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Triglycerides serve as crucial long-term energy storage molecules in microorganisms, providing a dense source of metabolic energy. Their breakdown is mediated by lipases, which hydrolyze triglycerides into glycerol and free fatty acids. Each of these components follows distinct metabolic pathways, ultimately contributing to ATP synthesis and cellular energy homeostasis.Glycerol MetabolismGlycerol, released from triglyceride hydrolysis, is phosphorylated by glycerol kinase to form...
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Quantitative Determination of De Novo Fatty Acid Synthesis in Brown Adipose Tissue Using Deuterium Oxide
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Inflammation Triggers Liver X Receptor-Dependent Lipogenesis.

Sophie R Liebergall1, Jerry Angdisen1, Shun Hang Chan1

  • 1Department of Pharmacology, University of Virginia School of Medicine, Charlottesville, Virginia, USA.

Molecular and Cellular Biology
|October 30, 2019
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Liver X receptors (LXRs) regulate cholesterol metabolism during inflammation. LXRs promote cholesterol synthesis in macrophages, aiding inflammation resolution and gene expression shutdown.

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Area of Science:

  • Immunology
  • Molecular Biology
  • Lipid Metabolism

Background:

  • Immune cell function is significantly influenced by lipid metabolism.
  • Inflammatory stimuli activate macrophages, altering their metabolic state.

Purpose of the Study:

  • To investigate the role of lipid metabolism, specifically cholesterol and fatty acid synthesis, in macrophage inflammatory responses.
  • To elucidate the function of liver X receptors (LXRs) in regulating lipogenesis and inflammation resolution.

Main Methods:

  • Macrophage activation via Toll-like receptors (TLRs) with proinflammatory stimuli.
  • Analysis of cholesterol and fatty acid synthesis pathways.
  • Investigation of liver X receptor (LXR) induction by type I interferons.
  • Assessment of LXR's role in cholesterol homeostasis and gene expression.

Main Results:

  • Cholesterol and fatty acid synthesis increase in macrophages 12-18 hours post-TLR activation.
  • Lipogenesis upregulation is dependent on LXR induction by type I interferons.
  • LXRs are essential for resuming cholesterol synthesis during inflammation, not just cholesterol efflux.
  • LXR activity is required for shutting down specific type I interferon-stimulated genes as inflammation resolves.

Conclusions:

  • Liver X receptors act as bidirectional regulators of cholesterol homeostasis, balancing efflux and synthesis.
  • LXRs play a critical role in the resolution of inflammation by modulating lipid metabolism and gene expression.
  • LXR-mediated regulation contributes to a negative-feedback loop for inflammatory responses.