Nilsson A, Landin B, Johansson B
Department of Internal Medicine, University Hospital of Lund, Sweden.
Biochim Biophys Acta. 1988 Nov 25;963(2):231-6. doi: 10.1016/0005-2760(88)90285-8.
A large part of the circulating apolipoprotein A-I (apoA-I) is produced by the intestine. Yet the plasma levels of apoA-I are retained or even increased in rats with thoracic duct drainage (Johansson, B. and Nilsson, A, (1981) FEBS Lett. 130, 305-308 and Franzén, J. et al. (1987) Biochim. Biophys. Acta 918, 11-15). In this study we examined the effects of biliary drainage and of combined biliary and lymphatic drainage on the plasma apoA-I levels, and also the effects of lymphatic drainage on the output of biliary lipids in the rat. 63 h of biliary drainage caused a 40% decrease of the serum apoA-I concentration. In contrast the concentration in rats with combined thoracic duct and biliary drainage was 153% of that in control rats. The biliary secretion of bile acids, phosphatidylcholine and cholesterol declined to a lower level in rats with combined thoracic duct and biliary drainage, but increased at the later time intervals to the same levels as in rats with bile fistulas only. Intravenous chyle infusion 3-36 h after commencing the biliary drainage did not prevent the decrease in biliary lipid output. The study thus provided no evidence that the reduced hepatic inflow of apoB-containing lipoproteins during biliary drainage is of importance for the reduced biliary lipid output. The loss of all the chyle lipoproteins leads, however, to an even more pronounced decrease in the biliary lipid secretion. The drainage of all the chyle constituents also leads to an increased apoA-I synthesis that more than compensates for the apoA-I loss in chyle, whereas biliary drainage only lowers the plasma apoA-I levels.
循环中的载脂蛋白A-I（apoA-I）很大一部分是由肠道产生的。然而，在胸导管引流的大鼠中，apoA-I的血浆水平保持不变甚至升高（约翰松，B.和尼尔森，A，（1981年）《欧洲生物化学会联合会快报》130，305 - 308以及弗兰岑，J.等人（1987年）《生物化学与生物物理学报》918，11 - 15）。在本研究中，我们研究了胆汁引流以及胆汁和淋巴联合引流对大鼠血浆apoA-I水平的影响，还研究了淋巴引流对大鼠胆汁脂质输出的影响。63小时的胆汁引流导致血清apoA-I浓度降低40%。相比之下，胸导管和胆汁联合引流的大鼠中该浓度是对照大鼠的153%。在胸导管和胆汁联合引流的大鼠中，胆汁酸、磷脂酰胆碱和胆固醇的胆汁分泌下降到较低水平，但在随后的时间间隔内增加到与仅患有胆瘘的大鼠相同的水平。在开始胆汁引流3 - 36小时后静脉输注乳糜并不能阻止胆汁脂质输出的减少。因此，该研究没有提供证据表明胆汁引流期间含apoB脂蛋白的肝内流入减少对胆汁脂质输出减少具有重要意义。然而，所有乳糜脂蛋白的流失导致胆汁脂质分泌更明显的减少。所有乳糜成分的引流也导致apoA-I合成增加，这足以弥补乳糜中apoA-I的损失，而胆汁引流只会降低血浆apoA-I水平。
