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母体乙醇摄入对胎鼠和新生鼠肝脏脂质生物合成的影响。

Effects of maternal ethanol consumption on hepatic lipid biosynthesis in foetal and neonatal rats.

作者信息

Rawat A K

出版信息

Biochem J. 1978 Jul 15;174(1):213-9. doi: 10.1042/bj1740213.

Abstract

Effects of prolonged maternal ethanol consumption were studied on hepatic lipid content, on the rates of fatty acid synthesis and on the activities of enzymes involved in fatty acid synthesis in the livers of foetal and suckling neonatal rats. Prolonged maternal ethanol consumption resulted in a significant increase in the contents of hepatic total lipids, triacylglycerols and plasma unesterified fatty acids in foetal and neonatal rats. Studies in vitro with 3H2O showed that maternal ethanol consumption did not result in a significant change in its rate of incorporation into lipid fractions of foetal and neonatal livers. The rates of fatty acid synthesis showed a pronounced decrease immediately after birth, compared with the foetal stage, but increased in the adult animals. On the other hand, the highest rates of lipid oxidation were observed in the neonatal stage. Maternal ethanol consumption resulted in a significant decrease in the rates of [14C]palmitate oxidation to 14CO2 by both the foetal and neonatal livers. Maternal ethanol consumption did not result in an increase in the activities of any of the lipid-synthesizing enzymes tested throughout the period of development. Although increased fatty acid synthesis does not seem to be the mechanism for the accumulation of these lipids, decreased oxidation of the lipids may be partly responsible for the lipid accumulation.

摘要

研究了母体长期摄入乙醇对胎鼠和乳鼠肝脏脂质含量、脂肪酸合成速率以及参与脂肪酸合成的酶活性的影响。母体长期摄入乙醇导致胎鼠和新生鼠肝脏中总脂质、三酰甘油含量以及血浆非酯化脂肪酸显著增加。用3H2O进行的体外研究表明,母体摄入乙醇并未导致其掺入胎鼠和新生鼠肝脏脂质组分的速率发生显著变化。与胎儿期相比,出生后脂肪酸合成速率立即显著下降,但在成年动物中有所增加。另一方面,在新生期观察到脂质氧化速率最高。母体摄入乙醇导致胎鼠和新生鼠肝脏将[14C]棕榈酸氧化为14CO2的速率显著降低。在整个发育期间,母体摄入乙醇并未导致所测试的任何脂质合成酶的活性增加。尽管脂肪酸合成增加似乎不是这些脂质积累的机制,但脂质氧化减少可能部分导致了脂质积累。

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本文引用的文献

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Lipid metabolism in the fetal and neonatal rabbit.
Metabolism. 1966 Sep;15(9):856-64. doi: 10.1016/0026-0495(66)90178-8.

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