Robins S J, Brunengraber H
J Lipid Res. 1982 May;23(4):604-8.
The contribution of de novo synthesis to the secretion of cholesterol and lecithin in bile was assessed in isolated rat livers, perfused with a lipid-free medium. Cholesterol and lecithin synthesis were measured by the incorporation of tritiated water and [14C]-choline, respectively. Taurocholate stimulated the secretion of biliary lipids to the same extent in perfused livers and in live rats. During the first hour of perfusion, and when hepatic synthesis was active, newly synthesized cholesterol accounted for about 10% of biliary cholesterol and newly synthesized lecithin for 3% of biliary lecithin. Fasting reduced the contribution of newly synthesized cholesterol in bile to less than 1% but did not change the rate of biliary cholesterol secretion. After 2 hours of perfusion, newly synthesized biliary cholesterol accounted for only 4% of total hepatic sterol synthesis. Biliary lecithin, synthesized hepatic lecithin. We conclude that new synthesis makes only a small contribution to biliary cholesterol and lecithin secretion, and that, in the absence of perfusate lipids, both biliary cholesterol and lecithin must be predominantly mobilized from a preformed hepatic pool.
在灌注无脂培养基的离体大鼠肝脏中,评估了从头合成对胆汁中胆固醇和卵磷脂分泌的贡献。分别通过掺入氚水和[14C] - 胆碱来测量胆固醇和卵磷脂的合成。牛磺胆酸盐在灌注肝脏和活体大鼠中刺激胆汁脂质分泌的程度相同。在灌注的第一小时内,当肝脏合成活跃时,新合成的胆固醇约占胆汁胆固醇的10%,新合成的卵磷脂占胆汁卵磷脂的3%。禁食使胆汁中新合成胆固醇的贡献降至不到1%,但并未改变胆汁胆固醇的分泌速率。灌注2小时后,新合成的胆汁胆固醇仅占肝脏总固醇合成的4%;胆汁卵磷脂由肝脏合成。我们得出结论,新合成对胆汁胆固醇和卵磷脂分泌的贡献很小,并且在没有灌注脂质的情况下,胆汁中的胆固醇和卵磷脂都必须主要从预先形成的肝脏池中动员出来。