Goheen S C, Larkin E C, Rao G A
Lipids. 1983 Apr;18(4):285-90. doi: 10.1007/BF02534703.
Rats were fed ethanol and a fat-free diet for 30 days to determine whether dietary fat is needed for the development of fatty liver. The severity of fatty liver was similar to that of rats fed an isocaloric diet with 35% fat. Small amounts (29 mg/day) of dietary arachidonic acid prevented alcoholic fatty liver. Rats fed either the alcohol (AF) or control (CF) fat-free diets developed essential fatty acid deficiency (EFAD) as measured by the triene/tetraene ratio of liver and plasma lipids. Rats fed arachidonic acid (AA, alcohol and CA, control diets) did not develop EFAD. Although EFAD alone did not cause the development of fatty liver, the combination of dietary ethanol and EFAD did. The ratios of 16:1/16:0 and 18:1/18:0 in liver lipids indicated that desaturase enzymes were less active and lipogenesis was reduced in rats fed the AA diet compared to those fed the AF diet. In contrast, stimulated lipogenesis appears to have been the cause of fatty liver in rats fed the AF diet.
给大鼠喂食乙醇和无脂饮食30天，以确定脂肪肝的发展是否需要膳食脂肪。脂肪肝的严重程度与喂食含35%脂肪的等热量饮食的大鼠相似。少量（29毫克/天）的膳食花生四烯酸可预防酒精性脂肪肝。喂食酒精（AF）或对照（CF）无脂饮食的大鼠出现了必需脂肪酸缺乏（EFAD），这通过肝脏和血浆脂质的三烯/四烯比值来衡量。喂食花生四烯酸（AA，酒精组和CA，对照组饮食）的大鼠没有出现EFAD。虽然单独的EFAD不会导致脂肪肝的发展，但膳食乙醇和EFAD共同作用则会导致脂肪肝。肝脏脂质中16:1/16:0和18:1/18:0的比值表明，与喂食AF饮食的大鼠相比，喂食AA饮食的大鼠中去饱和酶的活性较低，脂肪生成减少。相反，脂肪生成增加似乎是喂食AF饮食的大鼠患脂肪肝的原因。
