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Acylcarnitines activate proinflammatory signaling pathways.

Jennifer M Rutkowsky1, Trina A Knotts2, Kikumi D Ono-Moore3

  • 1Department of Anatomy, Physiology and Cell Biology, School of Veterinary Medicine, University of California, Davis, California;

American Journal of Physiology. Endocrinology and Metabolism
|April 25, 2014
PubMed
Summary
This summary is machine-generated.

Acylcarnitines, by-products of incomplete fatty acid breakdown, can activate inflammatory pathways. This suggests a link between metabolic dysfunction in type 2 diabetes and inflammation, though specific targets require further research.

Keywords:
TLRacylcarnitineinflammationpattern recognition receptorsβ-oxidation

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Area of Science:

  • Metabolic Biochemistry
  • Immunology
  • Cellular Signaling

Background:

  • Incomplete fatty acid β-oxidation is linked to insulin resistance and type 2 diabetes mellitus (T2DM).
  • Elevated plasma acylcarnitines are observed in T2DM and insulin resistance.
  • Previous work indicated potential pro-inflammatory activation by acylcarnitines.

Purpose of the Study:

  • To investigate if physiologically relevant L-acylcarnitines activate classical pro-inflammatory signaling pathways.
  • To determine the involvement of pattern recognition receptor (PRR)-associated pathways in acylcarnitine-induced inflammation.

Main Methods:

  • Assessed cyclooxygenase-2 expression in RAW 264.7 cells.
  • Measured pro-inflammatory cytokine expression and secretion using L-C14 carnitine.
  • Analyzed phosphorylation of JNK and ERK signaling pathways.
  • Utilized MyD88 knockdown to assess PRR pathway involvement.
  • Examined IL-8 secretion in human epithelial cells (HCT-116) lacking TLR2 and TLR4.

Main Results:

  • Acylcarnitines induced cyclooxygenase-2 expression in a chain length-dependent manner.
  • L-C14 carnitine dose-dependently stimulated pro-inflammatory cytokine expression and secretion.
  • L-C14 carnitine induced JNK and ERK phosphorylation.
  • MyD88 knockdown partially inhibited acylcarnitine's pro-inflammatory effects.
  • L-C14 carnitine induced IL-8 secretion in TLR-deficient cells, suggesting PRR-independent mechanisms.

Conclusions:

  • L-acylcarnitines possess the potential to activate inflammatory signaling pathways.
  • While PRR signaling may be involved, acylcarnitines can also promote inflammation through PRR-independent routes.
  • The precise molecular and tissue targets mediating acylcarnitine-induced inflammation remain to be elucidated.