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A more recent version of this article appeared on May 1, 2005

Papers In Press, published online ahead of print February 16, 2005
J. Lipid Res., doi:10.1194/jlr.M500003-JLR200
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Submitted on January 4, 2005
Revised on February 2, 2005
Accepted on February 6, 2005

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

Patricia Aspichueta, Silvia Pérez, Begoña Ochoa, and Olatz Fresnedo

Department of Physiology, University of the Basque Country Medical School, Leioa, Vizcaya 48940

Corresponding Author: ofpocolb{at}lg.ehu.es

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 and perivenous hepatocytes were isolated from fasted lipopolysaccharide-treated, fasted, and fed rats. They were used to asses their capacity to release VLDL apoB and lipid classes in relation to de novo lipid synthesis and the expression of crucial genes to VLDL production. Despite the common superior ability of periportal 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 periportal hepatocytes; this was accompanied by a preferential periportal rise 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 periportal and perivenous hepatocytes exhibited similar capabilities for VLDL formation/secretion in normal conditions; however, the endotoxic pressure did zonate periportally.


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This article has been cited by other articles:


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N. Bartolome, B. Arteta, M. J. Martinez, Y. Chico, and B. Ochoa
Kupffer cell products and interleukin 1? directly promote VLDL secretion and apoB mRNA up-regulation in rodent hepatocytes
Innate Immunity, August 1, 2008; 14(4): 255 - 266.
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 Innate ImmunityHome page
P. Aspichueta, B. Perez-Agote, S. Perez, B. Ochoa, and O. Fresnedo
Impaired response of VLDL lipid and apoB secretion to endotoxin in the fasted rat liver
Innate Immunity, June 1, 2006; 12(3): 181 - 191.
[Abstract] [PDF]


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