Beaugé F, Clément M, Nordmann J, Nordmann R
Chem Biol Interact. 1981 Dec;38(1):45-51. doi: 10.1016/0009-2797(81)90152-6.
Oral administration of a single dose of t-butanol (25 mmol/kg body wt.) to female Wistar rats results in an accumulation of triacylglycerols (TAGs) in the liver. This administration induces an early increase in the rate of palmitate uptake by the liver and a delayed enhancement of the blood free fatty acid (FFA) level. Whereas hepatic lactate/pyruvate ratio and liver fatty acid oxidation appear unimpaired, a highly significant enhancement of palmitate incorporation into liver TAGs occurs after t-butanol administration. This administration impairs the biosynthesis and/or secretion of very low density lipoproteins (VLDLs) as shown by the decrease in both the serum TAG level and the palmitate incorporation into serum TAGs. These data suggest that the metabolic disturbances reported may be related to the stress induced by the administration of t-butanol which is very slowly metabolized, as shown by the sustained blood alcohol level found over a 20-h period. This study also provides evidence that metabolism through the alcohol dehydrogenase (ADH) pathway is not a prerequisite for the ability of an alcohol to induce a fatty liver when administered to rats.
给雌性Wistar大鼠口服单剂量叔丁醇（25 mmol/kg体重）会导致肝脏中三酰甘油（TAGs）的积累。这种给药方式会使肝脏对棕榈酸的摄取速率早期增加，并使血液游离脂肪酸（FFA）水平延迟升高。虽然肝脏乳酸/丙酮酸比值和肝脏脂肪酸氧化似乎未受损害，但叔丁醇给药后，棕榈酸掺入肝脏TAGs的量显著增加。如血清TAG水平降低以及棕榈酸掺入血清TAGs减少所示，这种给药方式损害了极低密度脂蛋白（VLDLs）的生物合成和/或分泌。这些数据表明，所报道的代谢紊乱可能与叔丁醇给药所诱导的应激有关，叔丁醇代谢非常缓慢，如在20小时内持续的血液酒精水平所示。这项研究还提供了证据，表明当给大鼠给药时，通过乙醇脱氢酶（ADH）途径的代谢并非酒精诱导脂肪肝能力的先决条件。
