The dipeptide H-Trp-Arg-OH (WR) Is a PPARα agonist and reduces hepatic lipid accumulation in lipid-loaded H4IIE cells

Appl Biochem Biotechnol. 2015 Jan;175(2):1211-20. doi: 10.1007/s12010-014-1302-7. Epub 2014 Nov 7.

Abstract

Dipeptides absorbed by the intestinal epithelium are delivered to circulation, but their metabolic roles are not yet clearly understood. We investigated the biological activities of a dietary dipeptide, H-Trp-Arg-OH (WR), on the regulation of peroxisome proliferator-activated receptor (PPAR) α activity. Reporter gene assays revealed that WR dose-dependently induced PPARα transactivation. Surface plasmon resonance experiments demonstrated that WR interacts directly with the PPARα ligand binding domain, and time-resolved fluorescence energy transfer analyses revealed recruitment of a co-activator peptide, fluorescein-PGC1α, to PPARα, confirming the direct binding of WR to PPARα and occurrence of conformational changes. WR induced cellular fatty acid uptake and the expression of PPARα response genes in fatty acid oxidation, thus reducing intracellular triglyceride accumulation in lipid-loaded hepatocytes. In conclusion, the dietary dipeptide WR activates PPARα and reduces hepatic lipid accumulation in lipid-loaded hepatocytes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Biological Transport / drug effects
  • Cell Line
  • Dipeptides / pharmacology*
  • Fatty Acids / metabolism
  • Gene Expression Regulation / genetics
  • Hepatocytes / drug effects*
  • Hepatocytes / metabolism*
  • Humans
  • Hypolipidemic Agents / pharmacology*
  • Kinetics
  • Ligands
  • Lipid Metabolism / drug effects*
  • PPAR alpha / agonists*
  • PPAR alpha / genetics
  • Rats

Substances

  • Dipeptides
  • Fatty Acids
  • Hypolipidemic Agents
  • Ligands
  • PPAR alpha