat accumulation in livers of rats fed an ethanol-containing liquid diet. Initially, male Sprague-Dawley rats were housed individually in stainless steel, wire-bottomed cages with free access to a Lieber-Decarli control liquid diet. Rats were divided by body weight into three groups of eight each: one group of rats was fed the Lieber-Decarli control liquid diet devoid of ethanol (control), another was fed the Lieber-Decarli ethanol diet (ethanol), and third was fed the same ethanol diet except containing CPE. All three groups were fed their respective diets for 6 weeks. Serum and liver lipids were analyzed and liver histology performed. Body weight did not differ among the groups over the 6-wk duration. Histology images showed that CPE administration significantly improved fat accumulation in livers, which was induced by ethanol diet. Serum levels of transaminases and lipids also were reduced by CPE consumption. Taken together, the results indicate that CPE may protect ethanol-induced fatty liver by lowering fat accumulation in both the liver and blood. The protective effects of CPE appear to be due to its phenolic contents.

• Toxicological Research
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• v.24 no.2
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• pp.113-117
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• 2008

Chronic exposure to ethanol induces cumulative damage to the liver starting from fatty infiltration to cirrhosis depending on the dose and duration of exposure. The whole process leading to the development of alcoholic liver disease is very complex and the mechanisms involved are not fully understood. Among many experimental animal models, Lieber-DeCarli liquid diet provides moderate to severe pathophysiological outcome depending on the compositional changes. In the present study, we investigated the temporal changes in the early phase hepatic disease in rats fed with standard Lieber-DeCarli diet. Male Wistar rats were fed with Lieber-Decarli ethanol diet for 6 weeks and the liver samples were obtained after 2, 4 and 6 weeks. Mild fatty infiltration was observed in 2 weeks of feeding and it became evident in 4 and 6 week samples. The level of hepatic triglyceride showed a good agreement with the data obtained in the pathological analysis. Feeding mice with ethanol diet resulted in the maturation and translocation of SREBP-1 to nucleus in the liver. Western blot analysis of the pooled liver sample of control and ethanol fed animals showed a clear-cut time-dependent increase in the expression of nSREBP-1. These data provide important information for selecting proper time point in experimental intervention study in the field of drug development for alcoholic liver disease.

• Journal of Nutrition and Health
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• v.29 no.7
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• pp.721-728
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• 1996

The level of oxidative tissue damage caused by free radicals generated from ethanol oxidation was determined in the myocardium of chronic ethanol fed-rats and the protective action of various radical scavenging enzymes was monitored, also. Adult male Sprague-Dawley rats were given ethanol in an amount of 36% of total calories via Lieber-DeCarli liquid diet for 6 weeks. Control group was pair-fed with the diet containing isocaloric amount of dextrin-maltose instead of ethanol. Chronic ethanol administration resulted in the increased amount of myocardial thiobarbituric acid reactive substance(TBARS), th parameter of lipid peroxidation, under our experimental condition. Chronic ethanol ingestion did not cause any change in activities of either glutathione peroxidase or glutathione reductase and glucose-6-phosphate dehydrogenase were decreased after ethanol treatment. Therefore, chronic ethanol administration seemed to cause considerble changes in cellular defense function against oxidative tissue damage in rat myocardium through glutathione utilizing system and radical generation system. However the ultimate net result of chronic ethanol inestion on the myocardium of rat was the oxidative tissue damage revealed by increased TBARS content.

• Nutritional Sciences
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• v.8 no.2
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• pp.89-96
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• 2005

To determine the deleterious effects of chronic alcohol consumption on bone especially in adolescents or young adults, 8 week-old Sprague Dawley male rats were fed with Lieber-Decarli ethanol liquid diet, containing $36\%$ of energy as ethanol, ad libitum (ethanol group) or isocaloric normal liquid diet (control group) for 7 weeks. Body weight was significantly lower in ethanol group than that in control group after 1 week of feeding to the end. liver weight and the ratio of liver or kidney weight to body weight in ethanol group were significantly increased when compared to those in control group. Ethanol group showed significantly lower serum protein and albumin levels (p<0.05), higher total cholesterol and HDL-cholesterol levels (p<0.05), and AST, ALT and BUN activities than control group, but serum triglyceride, Ca and phosphate levels were not different. Ethanol group had significantly lower tibial trabecular bone area and serum osteocalcin level than control group (p<0.05), but urinary Ca and NTx (cross-linked N-telopeptide of type I collagen) concentrations and serum testosterone and parathyroid hormone levels were not different. In conclusion, chronic alcohol consumption in growing young male rats may result in osteopenia through the reduction of bone formation as well as liver malfunction.

• Journal of Nutrition and Health
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• v.40 no.2
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• pp.105-110
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• 2007

The study was designed to observe antioxidant activities of conjugated linoleic acid (CLA) by determining antioxidant enzyme protein levels [cytochrome P4502 El (CYP2E1), Copper, Zinc-superoxide dismutase (CuZn-SOD), glutathione peroxidase (CSH-Px), glutathione S-transferase (GST)] by Western blot analysis and the levels of ${\alpha}$-tocopherol and 2-thiobarbituric acid reactive substances (TBARS) in the liver of chronically ethanol-treated rats. Sixty Sprague Dawley male rats were divided into 3 groups (Control, EtOH, EtOH+CLA). All rats were fed Lieber-DeCarli liquid diet for 4 weeks by pair-feeding against the EtOH group. The liquid diet was supplemented with 1.77g CLA mixture per kg diet in the EtOH+CLA group. Isocaloric maltose dextrin was added in replace of 50g ethanol (36%kcal) for the Control group. Ethanol ingestion significantly increased the levels of CYP2E1 protein and TBARS, but significantly reduced CuZn-SOD protein level and increased GST protein level. There was no significant effect on the level of GSH-Px protein and ${\alpha}$-tocopherol in the liver by ethanol. CLA supplementation with ethanol significantly increased the levels of CuZn-SOD, GSH-Px and GST and also significantly attenuated TBARS level, whereas there was no significant effect on the levels of CYP2E1 protein and ${\alpha}$-tocopherol by CLA. Overall, the CLA supplemented to ethanol could significantly increase the levels of CuZn-SOD, GSH-Px and GST proteins and reduce the level of TBARS in the liver of chronically ethanol-treated rats.

• Journal of the Korean Society of Food Science and Nutrition
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• v.20 no.5
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• pp.409-417
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• 1991

To investigate effects of chronic alcohol consumption and tocopherol on lipid peroxidation and mitochondrial respiration 48 male rats of Sprague-Dawley strain were divided into 4 groups. Each group received for 3 weeks one of 4 experimental diets: tocopherol deficient control (TDC), tocopherol deficient-ethanol (TDE), tocopherol-supplemented control (TSC) and tocopherol-supplemented-ethanol (TSE). Composition of the diets was based on the Lieber and Decarli liquid diet and $\alpha$-tocopherol was supplemented at the level of 30mg/liter of diet, and ethanol supplied 36kcal%. TDC and TSC were pair-fed to TDE and TSE, respectively. Increase of body weight of tocopherol deficient-ethanol group was the lowest and the effect was diminished with tocopherol supplementation. Respiration of liver mitochondria was depressed in ethanol-administered groups and the effect became larger with tocopherol deficiency. Hepatic lipid peroxide level was not influenced by ethanol, but hepatic tocopherol content decreased with ethanol treatment. The result indicated that, although lipid perroxide level was unchanged with chronic ethanol consumption, oxidative stress exists in tissues of rate administered ethanol and may be relieved by tocopherol supplementation.