Experimental liver fibrosis induced in rats receiving high doses of alcohol and alternating between regular and vitamin-depleted diets.

Experientia Pub Date : 1996-07-15 DOI:10.1007/BF01925580
H Hirano, T Hirano, K Hirata, M Tamura, T Yamaura, T Hamada
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引用次数: 4

Abstract

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.

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实验性肝纤维化诱导大鼠接受高剂量的酒精,并在常规和缺乏维生素的饮食之间交替。
通过模拟人类酒精饮食模式诱导大鼠肝纤维化。酒精成瘾是通过逐渐增加饮用水中乙醇浓度来建立的;在最后阶段加入盐。接受酒精浓度超过50% (v/v)(类似于伏特加)的大鼠肝细胞表现出酒精透明(马洛里体)。酒精性肝纤维化是通过在常规饮食和高压灭菌(缺乏维生素)饮食之间交替诱导的,模拟人类酗酒者的不规则饮食习惯。在大鼠肝脏中,给予70% (v/v)乙醇(相当于苦艾酒)和25%生理盐水,并饲喂交替饮食,诱导细胞周围纤维化。除了大鼠饮酒发作(重度饮酒期)外,对照组大鼠和酒精大鼠之间的卡路里摄入量没有显著差异。这表明,无论是高脂肪饮食还是胆碱消耗饮食都不是诱发人类酗酒者酒精性纤维化的必要条件。
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