Ginsenoside-Rb 1 promotes adipogenesis through regulation of PPARγ and microRNA-27b

L. S. Chan, Patrick Y K YUE, T. W. Kok, M. H. Keung, Nai Ki MAK, Ricky N S WONG*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

22 Citations (Scopus)

Abstract

Ginsenoside-Rb 1 (Rb 1), one of the bioactive components in ginseng extract, is recently reported to be able to promote adipogenesis and peroxisome proliferator-activated receptor gamma (PPARγ) expression. Meanwhile, microRNA-27b (miR-27b) is also identified to regulate adipogenesis by targeting PPARγ2. In the present study, we attempted to link up the Rb 1-promoted adipogenesis with PPARγ binding and miR-27b regulation. First, we demonstrated that GW9662, an antagonist of PPARγ, could block Rb 1-induced 3T3-L1 differentiation with little toxicity towards cell proliferation. Then, expression levels for both of miR-27b and its primary transcript, pri-mir-27b, were found to decrease upon Rb 1 treatment. Again, GW9662 could attenuate the inhibitory effect of Rb 1 on both miR-27 and pri-mir-27b expression. Since Rb 1 was demonstrated to have binding activity towards PPARγ, we thus speculate that Rb 1 may act though PPARγ to downregulate mir-27b gene transcription and mature miR-27b activity, which in turn promotes PPARγ expression and adipogenesis. Enhancement on adipogenesis of adipose tissues is expected to prevent lipotoxicty in nonadipose tissues. Our data may give a better illustration to explain the antidiabetic effect of Rb 1 and provide a hint on treatment of lipid related metabolic diseases in the future.

Original languageEnglish
Pages (from-to)819-824
Number of pages6
JournalHormone and Metabolic Research
Volume44
Issue number11
DOIs
Publication statusPublished - 2012

Scopus Subject Areas

  • Endocrinology, Diabetes and Metabolism
  • Biochemistry
  • Endocrinology
  • Clinical Biochemistry
  • Biochemistry, medical

User-Defined Keywords

  • 3T3-L1 adipocytes
  • adipogenesis
  • ginsensoside-Rb
  • miR-27b
  • PPARγ

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