Effect of the type of dietary fat on the development of alcoholic liver disease.

根据我们对美国和日本酒精性肝病患者营养背景的研究，膳食脂肪的数量和类型被认为在酒精性肝病的发病机制中是重要的。我们研究了脂肪的数量和类型在酒精性肝病发展中的作用。将雄性Wistar大鼠与标准饮食、低蛋白饮食、低蛋白-高脂肪饮食（含或不含36 Cal%乙醇）等热量配对喂养。低蛋白乙醇组和低蛋白高脂乙醇组肝胶原结合羟脯氨酸和甘油三酯均高于标准乙醇组。此外，肝胶原结合羟脯氨酸和甘油三酯在低蛋白高脂肪乙醇组比低蛋白乙醇组高得多。低蛋白乙醇组可见明显的中央纤维硬化，尤其是低蛋白高脂肪乙醇组，并伴有小叶中心型脂肪肝。 关于我们 安吉。低蛋白高脂肪乙醇组血浆乙酸水平最高.本文研究了乙醇和脂肪在肝脏中的代谢产物乙酸对酒精性肝损伤发生、发展的影响。将雄性Sprague-Dawley大鼠与标准饮食、乙酸盐饮食（含有0.1 -mol乙酸钠）和具有或不具有46 Cal%乙醇的等热量配对喂养。与乙酸盐组和标准乙醇组相比，乙酸盐-乙醇组的乙醇消除率较低。脂肪和肝纤维化的变化是最突出的生化和组织病理学在醋酸酒精组。这些数据表明醋酸盐的作用可能是酒精性肝病发生发展的重要因素.将雄性Sprague-Dawley大鼠配对，用含或不含46 Cal%乙醇的牛肉油或红花油等热量喂养12周。我们检测了肝脏的白三烯，肝脏过氧化脂质，肝脏脂肪酸组成，肝脏P450活性，肝脏胶原结合羟脯氨酸和纤维化活性。肝脏脂质过氧化物、亚油酸、花生四烯酸和羟脯氨酸水平在乙醇组中最高。成纤维细胞活性和P450活性较其他各组明显增高。肝组织中白三烯含量与肝组织中花生四烯酸、亚油酸含量呈显著正相关。肝脏过氧化脂质水平与花生四烯酸或亚油酸水平之间也存在显著相关性。总之，含有更多亚麻油酸的植物油促进酒精性肝病的发展。我们推测，加速产生的白三烯来自花生四烯酸可能是一个重要的因素，在发展中的脂质过氧化反应和肝脏疾病的酒精性肝脏。少

The amount and type of dietary fat is thought to be important in the pathogenesis of alcoholic liver disease according to our studies on the nutritional background of the American and Japanese patients with alcoholic liver disease. We investigated the role of amount and type of fat in the development of alcoholic liver disease.1. Male Wistar rats were paired fed isocalorically with standard diet, low protein diet, low protein-high fat diet with or without 36 Cal% of ethanol. Hepatic collagen-bound hydroxyproline and triglyceride were higher in the low protein-ethanol group and the low protein-high fat-ethanol group than in the standard-ethanol group. Furthermore, hepatic collagen-bound hydroxyproline and trialyceride were much higher in the low protein-high fat-ethanol group compared to the low protein-ethanol group. Marked central fibrosclerosis was evident in the low protein-ethanol group and especially in the low protein-high fat-ethanol group accompanied with centrolobular fatty ch … More ange. Plasma level of acetate was the highest in the low protein-high fat-ethanol group.2. The influence of acetate, as the metabolic product of ethanol and fats in the liver, on the occurrence and progression of alcoholic liver injury was studied. Male Sprague-Dawley rats were paired fed isocalorically with standard diet, acetate diet (containing 0.1 -mol sodium acetate), and with or without 46 Cal% of ethanol. Ethanol elimination rate was lower in the acetate-'ethanol group compared to the acetate group and the standard-ethanol group. Fatty and fibrotic changes in the liver were most prominent biochemically and histopathologically in the acetate-alcohol group. these data suggested that the effect of acetate may be an important factor in the development of alcoholic liver disease.3. Male Sprague-Dawley rats were paired fed isocalorically with beef or safflower oil with or without 46 Cal% of ethanol for 12 weeks. We measured hepatic leukotrienes, hepatic lipid peroxide, fatty acid composition of liver, hepatic P450 activity, hepatic collagen-bound hydroxyproline and fibrogenic activity. Hepatic levels of lipid peroxide, linoleic acid, arachidonic acid and hydroxyproline iiere the highest in the safflox%rer-ethanol group. Fibrogenic activity and P450 activity were increased more significantly compared to those in the other paied groups. A significant positive correlation Y, 7as observed between hepatic level of leukotrienes and hepatic arachidonic acid or linoleic acid. A sigificant correlation was also found betx, ; een hepatic levels of lipid peroxide and arachidonic acid or linoleic acid.In conclusion, vegitable oil containing more lineleic acid facilitates development of alcoholic liver disease. We postulate that accelerated generation of leukotrienes derived from arachidonate may be an important factor in the development of lipid peroxidation and liver disease in the allcoholic liver. Less