Hummel L, Zimmermann T, Fischer H
Acta Biol Med Ger. 1982;41(10):961-5.
The study has been performed in order to obtain information on the mechanism responsible for the hypertriglyceridemia found in pregnant rats. The results show that the whole plasma triglyceride flux is increased by 65% in late gestation. It has been found that labeled VLDL triglyceride originating from pregnant rats shows no delay in plasma disappearance when injected into the circulation of non pregnant female rats. Contrariwise, labeled VLDL triglyceride originating from non pregnant rats when injected into pregnant rats shows a delay in disappearance from the circulation. From these results the conclusion can be drawn that the delay in labeled plasma triglyceride disappearance in late gestation is not caused by a possibly abnormal VLDL showing a decrease in affinity of lipoprotein substrate for lipoprotein lipase. Therefore, we interpret the delay in labeled plasma triglyceride disappearance in late gestation in terms of a lowered removal capacity of plasma triglyceride by extrahepatic tissue.
进行这项研究是为了获取有关孕鼠高甘油三酯血症发生机制的信息。结果显示，在妊娠后期，全血浆甘油三酯通量增加了65%。已发现，将源自孕鼠的标记极低密度脂蛋白（VLDL）甘油三酯注入未孕雌性大鼠的循环系统时，其在血浆中的消失并无延迟。相反，将源自未孕大鼠的标记VLDL甘油三酯注入孕鼠体内时，其从循环系统中的消失出现延迟。从这些结果可以得出结论，妊娠后期标记血浆甘油三酯消失延迟并非由可能异常的VLDL导致，即脂蛋白底物对脂蛋白脂肪酶的亲和力降低。因此，我们将妊娠后期标记血浆甘油三酯消失延迟解释为肝外组织对血浆甘油三酯的清除能力降低。
