Abstract:
BACKGROUND & AIMS:It is widely recognized that in the early stages of liver regeneration after partial hepatectomy, the hepatocytes accumulate a significant amount of lipids. The functional meaning of this transient steatosis and its effect on hepatocellular proliferation are not well defined. In addition, the basic mechanisms of this lipid accumulation are not well understood although some studies suggest the participation of the Low Density Lipoprotein Receptor (Ldlr). METHODS:To address these questions, we studied the process of liver regeneration in Ldlr null mice and wild type mice following partial hepatectomy. RESULTS:Ldlr deficiency was associated with a significant decrease in serum albumin concentration, during early stages of liver regeneration, and a delayed hepatic regeneration. Remnant livers of Ldlr(-)(/)(-) showed a time-shifted expression of interleukin-6 (IL6) and a defective activation of tumor necrosis factor-α (TNFα) and hepatocyte growth factor (HGF) expression in early phases of liver regeneration. Unexpectedly, Ldlr(-)(/)(-) showed no significant differences in the content of lipid droplets after partial hepatectomy compared to wild type mice. However, lipidomic analysis of the regenerating liver from Ldlr(-)(/)(-) revealed a lipid profile compatible with liver quiescence: high content of cholesterol esters and ceramide, and low levels of phosphatidylcholine. CONCLUSIONS:Ldlr deficiency is associated with significant changes in the hepatic lipidome that affect cytokine-growth factor signaling and impair liver regeneration. These results suggest that the analysis of the hepatic lipidome may help predict the success of liver regeneration in the clinical environment, specifically in the context of pre-existing liver steatosis.
journal_name
J Hepatoljournal_title
Journal of hepatologyauthors
Pauta M,Rotllan N,Vales F,Fernandez-Hernando A,Allen RM,Ford DA,Marí M,Jiménez W,Baldán A,Morales-Ruiz M,Fernández-Hernando Cdoi
10.1016/j.jhep.2013.05.026subject
Has Abstractpub_date
2013-10-01 00:00:00pages
731-7issue
4eissn
0168-8278issn
1600-0641pii
S0168-8278(13)00358-9journal_volume
59pub_type
杂志文章abstract:BACKGROUND/AIMS:The chemokine receptor CX3CR1 and its specific ligand fractalkine (CX3CL1) are known to modulate inflammatory and fibroproliferative diseases. Here we investigate the role of CX3CR1/fractalkine in HCV-induced liver fibrosis. METHODS:A genotype analysis of CX3CR1 variants was performed in 211 HCV-infect...
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