• Journal of the Korean Society of Food Science and Nutrition
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• v.27 no.1
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• pp.126-131
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• 1998

This study was undertaken to determine the effect of yellow and black soybeans on plasma and hepatic lipid composition and fecal lipid excretion in Sprague Dawley rats. Animals were fed with diets containing 52% yellow soybean, 50% black soybean, or 20% casein for 7 weeks. Feeding efficiency was significantly increased in the animals fed soybeans(p<0.05). Plasma cholesterol concentration was significantly lowered in the group fed yellow soybean compared with black soybean and casein-fed control (p<0.05). Hepatic triglyceride concentration was significantly lowered in soybean groups compared with casein-fed control(p<0.05), whereas hepatic cholesterol concentration was not affected by diet treatments. Soybean feeding significantly increased fecal weight, triglyceride and bile acid contents compared with casein feeding(p<0.05). It is concluded that soybean feeding in rats affects plasma and hepatic lipid levels by increasing the excretion of triglyceride and bile acids.

• Journal of Nutrition and Health
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• v.26 no.5
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• pp.532-546
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• 1993

This study was done to investigate the effects of different dietary oils on hepatic mitochondrial lipid compositon, adenine nucleotide translocase(AdNT) and ATPase activities in carcinogen treated rats. Sixty male Sprague-Dawley rats, weighing 50∼60g, were fed three different types of dietary oil, beef tallow(BT), corn oil(CO) and sardine oil(SO) at 15% by weight for 14 weeks. Three weeks after feeding rats were intraperitoneally injected with a single dose of diethylnitrosamine(200mg/Kg BW). After five weeks rate fed 0.02% acetylaminofluorene contating diet for 6 weeks, and after seven weeks 0.05% phenobarbital containing diet for 7 weeks. At 14th week, rats were sacrificed and hepatic mitochondrial lipid composition, AdNT and ATPase activities were determined. Percent liver weight per body weight was significantly by carcinogen treatment. Analysis of mitochondrial lipid composition showed that body cholesterol and phospholipid contents were not affected by dietary oils but significantly increased by carcinogen treatment. Individual phospholipid composition as well as phosphatidyl ethanolamine/phosphatidyl choline ratio were altered by either dietary oils or carcinogen treatment. Fatty acid composition was changed by dietary oils but not much by carcinogen treatment. AdNT activity was affected by dietary oils in only carcinogen treated groups. ATPase activity was affected by dietary oils in only carcinogen nontreated groups. These data indicate that both dietary oils and caricinogen treatment can change mitochondrial lipid composition and thereby change AdNT and ATPase activities. Particularly effects of carcinogen treatment on cholesterol/phopholipid ratio, phospholipid compositon and ATPase activity were different among dietary oil groups. Therefore it is suggested that different dietary oils can somewhat modulate the changes of mitochnodrial lipid composition and membrane bound enzyme activites during hepatocarcinogenesis.

• Journal of Nutrition and Health
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• v.31 no.2
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• pp.135-142
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• 1998

This study was undertaken to determine whether dehulled defatted flour has an effect on postprandial plasma lipoprotein composition, hepatic lipid composition, enzyme and hormone levels in rats. Control(casein) and experimental (dehulled defatted soy flour)diets were fed to rats for 7 weeks. all animals (S. D. rats, male) were sacrificed 2 hrs after the feeding of 5g of each diet. Defatted soy flour feeding significantly lowered postprandial plasma total cholesterol, chylomicron/VLDL-cholesterol, hepatic cholesterol and triglyceride(TG) as compared with casein feeding, whereas no significant effect on plasma TG was observed. Intestinal kipase activity was elevated , whereas trypsin activity was suppressed in the dehulled defatted soy flour group. Plasma glucagon, thyroid hormone and hepatic HMG-coA reductase levels were not affected by diet treatment. These results hypothesize that dehulled defatted soy flour affects cholesterol digestion and absorption in guts, thus delaying the appearance of chylomicron cholesterol in plasma or affecting the disappearance of chylomicron remnant to high-density-lipoprotein(HDL).

• Asian-Australasian Journal of Animal Sciences
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• v.16 no.8
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• pp.1171-1176
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• 2003

The effects of dietary conjugated linoleic acid (CLA) on lipid concentrations and fatty acid composition of various tissues were studied in young chicks. From 7 days of age, a total of 160 chicks were divided into 4 groups, placed into 4 pens per group (10 birds per pen) and fed one of four experimental diets containing 6% tallow (TO 6%), 4% tallow plus 2% CLA (TO 4%-CLA 2%), 2% tallow plus 4% CLA (TO 2%-CLA 4%) or 6% CLA (CLA 6%) for 3 weeks. There were no significant differences in growth performances and the relative weights of various organs, but relative liver weight of chicks fed dietary CLA at 4 and 6% levels was significantly higher (p<0.05) than that of TO 6% group. The chemical compositions of leg muscle were not affected by CLA feeding. However, hepatic total lipid of chicks fed 6% CLA diet was significantly higher (p<0.05) than those of TO 6% and TO 4%-CLA 2% groups. The concentrations of various lipid fractions in serum were not affected by CLA feeding. With the increase in dietary CLA levels, cis 9-trans 11 CLA, trans 10-cis 12 CLA and total CLA of leg muscle increased linearly. The relative proportions of C18:1 $\omega$ -9 and C20:4 $\omega$-6 fatty acids in the leg muscles of chicks fed the CLA containing diets were significantly lower (p<0.05) than those of TO 6% group. These results indicate that the levels of CLA isomers were increased linearly in dose-dependent manner after feeding of synthetic CLA source. But it was also observed that excessive amount of dietary CLA resulted in the possible adversely effects, such as increase of liver weight, hepatic lipid accumulation and serum GOT level.

• Journal of Nutrition and Health
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• v.26 no.5
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• pp.547-557
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• 1993

This study was done to investigate whether dietary fats differing in their fatty acid compositions change hepatic mitochondrial lipid composition and thereby change adenine nucleotide translocase activity. Male Sprague-Dawley rats were fed 5 different wxperimental diets for 6 weeks, which were different in their fatty acid compositions. The dietary fats were beef tallow(BT), olive oil(OO), corn oil(CO), perilla oil(PO) and sardine oil(SO) as a source of saturated fatty acid, oleic acid, n-6 linoleic acid, n-3 $\alpha$-linolenic acid and n-3 eiocosapentaenoic acid+docosahexaenoic acid respectively. Body weight of PO group was significantly higher than that of either BT or SO group. This increase in body weight of PO group was due to the increase of food intake. Although there was no difference in liver weight, % liver weight per body weight of SO group was significantly higher than BT and OO groups. Analysis of mitochondrial lipid composition showed that dietary oils differing their fatty acid compositions altered mitochondrial fatty acid patterns, especially n-6/n-3 ratio, cholesterol/phospholipid ratio and phopsholipid composition. The n-6/n-3 ratio was highest in CO group but lowest in SO group whereas the ratio of Chol/PL was highest in SO group but lowest in CO group. Such changes in mitochondrial lipids did not lead to a significant alteration in the activities of adenine nucleotide translocase, which is embedded in mitochodrial inner membrane.

• Journal of Nutrition and Health
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• v.38 no.4
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• pp.297-306
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• 2005

It is known that dehydroepiandrosterone (DHEA) shows a dual effect, prooxidant or antioxidant, depending on the do-sage or physiological status of animals. The purpose of this study was to determine the effects of DHEA administration at low dose on lipid peroxidation, protein carbonylation and fatty acid composition in liver. Sprague Dawley male rats were fed either com oil diet containing $15\%$ com oil or fish oil diet containing $2\%$ corn oil + $13\%$ sardine oil, with or without $0.2\%$ DHEA for 9 weeks. Atherogenic index and hepatic triglyceride and cholesterol levels were significantly reduced by DHEA administration in rats fed with fish oil diet. Hepatic lipid peroxide product (TBARS) and protein carbonyl levels were significantly higher in rats fed with fish oil diet than in rats fed with corn oil diet. However, DHEA administration significantly reduced the hepatic thiobarbituric acid-reactive substance (TBARS) and conjugated diene levels in rats fed with fish oil diet. Contents of C16 : 0, C16 : 1, C20 : 5 and C22 : 6 in hepatic microsome were higher in rats fed with fish oil diet than in rats fed with corn oil diet, and contents of C18 : 2 and C20 : 4 were lower than in rats fed with com oil diet. DHEA administration significantly increased C16 : 0 and C18 : 3 contents and reduced C18 : 2 content in rats fed with com oil diet, while it increased C16 : 0 and C18 : 1 and reduced C20 : 5 and C22 : 6 in rats fed with fish oil diet. On overall, DHEA administration increased saturated fatty acid (SFA) and reduced polyunsaturated fatty acid (PUFA) in hepatic microsome, thereby PUFA/SFA ratio was significantly (p < 0.0001) reduced without the change of n-3/n-6 ratio. Taken together, low dose of DHEA administration lowered PUFA/SFA ratio in hepatic microsomal membranes and also showed antioxidative effect especially in fish oil-induced highly oxidative stress condition through blocking increases of C20 : 5 and C22 : 6 contents.

• YAKHAK HOEJI
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• v.36 no.1
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• pp.73-79
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• 1992

To achieve better understanding of the effects of monosodium-L-glutamate(MSG) against $CCl_4$ fatty liver in Wister male rats, 5% MSG solution was given as drinking water and $CCl_4$ 0.1 ml/kg was injected subcutaneously twice a week for four weeks. It was showed that increased hepatic phospholipid and hepatic triacylglycerol levels by $CCl_4$ challenge were significantly decreased by additionnal MSG, respectively. However, MSG had no apparent effect on the elevated hepatic cholesterol level in the presence of $CCl_4$. Histologically, additional MSG markedly inhibited fatty degeneration, spotty necrosis, inflammation and periportal vascular proliferation manifested by $CCl_4$. respectively. These results indicated that effects of MSG against $CCl_4$ induced-fatty liver appeared to be involved with partial restoration of altered hepatic lipid composition.

• 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.

• Preventive Nutrition and Food Science
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• v.21 no.3
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• pp.171-180
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• 2016

Non-alcoholic fatty liver disease (NAFLD) is one of the most prevalent liver diseases associated with an altered lifestyle, besides genetic factors. The control and management of NAFLD mostly depend on lifestyle modifications, due to the lack of a specific therapeutic approach. In this context, we assessed the effect of carrot juice on the development of high fructose-induced hepatic steatosis. For this purpose, male weanling Wistar rats were divided into 4 groups, fed either a control (Con) or high fructose (HFr) diet of AIN93G composition, with or without carrot juice (CJ) for 8 weeks. At the end of the experimental period, plasma biochemical markers, such as triglycerides, alanine aminotransferase, and ${\beta}$-hydroxy butyrate levels were comparable among the 4 groups. Although, the liver injury marker, aspartate aminotransferase, levels in plasma showed a reduction, hepatic triglycerides levels were not significantly reduced by carrot juice ingestion in the HFr diet-fed rats (HFr-CJ). On the other hand, the key triglyceride synthesis pathway enzyme, hepatic stearoyl-CoA desaturase 1 (SCD1), expression at mRNA level was augmented by carrot juice ingestion, while their protein levels showed a significant reduction, which corroborated with decreased monounsaturated fatty acids (MUFA), particularly palmitoleic (C16:1) and oleic (C18:1) acids. Notably, it also improved the long chain n-3 polyunsaturated fatty acid, docosahexaenoic acid (DHA; C22:6) content of the liver in HFr-CJ. In conclusion, carrot juice ingestion decreased the SCD1-mediated production of MUFA and improved DHA levels in liver, under high fructose diet-fed conditions. However, these changes did not significantly lower the hepatic triglyceride levels.

• BMB Reports
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• v.36 no.3
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• pp.312-318
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• 2003

The purpose of this study was to investigate the effects of altering relative intakes of fat and carbohydrates on serum lipid profiles, hepatic acyl-CoA synthetase (ACS), carnitine palmitoyltransferase-I (CPT-I), and the acetyl-CoA carboxlyase (ACC) mRNA level in Sprague-Dawley rats. For four weeks the rats were fed either an AIN-76 diet or one of its modified diets that were supplemented with 20% beef tallow (high-fat diet, HF) and 66.3% sucrose (highsucrose diet, HS). The HS group had significantly higher serum triglyceride and total cholesterol concentrations when compared with the other groups. Serum LDL-cholesterol concentrations in the HS and HF groups were significantly higher when compared to the normal diet (ND) group. Serum HDL-cholesterol levels of the ND and HS groups were significantly higher than those of the HF group. The hepatic total lipid level of the HF group was significantly higher than those of other groups; triglyceride levels of the HS and HF groups were significantly higher than those of the ND group. Hepatic ACS mRNA levels of the HF group were significantly higher than those of the ND group. Hepatic CPT-I mRNA levels were higher in the HF group than other groups. Also, ACC mRNA levels in the liver increased in the HF group. In conclusion, changes in the composition of dietary fat and carbohydrates could affect the hepatic ACS, CPT-I, and ACC mRNA levels. These results facilitate our understanding of the coordinated regulation of the ACS, CPT-I, and ACC mRNA levels and will serve to enhance our understanding of the molecular mechanisms that underlie the regulation of fatty acid metabolism.