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(−)‐Epigallocatechin gallate suppresses adipocyte differentiation through the MEK/ERK and PI3K/Akt pathways
Author(s) -
Kim Hyojung,
Sakamoto Kazuichi
Publication year - 2012
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1042/cbi20110047
Subject(s) - pi3k/akt/mtor pathway , mapk/erk pathway , protein kinase b , gallate , chemistry , adipocyte , microbiology and biotechnology , epigallocatechin gallate , biology , signal transduction , biochemistry , polyphenol , adipose tissue , antioxidant , nuclear chemistry
EGCG [(−)‐epigallocatechin gallate], tea catechin, is one of the compounds that has been reported to act against obesity and diabetes. To determine the effect of EGCG on adipocyte differentiation, we treated 3T3‐L1 preadipocytes with different catechins. Oil Red O staining showed significantly reduced intracellular lipid accumulation, especially with EGCG. Cell cycle analysis showed that EGCG inhibited cell proliferation by disturbing the cell cycle during the clonal expansion of 3T3‐L1. RT‐PCR (real‐time PCR) demonstrated that EGCG noticeably reduced mRNA expression of PPARα (peroxisome proliferator‐activated receptor α), C/EBPα (CCAAT/enhancer‐binding protein α) and FoxO1 (forkhead box class O1). EGCG also caused a significant decrease in the transcription of FoxO1 – the forkhead transcription factor class O1 involved in adipocyte differentiation – via the PI3K (phosphoinositide 3‐kinase)/Akt and MEK [MAPK (mitogen‐activated protein kinase)/ERK (extracellular‐signal‐regulated kinase) kinase] pathways. These results suggest that EGCG suppresses the clonal expansion of adipocytes by inactivating FoxO1 via insulin signalling and stress‐dependent MAPK pathways.