Kaffarnik H, Schneider J
Klin Wochenschr. 1976 Aug 15;54(16):747-54. doi: 10.1007/BF01614291.
Reversible hyperlipoproteinemia may be observed after ethanol loads in healthy man before any ethanol-induced disease is being established. Different pathogenetic ways to this acute ethanol-induced hyperlipoproteinemia have been investigated or postulated in recent years. Two main sites have appeared: changes in the metabolism of lipids and their precursors which depend from acutal oxidation of ethanol in the liver, and ethanol-induced activation of lipolysis in adipose tissue, transmitted by the sympathico-adrenal system. The changes in liver metabolism during ethanol oxidation have been well confirmed in many experiments, they nevertheless do not seem to lead to hyperlipoproteinemia in many experimental designs in animals and after drinkable amounts of ethanol in healthy man when lipolysis of adipose tissue is blocked and no food is ingested. After the intake of a fatty meal these triglycerides are becoming importance as a source of fatty acids. A possible increased de novo synthesis of palmitic acid may to a minor degree contribute to hypertriglyceridemia.
在健康男性中,在任何乙醇诱导的疾病发生之前,乙醇负荷后可能会观察到可逆性高脂蛋白血症。近年来,人们对这种急性乙醇诱导的高脂蛋白血症的不同发病机制进行了研究或推测。主要出现了两个部位:脂质及其前体代谢的变化,这取决于肝脏中乙醇的实际氧化,以及乙醇诱导的脂肪组织中脂肪分解的激活,通过交感-肾上腺系统传递。乙醇氧化过程中肝脏代谢的变化在许多实验中得到了充分证实,但在许多动物实验设计中,以及在健康男性摄入可饮用剂量的乙醇后,当脂肪组织的脂肪分解被阻断且不摄入食物时,它们似乎不会导致高脂蛋白血症。摄入脂肪餐后,这些甘油三酯作为脂肪酸的来源变得很重要。棕榈酸可能增加的从头合成可能在较小程度上导致高甘油三酯血症。