Author: Labrie, Marilyne; Lalonde, Simon; Najyb, Ouafa; Thiery, Maxime; Daneault, Caroline; Des Rosiers, Chrisitne; Rassart, Eric; Mounier, Catherine
Title: Apolipoprotein D Transgenic Mice Develop Hepatic Steatosis through Activation of PPAR? and Fatty Acid Uptake Document date: 2015_6_17
ID: 0wtq1c15_49
Snippet: Another mechanism by which PPARγ may be implicated in hepatic lipid accumulation could be by the induction of LD formation and maturation [28] [29] [30] . In the present study, we demonstrated that the expression of Plin2, Cide A and C, three targets of PPARγ, was increased in H-apoD Tg mice. At the opposite, the expression of Cide B, which is not a PPARγ target, was unaltered. Listenburger et al [33] showed that Plin2 lowers the rate of TG tu.....
Document: Another mechanism by which PPARγ may be implicated in hepatic lipid accumulation could be by the induction of LD formation and maturation [28] [29] [30] . In the present study, we demonstrated that the expression of Plin2, Cide A and C, three targets of PPARγ, was increased in H-apoD Tg mice. At the opposite, the expression of Cide B, which is not a PPARγ target, was unaltered. Listenburger et al [33] showed that Plin2 lowers the rate of TG turnover in LD by reducing the association of ATGL with LD and therefore the hydrolysis of TG [61] while Cide A and C are implicated in the fusion of LD [62] [63] [64] [65] . This may explain the 5-fold increase in LDs' size observed in the liver of H-apoD Tg mice.
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