Rogers A E, Fox J G, Murphy J C
Drug Nutr Interact. 1981;1(1):3-14.
Development of alcohol-related liver and other diseases appears to be modified by host and environmental factors that include diet and nutritional status, exposure to other drugs and toxins, and infection. The relative importance of alcohol toxicity and malnutrition in the induction of fatty liver and cirrhosis, the subject of this report, has been debated. Male rhesus (M mulatta) monkeys were fed purified liquid diets, adequate or marginally deficient in lipotropes (choline, methionine, and folate), containing ethanol to supply 40-50% of calories for 1.5-4.5 years. Controls, fed the diets with sucrose and fat isocalorically substituted for ethanol, grew well and were clinically normal. Ethanol-fed monkeys in both diet groups failed to gain weight and were slightly anemic, with mild derangements of serum electrolytes and small amounts of fat in their livers. None had fibrosis or cirrhosis until the severity of the lipotrope-deficiency was increased; then two of four deficient animals developed cirrhosis and one developed fibrosis. (The severe deficiency induced weight loss and fatty liver, but not fibrosis, in one of two controls.) We conclude that alcohol does not induce hepatic fibrosis or cirrhosis in rhesus monkeys fed a nutritionally complete diet, a result supported by studies in rats and another monkey, M radiata. Alcohol does induce cirrhosis when fed in combination with a lipotrope-deficient diet that is not, by itself, cirrhogenic.
酒精性肝病及其他疾病的发生发展似乎会受到宿主和环境因素的影响，这些因素包括饮食和营养状况、接触其他药物和毒素以及感染。本报告的主题是酒精毒性和营养不良在脂肪肝和肝硬化诱发过程中的相对重要性，这一问题一直存在争议。给雄性恒河猴（食蟹猴）喂食纯化的流质饮食，这些饮食中促脂物质（胆碱、蛋氨酸和叶酸）充足或略微缺乏，同时含有乙醇，乙醇提供40 - 50%的热量，持续1.5 - 4.5年。对照组以蔗糖和脂肪等热量替代乙醇喂食，生长良好且临床正常。两个饮食组中喂食乙醇的猴子体重均未增加，且有轻微贫血，血清电解质有轻度紊乱，肝脏中有少量脂肪。在促脂物质缺乏程度加重之前，没有猴子出现纤维化或肝硬化；之后，四只缺乏促脂物质的动物中有两只发展为肝硬化，一只发展为纤维化。（严重缺乏促脂物质在两只对照组动物中的一只中导致体重减轻和脂肪肝，但未导致纤维化。）我们得出结论，在喂食营养完整饮食的恒河猴中，酒精不会诱发肝纤维化或肝硬化，这一结果得到了大鼠和另一种猴子（帚尾猴）研究的支持。当与本身不会导致肝硬化的促脂物质缺乏饮食一起喂食时，酒精确实会诱发肝硬化。
