• 한국환경성돌연변이발암원학회지
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• 제17권2호
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• pp.78-91
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• 1997

Peroxisome is a single membrane-bounded organelle found in hepatic parenchymal cells and kidney tubular epithelial cells. A number of enzymes exist in peroxisome contributing to anabolic and catabolic peroxisomal functions. Extramitochontriai $\beta$-oxidation of fatty acid is a major function of peroxisome. Peroxisomes can be proliferated by many structually unrelated compounds such as hypolipidemic drugs, plasticizers, pesticides, some pharmaceutical agents and high fat diet. These chemicals, called peroxisome proliferators, act via the peroxisome proliferator activated receptor, to induce peroxisome proliferation, hepatomegaly and hepatocellular carcinoma in rodent. The clear mechanisms of peroxisome proliferator-induced hepatocarcinogenesis have been not demonstrated. Since they are not genotoxic, biochemical changes or changes in gene expressions may be involved. A free radical theory has been suggested based on the finding of oxidative damages of macromolecules by hydrogen peroxide released in the peroxisomal $\beta$-oxidation of fatty acid. Increased cell proliferation by a peroxisome proliferator has been also thought to be an important factor in the hepatocarcinogenesis as suggested in other cases of nongenotoxic carcinogenesis. The alternation of eicosanoid concentrations by peroxisome proliferators may be important in the peroxisome proliferator-induced hepatocarcinogenesis since peroxisome proliferators decrease the concentration of eicosanoids, and the peroxisome proliferator ciprofibrate-eicosanoid combination is comitogenic and costimulates some mitogenic signals in hepatocytes. All of proposed mechanisms should be considered in the peroxisome prolifrator-induced hepatocarcinogenesis.

• Asian-Australasian Journal of Animal Sciences
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• 제10권4호
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• pp.402-407
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• 1997

This study was conducted to investigate the effects of effects of enprostil, a prostaglandin $E_2$, analogue, on liver triacylglycerol content and factors that regulate liver lipid metabolism in mice. Mice received vehicle or $10{\mu}g$ enprostil/kg body weight intraperitoneally every 6 h, and were killed at 0, 6, 12, 18 and 24 h after the first injection. Enprostil significantly lowered liver triacylglycerol content after 12 h of the first injection. However, the peroxisomal ${\beta}$-oxidation activity was inconsistent with the result of liver triacylglycerol content, because its activity was lovered by enprosil. In another experiment, the effect of enprostil on lipid metabolism in mice was investigated in a short period. Mice received $10{\mu}g$ enprostil/kg body weight intraperitoneally, and were killed after 0, 5, 10, 30 and 60 min. After 30 min, malic enzyme activity was significantly increased by the administration of enprostil compared with the activity at 5 min after. No significant changes in liver carnitine palmitoyltransferase and peroxisomal ${\beta}$-oxidation activities were observed. Plasma free fatty acid concentrations were markedly reduced from 5 through 60 min after the administration of enprostil. Consequently, enprostil suppressive effect on liver triacylglycerol concentration might result from the decreased entry of free fatty acid into liver.

• 한국식품과학회지
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• 제22권3호
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• pp.332-336
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• 1990

레놀레산이 함유된 액상 모델시스템에 있어서 지방산의 산화반응에 미치는 양조간장(분말)의 항산화 특성에 대한 일련의 연구를 행하여 다음과 같은 결과를 얻었다. 양조간장은 산화반응 과정 중 과산화물 생성을 억제하였으며, 반응에 첨가된 양조간장의 함량이 높을수록 항산화 작용이 더 큰 결과를 보였다. 이를 기존 항산화제와 비교하였을 때 알파-토코페롤0.05% 첨가수준의 항산화성은 양조간장 분말 $0.2{\sim}0.5%$ 범위에 있었다. 그리고 10ppm의 염화제일철이 함유된 산화반응에 있어서 양조간장은 미량금속의 산화촉진작용을 저하시켰으며 구연산과 공존할 때 항산화작용의 상승효과도 있었다. 또한, 양조간장은 oxidative free radical과 반응하였을때 수소공여성이 인정되었으며 리놀레산 혼합물의 리폭시제나이제 촉매적 산화반응을 억제하는 효과도 보였다.

• 한국식생활문화학회지
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• 제21권1호
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• pp.81-85
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• 2006

Seasoning oil(SO-1) was manufactured from soybean oil, with ${\beta}-carotene$, oleoresin paprika and 3 kinds of flavors. Color of it's SO-1 was red. Total content of trans fatty acid of SO-1 was low level 0.84%, compare to the butter's and margarine's 1.35%, 28.31%, respectively. Total volatile components of SO-1 was 201,313.11ppm, was higher than soybean oil's, butter's, margarine's and SO-2's(removed 3 kinds of flavors from SO-1), it's value of 63.54ppm, 481.24ppm, 168.95ppm and 205.73ppm, respectively. And smoke point(SP) of SO-1 was higher than others. SP of SO-1, after 6 months later at room temperature, was 240, in contrast with soybean oil's 228. This SO-1, added ${\beta}-carotene$ and flavor components, had a masking effect of burnt flavor. From these results, SO-1 can be replaced of butter or margarine as a substituted oil.

• Journal of Nutrition and Health
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• 제29권7호
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• pp.703-712
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• 1996

This study planned to compare the effects of source and amount of dietary n-3 fatty acid, tuna oil and perilla oil, on lipid metabolism and eicosanoids production in Spargue-Dawley strain male rats. Weaning rats were fed 5 different experimantal diets for 4 weeks. (S : beef tallow 50%+sesame oil 50%, T1 : beef tallow 50%+sesame oil 40%+tuna oil 10%, T2 : beef tallow 50%+sesame oil 25%+tuna oil 25%, P1 : beef tallow 50%+sesame oil 40%+perilla oil 10%, P2 : beef tallow 50%+sesame oil 25%+perilla oil 25%) Food intake was higher in T2 group than in other groups, but body weight gain and food efficiency tate were not different among groups. Plasma total lipid and triglyceride were significantly lower in groups fed perilla oil as much as groups fed tuna oil than in S. But tuna oil reduced plasma cholesterol level more than perilla oil. Liver total lipid per unit, cholesterol and triglyceride were not affected by dietary fat sources. Peroxisomal $\beta$-oxidation was higher in T1 and T2 than in P1 and P2. Activities of glucose 6 phosphate dehydrogenase and malic enzyme were lower in T1 and T2 than in group fed sesame oil only. Plasma TXB2 was affected by n-3 fatty acid consumption, and it was lower in perilla oil groups as much as tuna oil groups than in S. But 6-keto PGF1$\alpha$ was not different among experimental groups. The results of this study indicated that tuna oil and perilla oil both decreased plasma lipids, however, the mechanism may be different. And tuna oil and perilla oil had a similar effects on eicosanoids production.

• Journal of Nutrition and Health
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• 제29권9호
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• pp.925-933
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• 1996

This study intended to compare the hypolipidemic effects among six experimental groups fed by three different dietary carbohydrates on hyperlipodemic rats. Sixty experimental animals were divided into 6 groups, SB, ST, SP and CB, CT, CP after production of hyperlipidemia fed by SB diet on Sprague-Dawley rats for 4 weeks. Rats were fed by six experimental diets for eight weeks. Hyjperlipidemic rats showed three times higher in plasma TG level not in cholesterol content compare to control group fed by stock diet. Two different dietary carbohydrates seem to be effective in body weight gain and fat cumulation as weight of epididymal fat pad. In comparison of S and C groups, C fed groups showed lowering effect in plasma TG and total lipid contents, but among S fed groups, ST and SP group showed lower than SB in this respects. Dietary carbohydrates seem to be more effective than fat in plasma lipid contents. When we compare among three different fat groups, only T groups with different carbohydrates increased in peroxisomal lipid oxidation and decreased in lipogenic enzyme activites. As same token, sucrose fed group with three fat sources seem to increase activiteies enzyme activities. In epididymal fat pad and Heart, SP and CP effect more in LPL activites than other groups. In conclusion, we can recommed to consume polysaccharides rather than disaccharide and n-3 fatty acids such as perilla and tuna oils to alleviate hypertringlycemic condition.

• Journal of Nutrition and Health
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• 제26권7호
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• pp.887-898
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• 1993

In order to determine the effect of iron depletion and subsequent supplementation on the muscle capacity for peroxisomal (PO) and mitochondrial(MO) $\beta$-oxidation during high fat feeding, weanling rats were fed a 44% (HF) or 2.5% (LF) fat diet with (+Fe) or without (-Fe) iron for 6 or 9 weeks. After 1 week rats fed HF+Fe or HF-Fe had 50-100% more PO and MO in heart, soleus, psoas and gastrocnemius than did rats fed low fat, but after 3 weeks rats fed HF-Fe had lower muscle PO and MO. In muscles of iron depleted rats PO and MO were not increased by supplementation with iron for 3 weeks. After 6 weeks MO and PO in skeletal muscles of rats fed HF+Fe were lower than after 3 weeks. It is concluded that adequate iron is necessary for miaximum response of muscle PO and MO to high fat feeding. However, after 6 weeks both PO and MO have returned to levels similar to those of rats fed low fat diets, hence, the elevated catalase activities seen at this time do not reflect peroxisomal $\beta$-oxidation.

• Toxicological Research
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• 제27권4호
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• pp.211-216
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• 2011

Herbal medicines are widely used in many countries for the treatment of many diseases. Although the use of herb extracts as alternative medicine is growing, their toxicological properties have not been thoroughly investigated. In this study, we have investigated the effects of water and ethanol extracts of 18 herbs on the hepatic lipid metabolism and steatogenic hepatotoxicity. Ethanol extracts of Cirsium japonicum, Carthamus tinctorius, Rehmanniae glutinosa (preparata), Polygala tenuifolia, Foeniculum vulgare, Polygonum multiflorum, and Acorus gramineus and water extracts of Polygonum multiflorum and Rehmanniae glutinosa induced lipid accumulation in Sk-hep1 human hepatoma cells as determined by Nile red staining. These extracts increased the luciferase activity of sterol regulatory element (SRE) and decreased that of peroxisome proliferator response element (PPRE), indicating the possibilities of enhanced fatty acid synthesis and decreased fatty acid oxidation. To identify the components responsible for the fat accumulation, we tested 50 chemicals isolated from the nine herbs. Apigenin, luteolin, pectolinarin and lupeol from Cirsium japonicum, 8-methoxypsoralen and umbelliferone from Foeniculum vulgare and pomonic acid and jiocerebroside from Rehmanniae glutinosa significantly increased the accumulation of lipid droplets. These results suggest that ethanol extracts of Cirsium japonicum, Carthamus tinctorius, Rehmanniae glutinosa (preparata), Polygala tenuifolia, Foeniculum vulgare, Polygonum multiflorum, and Acorus gramineus and water extracts of Polygonum multiflorum and Rehmanniae glutinosa can cause fatty liver disease by decreasing ${\beta}$-oxidation of fatty acid and increasing lipogenesis.

• Clinical and Experimental Pediatrics
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• 제45권9호
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• pp.1083-1089
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• 2002

목 적 : 지속적으로 증가하는 소아 비만은 성인 비만으로 이행되기 쉽고 합병증으로 고혈압, 지방간, 동맥경화증이 동반될 수 있다. Carnitine은 장쇄 지방산이 미토콘드리아로 이동할 때 필요한 조효소로 지방산 대사에서 중요한 역할을 한다. 지방간을 가진 비만 소아에서 혈중 지방산과 carnitine 농도를 측정함으로써 L-carnitine을 임상적으로 비만 치료에 적용할 수 있는지를 알아보고자 본 연구를 실시하였다. 방 법 : 7-18세의 지방간으로 진단받은 비만아 9명과 정상 대조군 소아 10명을 대상으로 하였다. 혈장을 sodium borate를 섞어 원심분리 후 하층을 methylene chloride를 이용하여 계층 분리하였고, MSTFA와 acetonitrile을 넣고 유도체화 반응을 시켰다. GC-MS 자동 분석기로 혈청 지방산 fraction을 정량 분석하였고, carnitine(free, acyl, total)은 cycling technique을 이용하여 415 nm에서 정량 분석하였다. 결 과 : 혈중 총 지방산은 지방간이 동반된 비만아 군에서 대조군에 비해 유의하게 증가하였고 특히 장쇄 지방산(myristic acid, palmitoleic acid, palmitic acid, linoleic acid, oleic acid, stearic acid)이 의미 있게 증가되어 있었다. 총 carnitine과 유리 carnitine 농도가 비만아에서 정상아에 비해 유의하게 증가하였으나 acyl carnitine은 유의한 차이가 없었다. 결 론 : 지방간이 동반된 비만아에서 장쇄 지방산이 뚜렷이 증가되었으며, 비만아군에서 정상아에 비해 혈청 carnitine이 증가되어 있음을 알 수 있었다. 이것을 기초로 하여 비만아에서 L-carnitine 투여 후 지방산 대사의 변화에 대해 추후에 연구할 예정이다.

• BMB Reports
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• 제47권1호
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• pp.15-20
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• 2014

Intracellular lipid-binding proteins (LBPs) impact fatty acid homeostasis in various ways, including fatty acid transport into mitochondria. However, the physiological consequences caused by mutations in genes encoding LBPs remain largely uncharacterized. Here, we explore the metabolic consequences of lbp-5 gene deficiency in terms of energy homeostasis in Caenorhabditis elegans. In addition to increased fat storage, which has previously been reported, deletion of lbp-5 attenuated mitochondrial membrane potential and increased reactive oxygen species levels. Biochemical measurement coupled to proteomic analysis of the lbp-5(tm1618) mutant revealed highly increased rates of glycolysis in this mutant. These differential expression profile data support a novel metabolic adaptation of C. elegans, in which glycolysis is activated to compensate for the energy shortage due to the insufficient mitochondrial ${\beta}$-oxidation of fatty acids in lbp-5 mutant worms. This report marks the first demonstration of a unique metabolic adaptation that is a consequence of LBP-5 deficiency in C. elegans.