Hamilton R L, Guo L S, Felker T E, Chao Y S, Havel R J
J Lipid Res. 1986 Sep;27(9):967-78.
Uniformly fatty livers from orotic acid-fed rats secreted almost no very low density lipoproteins (VLDL) but normal amounts of nascent high density lipoproteins (HDL) accumulated in perfusates. When lecithin:cholesterol acyltransferase (LCAT) was inhibited, nascent HDL were uniformly discoidal and lacked cholesteryl esters. Lipid and apoprotein compositions of nascent HDL from normal and fatty livers were similar whether LCAT was inhibited or not. Apolipoprotein B-100 was not detected in perfusates of uniformly fatty livers, but small amounts of apolipoprotein B-48 were present in HDL2 fractions. Nascent lipoproteins were not seen in Golgi compartments, but lipid-rich particles were clearly evident in endoplasmic reticulum cisternae adjacent to the cis face of the Golgi complex, suggesting that orotic acid blocks VLDL secretion by preventing translocation of nascent particles from the endoplasmic reticulum to the cis Golgi compartment. The accumulation of normal amounts of discoidal HDL in liver perfusates despite virtual absence of triglyceride-rich lipoproteins in Golgi secretory compartments, the space of Disse, and the perfusate is inconsistent with the concept that nascent HDL are exclusively a product of surface remnants cast off during lipolysis of chylomicrons and VLDL.
用乳清酸喂养的大鼠的均匀脂肪肝几乎不分泌极低密度脂蛋白（VLDL），但灌流液中积累了正常量的新生高密度脂蛋白（HDL）。当卵磷脂胆固醇酰基转移酶（LCAT）被抑制时，新生HDL呈均匀的盘状且缺乏胆固醇酯。无论LCAT是否被抑制，正常肝脏和脂肪肝中新生HDL的脂质和载脂蛋白组成都相似。在均匀脂肪肝的灌流液中未检测到载脂蛋白B-100，但在HDL2组分中存在少量载脂蛋白B-48。在高尔基体区室中未见新生脂蛋白，但在高尔基体复合体顺面相邻的内质网池中有明显的富含脂质的颗粒，这表明乳清酸通过阻止新生颗粒从内质网转运至顺面高尔基体区室来阻断VLDL分泌。尽管在高尔基体分泌区室、狄氏间隙和灌流液中几乎不存在富含甘油三酯的脂蛋白，但肝脏灌流液中仍积累了正常量的盘状HDL，这与新生HDL完全是在乳糜微粒和VLDL脂解过程中脱落的表面残余物产物这一概念不一致。
