Beaugé F, Clément M, Nordmann J, Nordmann R
Chem Biol Interact. 1979 Jul;26(2):155-66. doi: 10.1016/0009-2797(79)90019-x.
Besides ethanol, other aliphatic alcohols such as n-propanol and isopropanol induce a triacylglycerol (TAG) accumulation in the liver. To determine whether a common mechanism is responsible for the effects of these three alcohols on hepatic lipid metabolism, each was administered by gastric tube to female Wistar rats at the dose of 50 mmol/kg body wt. Whichever alcohol was administered, the hepatic triacylglycerol accumulation was found to be related to the duration of elevated blood alcohol concentration. After administration of n-propanol or isopropanol, the liver [14C]palmitate uptake was increased whereas hepatic palmitate oxidation to 14CO2 was impaired and palmitate esterification into TAG enhanced; these perturbations were however more discrete than after ethanol administration. In contrast to ethanol and n-propanol which, at the dose presently used, increase precursor incorporation into blood TAG, isopropanol inhibits this incorporation. Interference with the process of very low density lipoprotein (VLDL) synthesis and/or secretion, which appears only at a late stage of isopropanol intoxication, is probably responsible for the intensity and duration of the fatty liver observed after administration of this alcohol.
除乙醇外，其他脂肪醇如正丙醇和异丙醇会诱导肝脏中三酰甘油（TAG）的积累。为了确定这三种醇对肝脏脂质代谢的影响是否存在共同机制，将每种醇以50 mmol/kg体重的剂量通过胃管给予雌性Wistar大鼠。无论给予哪种醇，肝脏三酰甘油的积累都与血液酒精浓度升高的持续时间有关。给予正丙醇或异丙醇后，肝脏对[14C]棕榈酸的摄取增加，而肝脏将棕榈酸氧化为14CO2的过程受到损害，棕榈酸酯化生成TAG增强；然而，这些干扰比给予乙醇后更为分散。与目前所用剂量的乙醇和正丙醇会增加前体掺入血液TAG不同，异丙醇会抑制这种掺入。对极低密度脂蛋白（VLDL）合成和/或分泌过程的干扰可能是导致给予这种醇后观察到的脂肪肝的强度和持续时间的原因，这种干扰仅在异丙醇中毒的后期出现。
