Synthesis and function of hepatic very-low-density lipoprotein
Synthesis and function of hepatic very-low-density lipoprotein
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DOI：
10.1042/bst0320059
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发表时间：
2004-02-01
影响因子：
3.9
通讯作者：
Hebbachi, AM
中科院分区：
文献类型：
--
作者：
Gibbons, GF;Wiggins, D;Hebbachi, AM
用于在肝细胞分泌器中组装极低密度脂蛋白（VLDL）的大多数三酰甘油（TAG）通过胞质TAG池的脂解，然后再酯化而动员。所涉及的脂肪酶包括芳基乙酰胺脱乙酰酶和/或三酰基甘油水解酶。一些脂解的再酯化产物获得富含载脂蛋白B的VLDL前体以形成成熟的VLDL。然而，有些在胰岛素刺激和微粒体三酰甘油转移蛋白（MTP）抑制的过程中返回到胞质池。磷脂还在涉及ADP-核糖基化因子-1（ARF-1）介导的磷脂酶D活化的过程中促进VLDL TAG。TAG在肝脏中的暂时储存，随后其作为VLDL动员和分泌，形成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。
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.