Hirano H, Hirano T, Hirata K, Tamura M, Yamaura T, Hamada T
Department of Biochemistry, University of Occupational and Environmental Health, Kitakyushu, Japan.
Experientia. 1996 Jul 15;52(7):710-5. doi: 10.1007/BF01925580.
Liver fibrosis was induced in rats by simulating human alcoholic eating and drinking patterns. Alcohol addiction was established by gradually increasing the ethanol concentration in the drinking water; salts were added at the terminal stage. The hepatocytes of rats receiving alcohol concentrations exceeding 50% (v/v) (similar to vodka) exhibited alcoholic hyaline (Mallory bodies). Alcoholic liver fibrosis was induced by alternating between regular and autoclaved (vitamin-depleted) diets, simulating the irregular eating habits of human alcoholics. In the livers of rats receiving 70% (v/v) ethanol (comparable to absinthe) with 25% saline and fed the alternating diets, pericellular fibrosis was induced. No significant difference in calorie intake between control and alcohol rats was detected except when rats underwent drinking bouts (heavy drinking phase). This indicates that neither a high-fat diet nor a choline-depleted diet is necessary to induce the alcoholic fibrosis seen in human alcoholics.
通过模拟人类饮酒模式在大鼠中诱导肝纤维化。通过逐渐增加饮用水中的乙醇浓度建立酒精成瘾;在末期添加盐分。接受超过50%(v/v)(类似于伏特加)酒精浓度的大鼠肝细胞出现酒精性透明小体(马洛里小体)。通过在常规饮食和高压灭菌(缺乏维生素)饮食之间交替,模拟人类酗酒者的不规律饮食习惯,诱导酒精性肝纤维化。在接受70%(v/v)乙醇(相当于苦艾酒)加25%盐水并采用交替饮食的大鼠肝脏中,诱导出细胞周围纤维化。除了大鼠经历饮酒发作(大量饮酒阶段)外,对照组和酒精喂养组大鼠的热量摄入没有显著差异。这表明,诱导人类酗酒者出现的酒精性纤维化既不需要高脂饮食也不需要胆碱缺乏饮食。