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알코올과 식이엽산수준이 혈장 Homocysteine, 간기능, 간 조직검사에 미치는 영향
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  • 알코올과 식이엽산수준이 혈장 Homocysteine, 간기능, 간 조직검사에 미치는 영향
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장남수,김기남,김연수,서종복,권오옥
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韓國營養學會誌
권/호정보
1998년|31권 7호|pp.1121-1129 (9 pages)
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한국영양학회
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이 논문은 한국과학기술정보연구원과 논문 연계를 통해 무료로 제공되는 원문입니다.
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The critical role of folate vitamin in the remethylation pathway for methionine synthesis from homocysteine has been well documented. Hyperhomocysteinemia resulting from inadequate folate nutrition has been implicated in increased incidence of macrovascular diseases, colorectal cancer, neural tube defects, etc. Chronic exposure to ethanol impairs folate nutrition and one-carbon metabolism in the liver, which often results in fatty liver due to a defective remethylation process. This study was carried out to investigate the chronic effects of moderate levels of alcohol and dietary 131ate on plasma homocysteine levels, and on histopathology and biochemical functions of the liver Rats were raised on experimental diets with three levels of folate(0, 2, 8mg/kg diet), and 50% ethanol(1.8m1/kg body weight) was administered intragastrically by intubation tubes three times a week for 10 weeks. Plasma homocysteine concentrations were found to be significantly influenced by dietary folate intake and alcohol administration. Among all treatment groups, Plasma homocysteine levels were highest in the animals receiving a combined treatment of folate deficient diet and alcohol administration. Plasma homocysteine concentration was negatively correlated with folate concentration in the plasma(p<0.01) and liver(p<0.05). Among alcohol treated rats, increase in plasma homocysteine values due to ethanol was prevented by 131ate supplementation. When liver histological tests were performed, macrovascular and microvascular fatty changes and spotted necrosis were observed more frequently in folate-deficient animals diet than those on folate-adequate and folate-supplemented diets in alcohol-treated rats. These results indicate that folate supplementation above the recommended level might be beneficial in the prevention of alcohol-related hyperhomocystei-nemia and abnormal histologic changes in the liver due. (Korean J Nutrition 31(7) : l121-l129, 1998)