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    Changes in LXR signaling influence early-pregnancy lipogenesis and protect against dysregulated fetoplacental lipid homeostasis.

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    Authors
    Nikolova, Vanya
    Papacleovoulou, Georgia
    Bellafante, Elena
    Borges Manna, Luiza
    Jansen, Eugene
    Baron, Silvère
    Abu-Hayyeh, Shadi
    Parker, Malcolm
    Williamson, Catherine
    Type
    Article
    Language
    en
    
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    Title
    Changes in LXR signaling influence early-pregnancy lipogenesis and protect against dysregulated fetoplacental lipid homeostasis.
    Published in
    Am J Physiol Endocrinol Metab 2017; 313(4):E463-72
    Publiekssamenvatting
    Human pregnancy is associated with enhanced de novo lipogenesis in the early stages followed by hyperlipidemia during advanced gestation. Liver X receptors (LXRs) are oxysterol-activated nuclear receptors that stimulate de novo lipogenesis and also promote the efflux of cholesterol from extrahepatic tissues followed by its transport back to the liver for biliary excretion. Although LXR is recognized as a master regulator of triglyceride and cholesterol homeostasis, it is unknown whether it facilitates the gestational adaptations in lipid metabolism. To address this question, biochemical profiling, protein quantification, and gene expression studies were used, and gestational metabolic changes in T0901317-treated wild-type mice and Lxrab-/- mutants were investigated. Here, we show that altered LXR signaling contributes to the enhanced lipogenesis in early pregnancy by increasing the expression of hepatic Fas and stearoyl-CoA desaturase 1 (Scd1). Both the pharmacological activation of LXR with T0901317 and the genetic ablation of its two isoforms disrupted the increase in hepatic fatty acid biosynthesis and the development of hypertriglyceridemia during early gestation. We also demonstrate that absence of LXR enhances maternal white adipose tissue lipolysis, causing abnormal accumulation of triglycerides, cholesterol, and free fatty acids in the fetal liver. Together, these data identify LXR as an important factor in early-pregnancy lipogenesis that is also necessary to protect against abnormalities in fetoplacental lipid homeostasis.
    DOI
    10.1152/ajpendo.00449.2016
    PMID
    28420650
    URI
    http://hdl.handle.net/10029/621221
    ae974a485f413a2113503eed53cd6c53
    10.1152/ajpendo.00449.2016
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