Schubotz R, Mühlfellner G, Schneider J, Mühlfellner O, Kaffarnik H
Res Exp Med (Berl). 1976 May 15;167(2):139-48. doi: 10.1007/BF01851595.
This investigation decided to answer the question of the origin of fatty acids for the increased synthesis of triglycerides in acute ethanol-induced hyperlipoproteinemia. Healthy persons ingested 0.5 g of ethanol/kg body weight initially and 0,15 g of ethanol/kg and hour for 12 hours. The fatty acids of plasma triglycerides were determined before and after ingestion of ethanol in persons fasting and nourished isocaloricaly, with and without blocking peripheral lipolysis by nicotinic acid and with addition of glucose. The fasting persons triglycerides fatty acids increased to 165.7 % of the initial value after 12 hours of ethanol ingestion, with a preferential increase in palmitic-, oleic- and stearic acid. When lipolysis in adipose tissue was blocked by 0.5 g of nicotinic adic/hour the triglyceride-fatty acids reached only 116.2% after 12 hours, with a decrease in oleic acid, which is present in adipose tissue to a higher degree than in plasma triglycerides. When nourished isocaloricaly, the enhancement of plasma triglyceride-fatty acids could not be suppressed by nicotinic acid. The changes in concentration and pattern of triglyceride-fatty acids announce that the fatty acids used for increased synthesis of triglycerides in fasting persons come from adipose tissue preferentially. In contrast ethanol-ingested hyperlipoproteinemia during ingestion of a food which cannot be suppressed by nicotinic acid, seems to orginate from fatty acids of the food and for de novo synthesis of fatty acids in the liver.
本研究旨在回答急性乙醇诱导的高脂蛋白血症中甘油三酯合成增加时脂肪酸的来源问题。健康人最初按0.5 g乙醇/千克体重摄入,之后12小时内按0.15 g乙醇/千克体重·小时摄入。在禁食和等热量营养状态下的人群中,分别在摄入乙醇前后,测定血浆甘油三酯的脂肪酸含量,同时观察使用烟酸阻断外周脂肪分解以及添加葡萄糖的情况下脂肪酸含量的变化。禁食人群在摄入乙醇12小时后,甘油三酯脂肪酸含量增至初始值的165.7%,其中棕榈酸、油酸和硬脂酸优先增加。当用0.5 g烟酸/小时阻断脂肪组织中的脂肪分解时,12小时后甘油三酯脂肪酸仅达到116.2%,油酸含量下降,脂肪组织中油酸的含量高于血浆甘油三酯中的含量。在等热量营养状态下,烟酸无法抑制血浆甘油三酯脂肪酸的增加。甘油三酯脂肪酸浓度和模式的变化表明,禁食人群中用于增加甘油三酯合成的脂肪酸优先来自脂肪组织。相比之下,在摄入食物期间发生的乙醇诱导的高脂蛋白血症,若不能被烟酸抑制,则似乎源于食物中的脂肪酸以及肝脏中脂肪酸的从头合成。