Grunnet N, Jensen F, Kondrup J, Dich J
Alcohol. 1985 Jan-Feb;2(1):157-61. doi: 10.1016/0741-8329(85)90035-7.
In a previous report it was shown that ethanol increases the rate of accumulation of triacylglycerol by 90% in hepatocytes in primary culture. This represents the first known suitable model for in vitro studies of the ethanol-induced fatty liver. The biochemical alterations causing this accumulation of triacylglycerol remain to be elucidated, however. In the present report it is shown that (1) the effect of ethanol exhibits a time lag of 6-9 hours (2) the increment in the content of triacylglycerol caused by ethanol is increased by increased concentrations of fatty acids (3) the fatty acid uptake is not affected by ethanol (4) fatty acid synthesis is inhibited 20% by ethanol (5) the contents of diacylglycerol and phospholipids are not affected by ethanol (6) addition of ethanol increases the cytosolic and mitochondrial redox levels. It is concluded that ethanol is likely to exert its effect on the accumulation of triacylglycerol by redistributing fatty acids between oxidation and triacylglycerol synthesis and/or between storage and secretion of triacylglycerol.
在之前的一份报告中显示,乙醇使原代培养的肝细胞中三酰甘油的积累速率提高了90%。这是首个已知的适合用于乙醇诱导脂肪肝体外研究的模型。然而,导致这种三酰甘油积累的生化改变仍有待阐明。在本报告中表明:(1)乙醇的作用存在6 - 9小时的时间滞后;(2)乙醇引起的三酰甘油含量增加会因脂肪酸浓度升高而增加;(3)乙醇不影响脂肪酸摄取;(4)乙醇使脂肪酸合成受到20%的抑制;(5)乙醇不影响二酰甘油和磷脂的含量;(6)添加乙醇会提高胞质和线粒体的氧化还原水平。得出的结论是,乙醇可能通过在脂肪酸氧化与三酰甘油合成之间和/或三酰甘油储存与分泌之间重新分配脂肪酸,来对三酰甘油的积累产生影响。