Gibbons G F, Wiggins D, Brown A-M, Hebbachi A-M
Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Churchill Hospital, Oxford OX3 7LJ, UK.
Biochem Soc Trans. 2004 Feb;32(Pt 1):59-64. doi: 10.1042/bst0320059.
Most of the triacylglycerol (TAG) utilized for the assembly of very-low-density lipoprotein (VLDL) in the secretory apparatus of the hepatocyte is mobilized by lipolysis of the cytosolic TAG pool, followed by re-esterification. The lipases involved include arylacetamide deacetylase and/or triacylglycerol hydrolase. Some of the re-esterified products of lipolysis gain access to an apolipoprotein-B-rich VLDL precursor to form mature VLDL. Some, however, are returned to the cytosolic pool in a process that is stimulated by insulin and inhibited by microsomal triacylglycerol transfer protein (MTP). Phospholipids also contribute to VLDL TAG in a process which involves ADP-ribosylation factor-1 (ARF-1)-mediated activation of phospholipase D. The temporary storage of TAG in the liver, followed by its mobilization and secretion as VLDL, form part of a process by which the liver protects vulnerable body tissues from excess lipotoxic non-esterified ('free') fatty acids in the plasma.
肝细胞分泌装置中用于组装极低密度脂蛋白(VLDL)的大部分三酰甘油(TAG)通过胞质TAG池的脂解作用被动员起来,随后进行重新酯化。所涉及的脂肪酶包括芳基乙酰胺脱乙酰酶和/或三酰甘油水解酶。脂解的一些重新酯化产物进入富含载脂蛋白B的VLDL前体以形成成熟的VLDL。然而,一些产物在受胰岛素刺激且被微粒体三酰甘油转移蛋白(MTP)抑制的过程中返回胞质池。磷脂也通过涉及ADP - 核糖基化因子-1(ARF-1)介导的磷脂酶D激活的过程对VLDL TAG有贡献。TAG在肝脏中的临时储存,随后作为VLDL被动员和分泌,是肝脏保护脆弱身体组织免受血浆中过量脂毒性非酯化(“游离”)脂肪酸影响的过程的一部分。