Selected article for: "aa apod preferential ligand and aa concentration"

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_46
    Snippet: Our in vitro studies strongly suggest that apoD acts as an AA transporter, leading to the activation of PPARγ. AA is the preferential ligand of apoD [3] and a precursor for prostaglandins which are also natural PPARγ activators [22, 23] . We showed that activation of PPARγ by AA in HepG2 cells is significantly potentiated by apoD. In agreement with our study, Thomas et al. [56] demonstrated in cultured embryonic kidney (HEK) 293T cells that ap.....
    Document: Our in vitro studies strongly suggest that apoD acts as an AA transporter, leading to the activation of PPARγ. AA is the preferential ligand of apoD [3] and a precursor for prostaglandins which are also natural PPARγ activators [22, 23] . We showed that activation of PPARγ by AA in HepG2 cells is significantly potentiated by apoD. In agreement with our study, Thomas et al. [56] demonstrated in cultured embryonic kidney (HEK) 293T cells that apoD stabilizes AA at the plasma membrane and inhibits the release of AA in the extracellular media. Here, we show that plasmatic AA is decreased in H-apoD Tg compared to WT mice while hepatic concentration is enriched. Interestingly, increased hepatic concentration of AA has been associated with fatty liver [57] as observed in H-apoD Tg mice.

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