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Type II nuclear hormone receptors, coactivator, and target gene repression in adipose tissue in the acute-phase

Biao Lu1, Arthur H Moser, Judy K Shigenaga

  • 1Metabolism Section, Department of Veterans Affairs Medical Center, University of California San Francisco, San Francisco, CA 94121, USA.

Journal of Lipid Research
|July 19, 2006
PubMed

Insights

The acute-phase response (APR) suppresses key nuclear hormone receptors and coactivators in adipose tissue. This downregulation of lipid metabolism pathways may redirect lipids to vital organs during inflammation.

Area of Science:

  • Metabolic regulation
  • Molecular endocrinology
  • Inflammation and immunity

Background:

  • The acute-phase response (APR) alters lipid metabolism and suppresses type II nuclear hormone receptors in several organs.
  • The role of APR in adipose tissue's lipid metabolism regulation remains less understood.

Purpose of the Study:

  • To investigate the impact of the APR on nuclear hormone receptors and their coactivators in adipose tissue.
  • To elucidate the mechanisms by which APR affects lipid and carbohydrate metabolism in adipocytes.

Main Methods:

  • In vivo studies using mice treated with lipopolysaccharide (LPS) to induce APR.
  • In vitro studies using 3T3-L1 adipocytes treated with tumor necrosis factor-alpha (TNF-alpha).
  • Quantitative mRNA analysis of nuclear receptors, coactivators, and target genes; assessment of transcriptional activity.

Main Results:

  • LPS treatment in mice caused a significant decrease in mRNA levels of multiple nuclear hormone receptors (e.g., PPARgamma, LXRs, RXRs) and coactivators (e.g., SRC1, PGC1alpha) in adipose tissue.
  • Expression of key genes involved in triglyceride and carbohydrate metabolism, including PPARgamma-regulated TG synthetic enzymes, was reduced during APR.
  • TNF-alpha treatment in 3T3-L1 adipocytes mimicked these effects, reducing receptor and coactivator expression and impairing transcriptional activity.

Conclusions:

  • The APR significantly suppresses the expression of nuclear hormone receptors and coactivators in adipose tissue.
  • This suppression leads to downregulation of triglyceride biosynthesis and alters carbohydrate metabolism.
  • These changes likely represent a coordinated metabolic adaptation to redirect lipids to essential organs during inflammatory states.

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