Endotoxin promotes preferential periportal upregulation of VLDL secretion in the rat liver

极低密度脂蛋白 载脂蛋白B 微粒体甘油三酯转移蛋白 内分泌学 分泌物 内科学 脂肪生成 脂多糖 肝细胞 脂质代谢 体内 化学 甘油三酯 生物 脂蛋白 生物化学 体外 胆固醇 医学 生物技术
作者
Patricia Aspichueta,Silvia Rojí Pérez,Begoña Ochoa,Olatz Fresnedo
出处
期刊:Journal of Lipid Research [Elsevier]
卷期号:46 (5): 1017-1026 被引量:33
标识
DOI:10.1194/jlr.m500003-jlr200
摘要

Zonation affects liver parenchymal cell function and metabolism as well as nonparenchymal cell activation, but whether VLDL production is zonated has yet to be elucidated. Infection induces enhanced VLDL secretion by the liver. Ex vivo studies were undertaken to examine the liver heterogeneity for VLDL formation and secretion and their in vivo response to endotoxin. Highly pure periportal (PP) and perivenous (PV) hepatocytes were isolated from fasted lipopolysaccharide-treated, fasted, and fed rats. They were used to assess their capacity to release VLDL-apolipoprotein B (apoB) and lipid classes in relation to de novo lipid synthesis and the expression of genes crucial to VLDL production. Despite the common superior ability of PP hepatocytes for lipid release and zonal differences in lipid synthesis, zonated secretion of VLDL particles was observed in septic but not in normal fed or fasted livers. The endotoxin-induced apoB secretion was more accentuated in PP hepatocytes; this was accompanied by a preferential PP increase in apoB and microsomal triglyceride transfer protein mRNA levels, whereas lipogenesis indicators were, if anything, similarly modified in hepatocytes of either acinar origin. We conclude that PP and PV hepatocytes exhibited similar capabilities for VLDL formation/secretion in normal conditions; however, the endotoxic pressure did zonate periportally.

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