Apolipoprotein D Transgenic Mice Develop Hepatic Steatosis through Activation of PPAR? and Fatty Acid Uptake

Labrie, Marilyne; Lalonde, Simon; Najyb, Ouafa; Thiery, Maxime; Daneault, Caroline; Des Rosiers, Chrisitne; Rassart, Eric; Mounier, Catherine

We then measured the expression level of key proteins known to be involved in LD formation. The expression of the PPARγ target gene Plin2 [51] was increased by 1.98-fold in Tg mice (Fig 2A) . Similar observations were made regarding Cide A and Cide C (1.47 and 1.45-fold respectively), two other targets of PPARγ that are implicated in LD fusion [52] (Fig 2B and 2D) . A well-documented independent gene of PPARγ regulation, Cide B remained unchanged ( Fig 2C) . Conversely, the expression of genes coding for several lipases (adipose triglyceride lipase (ATGL), hormone sensitive lipase (HSL) and monoglyceride lipase (MGL)) as well as for the ATGL coactivator comparative gene identification 58 (CGI-58) remained identical (data not shown). Consistently with an elevated expression of proteins involved in hepatic LD formation and fusion, we found that the size of the hepatic LD in H-apoD Tg mice was drastically increased (5.45-fold) compared to WT. However, we did not detect a significant modification in the number of LD between the Tg and WT mice suggesting that the observed phenomenon was a result of both LD fusion and formation of new LD (Fig 2E) . Hepatic FFA uptake