Schneider J, Kaffarnik H
Leber Magen Darm. 1978 Oct;8(5):255-64.
Fatty liver and hyperlipoproteinemia are the main clinical manifestations of interrelationships between ethanol and fat metabolism. Elevation of VLDL is observed more, hyperchylomicronemia less frequently. In metabolic healthy volunteers reversible hypertriglyceridemia can be provoked as well. The pathogenesis of ethanol-induced hyperlipoproteinemia is based on metabolic alterations directly dependent on the oxidation of ethanol in the liver as well as on indirect effects: Besides decreased oxidation and increased de-novo-synthesis by the liver, the sources of fatty acids for the enhanced production of VLDL are the adipose tissue and alimentary fat. VLDL concentrations have been shown to correlate with risk of atherogenesis in the middle-aged. Enhancement of alpha/beta (HDL/LDL)-cholesterol which would indicate an antiatherogenetic effect have been observed in relation to ethanol intake. At the moment it is premature to conclude that ethanol-induced changes in plasma lipoproteins may favour or delay atherogenesis.
脂肪肝和高脂蛋白血症是乙醇与脂肪代谢相互关系的主要临床表现。观察到更多的是极低密度脂蛋白(VLDL)升高,而高乳糜微粒血症较少见。在代谢健康的志愿者中也可引发可逆性高甘油三酯血症。乙醇诱导的高脂蛋白血症的发病机制基于直接依赖肝脏中乙醇氧化的代谢改变以及间接作用:除了肝脏氧化减少和从头合成增加外,用于增强极低密度脂蛋白产生的脂肪酸来源是脂肪组织和食物脂肪。已表明极低密度脂蛋白浓度与中年人群动脉粥样硬化发生风险相关。关于乙醇摄入,已观察到α/β(高密度脂蛋白/低密度脂蛋白)胆固醇升高,这表明具有抗动脉粥样硬化作用。目前得出乙醇诱导的血浆脂蛋白变化可能有利于或延缓动脉粥样硬化发生的结论还为时过早。