Parekh A C, Mathur R K, Dave C V
Res Commun Chem Pathol Pharmacol. 1977 Mar;16(3):535-40.
The transient hypocholesterolemia phenomenon observed in rats, injected i.v. with amphotericin B (1.5 mg/kg/day) for three weeks, was investigated by in vitro [14C] acetate incorporation into the liver cholesterol. The incorporation of acetate in liver slices of treated animals increased more than two-fold (p less than 0.02) when compared with controls.When amphotericin B was added in vitro to liver slices of control rats, the incorporation of acetate into cholesterol decreased to about 65% of that observed with the corresponding controls (p less than 0.01). The results are consistent with the hypothesis that initially amphotericin B causes inhibition of de novo cholesterol synthesis resulting in hypocholesterolemia which disappears on continued treatment possibly due to compensatory increased rate of cholesterol biosynthesis.
对静脉注射两性霉素B（1.5毫克/千克/天）三周的大鼠所观察到的短暂性低胆固醇血症现象，通过体外[14C]乙酸掺入肝脏胆固醇的方法进行了研究。与对照组相比，经处理动物的肝脏切片中乙酸的掺入量增加了两倍多（p<0.02）。当在体外将两性霉素B添加到对照大鼠的肝脏切片中时，乙酸掺入胆固醇的量降至相应对照组观察值的约65%（p<0.01）。这些结果与以下假设一致：最初两性霉素B会抑制胆固醇的从头合成，导致低胆固醇血症，而持续治疗后这种现象消失可能是由于胆固醇生物合成速率的代偿性增加。
