Luteolin inhibits adipogenic differentiation by regulating PPARgamma activation

Biofactors. 2009 Jul-Aug;35(4):373-9. doi: 10.1002/biof.38.

Abstract

Luteolin (3',4',5,7-tetrahydroxyflavone), a flavonoid, has been known to possess antimutagenic, antitumorigenic, antioxidant, and anti-inflammatory properties. In this study, we investigated the role of luteolin in the regulation of adipogenic differentiation in 3T3-L1 preadipocytes. Luteolin inhibited intracellular triglyceride accumulation in a dose-dependent manner without cytotoxicity. Western blot and reverse transcription-polymerase chain reaction analyses showed that this inhibition was accompanied by attenuated expression of the adipogenic transcription factors: peroxisome proliferator-activated receptor gamma (PPARgamma) and CCAAT/enhancer-binding protein alpha. Luteolin inhibited the PPARgamma transactivation stimulated by rosiglitazone, a synthetic agonist, in COS-7 cells and inhibited rosiglitazone-induced adipogenic differentiation in 3T3-L1 cells. These data suggest that luteolin exerts antiadipogenic effects by suppressing adipogenic transcription factors and by inhibiting the transactivation of PPARgamma.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3T3-L1 Cells
  • Adipocytes / drug effects
  • Animals
  • CCAAT-Enhancer-Binding Protein-alpha / biosynthesis
  • COS Cells
  • Cell Differentiation / drug effects*
  • Chlorocebus aethiops
  • Luteolin / pharmacology*
  • Mice
  • PPAR gamma / drug effects
  • PPAR gamma / metabolism*
  • Rosiglitazone
  • Thiazolidinediones / antagonists & inhibitors

Substances

  • CCAAT-Enhancer-Binding Protein-alpha
  • PPAR gamma
  • Thiazolidinediones
  • Rosiglitazone
  • Luteolin