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在酒精性肝病的发病机制中起着重要的作用。我们调查了脂肪的数量和类型在酒精性肝病发生发展中的作用。雄性Wistar大鼠按等热量配对饲养，分别给予标准饲料、低蛋白饲料、低蛋白高脂饲料加或不加36Cal%乙醇。低蛋白乙醇组和低蛋白高脂乙醇组大鼠肝脏胶原结合羟脯氨酸和甘油三酯均高于标准乙醇组。此外，低蛋白-高脂-乙醇组的肝脏胶原结合羟脯氨酸和甘油三酯显著高于低蛋白-乙醇组。明显的中心性纤维硬化在低蛋白-高脂肪-酒精组明显，尤其是在低蛋白-高脂肪-乙醇合并中心小叶脂肪…组。更多的角度。结果：1.低蛋白高脂乙醇组的血浆醋酸酯水平最高。研究乙醇和脂肪在肝脏中的代谢产物--乙酸酯对酒精性肝损伤发生发展的影响。雄性SpragueDawley大鼠按等热量配对饲养，分别给予标准饲料、醋酸盐饲料(含0.1mol醋酸钠)和46Cal%乙醇。乙酸乙醇组的乙醇清除率低于乙酸乙酸组和标准乙醇组。在生化和组织病理学方面，醋酸乙醇组的肝脏脂肪和纤维化改变最为显著。提示醋酸盐的作用可能是酒精性肝病发生发展的重要因素。雄性SpragueDawley大鼠按等热量配对饲喂含或不含46Cal%乙醇的牛肉或红花油，连续12周。测定肝脏白三烯、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及肝纤维化活性。肝脏过氧化脂质、亚油酸、花生四烯酸和羟脯氨酸水平以红花乙醇组最高。纤维形成活性和P450活性较其他PAE组显著升高。肝脏白三烯水平与肝脏花生四烯酸、亚油酸呈显著正相关。甚至肝脏的过氧化脂质和花生四烯酸或亚油酸的水平也有显著的相关性。总而言之，含有更多亚麻酸的植物油有助于酒精性肝病的发生。我们推测，花生四烯酸衍生的白三烯的加速生成可能是异丙肾上腺素肝脏脂质过氧化和肝病发生的重要因素。较少

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