Bosma A, Seifert W F, van Thiel-de Ruiter G C, van Leeuwen R E, Blauw B, Roholl P, Knook D L, Brouwer A
TNO Institute of Ageing and Vascular Research (IVVO-TNO), Leiden, The Netherlands.
J Hepatol. 1994 Sep;21(3):394-402. doi: 10.1016/s0168-8278(05)80319-8.
Rats were malnourished for 12 months with a highly inadequate fat-rich, calorie-sufficient but otherwise poly-deficient liquid diet composed of mashed potatoes with mayonnaise, comparable with the nutritional intake of many chronic alcoholics. When alcohol was incorporated into this diet, administered as whisky in drinking water available ad libitum, the livers of all eight rats showed increased fibrosis and cirrhosis as compared to the livers of the eight non-alcohol-treated, isocalorically fed, paired control rats. Alcohol-treated rats developed fibrosis and cirrhosis on a dietary fat content of 38% of total caloric intake and low blood alcohol levels, ranging from 50 to 126 mg/dl, due to gradual intake over the day and to low absolute intake (mean 11.9 +/- 0.6 g/kg per day). None of the rats died spontaneously. Malnutrition is likely to be an important factor in the development of the fibrosis of alcoholic liver disease, and this rat model may be used to study aspects of the pathogenesis.
用一种脂肪含量极高但热量充足、其他方面却营养多缺乏的流质饮食(由加蛋黄酱的土豆泥组成)使大鼠营养不良12个月,这种饮食与许多慢性酗酒者的营养摄入相当。当将酒精加入这种饮食中,以威士忌的形式随意添加到饮用水中时,与8只未接受酒精处理、等热量喂养的配对对照大鼠的肝脏相比,所有8只大鼠的肝脏均出现了纤维化和肝硬化加重的情况。酒精处理的大鼠在饮食脂肪含量占总热量摄入38%且血液酒精水平较低(50至126毫克/分升)的情况下出现了纤维化和肝硬化,这是由于一天中逐渐摄入以及绝对摄入量较低(平均每天11.9±0.6克/千克)所致。没有大鼠自发死亡。营养不良可能是酒精性肝病纤维化发展的一个重要因素,这种大鼠模型可用于研究发病机制的各个方面。