Sabourault D, Giudicelli Y, Nordmann R, Nordmann J
Biochim Biophys Acta. 1976 May 27;431(2):241-8. doi: 10.1016/0005-2760(76)90144-2.
The intraperitoneal administration of 2-mercaptoethanol or 2-mercaptoacetate (40 muM/100 g body weight) to the rat induces a fatty liver, a marked and early increase of free fatty acids and a decrease of triacylglycerol and phospholipids in the blood. These changes are accompanied by a decrease of the ketone body level and the beta-hydroxybutyrate/acetoacetate ratio in the liver. Under the same experimental conditions, however, administration of 2-mercaptopropionate fails to induce a fatty liver and does not modify the hepatic ketone body level or the blood triacylglycerol and free fatty acid levels. These results led us to conclude that fatty liver induction is not a general feature of foreign thiols, and suggest that increased peripheral fat mobilization as well as decreased hepatic lipoprotein synthesis and/or release are responsible for the 2-mercaptoethanol- and 2-mercaptoacetate-induced fatty liver.
给大鼠腹腔注射2-巯基乙醇或2-巯基乙酸（40μM/100g体重）会诱导脂肪肝的形成，使血液中游离脂肪酸显著且早期升高，同时三酰甘油和磷脂减少。这些变化伴随着肝脏中酮体水平以及β-羟基丁酸/乙酰乙酸比值的降低。然而，在相同实验条件下，注射2-巯基丙酸不会诱导脂肪肝形成，也不会改变肝脏酮体水平或血液中三酰甘油和游离脂肪酸水平。这些结果使我们得出结论，脂肪肝诱导并非外来硫醇的普遍特征，并表明外周脂肪动员增加以及肝脏脂蛋白合成和/或释放减少是2-巯基乙醇和2-巯基乙酸诱导脂肪肝的原因。
