Ginsenoside Rb1 promotes browning through regulation of PPARγ in 3T3-L1 adipocytes

Biochem Biophys Res Commun. 2015 Oct 23;466(3):530-5. doi: 10.1016/j.bbrc.2015.09.064. Epub 2015 Sep 14.


Browning of white adipocyte tissue (WAT) has received considerable attention due to its potential implication in preventing obesity and related comorbidities. Ginsenoside Rb1 is reported to improve glycolipid metabolism and reduce body weight in obese animals. However whether the body reducing effect mediates by browning effect remains unclear. For this purpose, 3T3-L1 adipocytes were used to study the effect of ginsenoside Rb1 on browning adipocytes specific genes and oxygen consumptions. The results demonstrate that 10 μM of ginsenoside Rb1 increases basal glucose uptake and promoted browning evidenced by significant increases in mRNA expressions of UCP-1, PGC-1α and PRDM16 in 3T3-L1 mature adipocytes. Further, ginsenoside Rb1 also increases PPARγ activity. And the browning effect is abrogated by GW9692, a PPARγ antagonist. In addition, ginsenoside Rb1 increases basal respiration rate, ATP production and uncoupling capacity in 3T3-L1 adipocytes. Those effects are also blunted by GW9692. The results suggest that ginsenoside Rb1 promote browning of 3T3-L1 adipocytes through induction of PPARγ. Our finding offer a new source to discover browning agonists and also useful to understand and extend the applications of ginseng and its constituents.

Keywords: 3T3-L1 adipocytes; Browning; Ginsenoside Rb1; Mitochondrial respiration; PPARγ.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 3T3-L1 Cells
  • Adipocytes, Brown / cytology
  • Adipocytes, Brown / drug effects*
  • Adipocytes, Brown / metabolism*
  • Adipocytes, White / cytology
  • Adipocytes, White / drug effects*
  • Adipocytes, White / metabolism*
  • Anilides / pharmacology
  • Animals
  • Cell Differentiation
  • DNA-Binding Proteins / genetics
  • Energy Metabolism / drug effects
  • Ginsenosides / pharmacology*
  • Glucose / metabolism
  • Ion Channels / genetics
  • Mice
  • Mitochondrial Proteins / genetics
  • Oxygen Consumption / drug effects
  • PPAR gamma / agonists
  • PPAR gamma / antagonists & inhibitors
  • PPAR gamma / metabolism*
  • Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Transcription Factors / genetics
  • Uncoupling Protein 1


  • 2-chloro-5-nitrobenzanilide
  • Anilides
  • DNA-Binding Proteins
  • Ginsenosides
  • Ion Channels
  • Mitochondrial Proteins
  • PPAR gamma
  • Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
  • Ppargc1a protein, mouse
  • Prdm16 protein, mouse
  • RNA, Messenger
  • Transcription Factors
  • Ucp1 protein, mouse
  • Uncoupling Protein 1
  • ginsenoside Rb1
  • Glucose