title: (-)-Epigallocatechin-3-gallate blocks 3T3-L1 adipose conversion by inhibition of cell proliferation and suppression of adipose phenotype expression.
abstract: OBJECTIVE
  A major objective in the treatment of obese individuals is the development of agents that reduce body fat and improve metabolic homeostasis. Among a variety of biological effects, green tea exerts an anti-obesity effect; however, the mechanisms behind its activity on adipose tissue are uncertain. Tea contains high levels of (-)-epigallocatechin-3-gallate (EGCG), which is one of its main bioactive substances. Therefore, we studied the effects of EGCG on mouse embryonic fibroblast-adipose like cell line (3T3-L1) preadipocyte proliferation and differentiation.
  
  
  METHODS
  3T3-L1 cells were incubated with physiologically attainable (0.1-1 μM) and pharmacological (5μM, 10μM) concentrations of EGCG for various lengths of time. Cell proliferation was assessed by cell counting and cell cycle analysis. Adipose conversion was evaluated by lipid accumulation and expression of CCAAT/enhancer binding protein alpha (C/EBPα) and peroxisome proliferator-activated receptor gamma (PPARγ) transcription factors.
  
  
  RESULTS
  A dose dependent suppressive effect on preadipocyte proliferation was observed, with the highest reduction in cell number at 10μM EGCG. On the other hand, adipose conversion was fully inhibited with 10μM EGCG. Flow-cytometric analysis showed that 3T3-L1 cells treated with EGCG underwent an arrest of cell cycle at G2/M. The inhibition of the expression of C/EBPα and PPARγ was accompanied by the inhibitory effect of EGCG. Microscopic observation showed that 3T3-L1 cells treated with EGCG maintained the fibroblastic shape and failed to accumulate cytoplasmic fat droplets even after the induction of differentiation.
  
  
  CONCLUSIONS
  Our results suggest that EGCG reduces adipogenesis through an arrest of cell cycle and a blockage of adipose phenotype expression. These results also suggest that the anti-obesity activity of green tea may be partially attributed to its suppressive effects in adipogenesis.
authors: Department of Pharmacology & Pharmacy, The University of Hong Kong, Hong Kong SAR.
authors: Cheuk Ying
authors: CY
authors: Chan
authors: Lai
authors: L
authors: Wei
authors: Federico
authors: F
authors: Castro-Muñozledo
authors: Wing Leung
authors: WL
authors: Koo
mesh_terms: D041721:3T3-L1 Cells; D017667:Adipocytes / Q000187:drug effects; D000273:Adipose Tissue / Q000166:cytology / Q000187:drug effects*; D000818:Animals; D016588:Anticarcinogenic Agents / Q000494:pharmacology*; D001391:Azo Compounds; D015153:Blotting, Western; D022763:CCAAT-Enhancer-Binding Protein-alpha / Q000096:biosynthesis; D002392:Catechin / Q000031:analogs & derivatives* / Q000494:pharmacology; D002452:Cell Count; D002453:Cell Cycle / Q000187:drug effects; D002454:Cell Differentiation / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects; D004396:Coloring Agents; D004305:Dose-Response Relationship, Drug; D005434:Flow Cytometry; D051379:Mice; D047495:PPAR gamma / Q000037:antagonists & inhibitors / Q000096:biosynthesis; D010641:Phenotype; D060888:Real-Time Polymerase Chain Reaction; D015398:Signal Transduction / Q000187:drug effects
chemical_list: D016588:Anticarcinogenic Agents; D001391:Azo Compounds; D022763:CCAAT-Enhancer-Binding Protein-alpha; D004396:Coloring Agents; D047495:PPAR gamma; D002392:Catechin; C045651:epigallocatechin gallate; C011049:oil red O