Havel R J
Cardiovascular Research Institute, University of California, San Francisco, USA.
Curr Opin Lipidol. 1995 Oct;6(5):312-6. doi: 10.1097/00041433-199510000-00011.
Recent studies support a sequential model for hepatic processing and catabolism of chylomicron remnants. Removal of chylomicron remnants by the liver involves interaction with several macromolecules on the cell surface, including the LDL receptor and heparan-sulfate-bound hepatic lipase and apolipoprotein E. Endocytosis of chylomicron remnants into hepatocytes is mediated by apolipoprotein E and normally occurs through the LDL receptor. Interaction of chylomicron remnants with the LDL receptor-related protein, or another endocytic receptor with similar properties, occurs slowly, requiring modification of surface-bound chylomicron remnants, and serves as a backup mechanism that is utilized primarily when LDL receptors are deficient or down-regulated.
近期研究支持乳糜微粒残粒肝脏加工和分解代谢的顺序模型。肝脏清除乳糜微粒残粒涉及与细胞表面几种大分子的相互作用,包括低密度脂蛋白受体、硫酸乙酰肝素结合的肝脂酶和载脂蛋白E。乳糜微粒残粒被肝细胞内吞是由载脂蛋白E介导的,通常通过低密度脂蛋白受体发生。乳糜微粒残粒与低密度脂蛋白受体相关蛋白或具有类似性质的另一种内吞受体的相互作用发生缓慢,需要对表面结合的乳糜微粒残粒进行修饰,并且作为一种备用机制,主要在低密度脂蛋白受体缺乏或下调时发挥作用。