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KMID : 0624620160490020111
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BMB Reports
2016 Volume.49 No. 2 p.111 ~ p.115
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Caffeine inhibits adipogenesis through modulation of mitotic clonal expansion and the AKT/GSK3 pathway in 3T3-L1 adipocytes
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Kim Hyo-Jung
Yoon Bo-Kyung
Park Hyoun-Kyoung
Seok Jo-Woon
Choi Hyeon-Jin
Yu Jung-Hwan
Choi Yoon-Jeong
Song Su-Jin
Kim A-Ra
Kim Jae-Woo
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Abstract
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Caffeine has been proposed to have several beneficial effects on obesity and its related metabolic diseases; however, how caffeine affects adipocyte differentiation has not been elucidated. In this study, we demonstrated that caffeine suppressed 3T3-L1 adipocyte differentiation and inhibited the expression of CCAAT/enhancer binding protein (C/EBP)α and peroxisome proliferator-activated receptor (PPAR)γ, two main adipogenic transcription factors. Anti-adipogenic markers, such as preadipocyte secreted factor (Pref)-1 and Kr?ppel-like factor 2, remained to be expressed in the presence of caffeine. Furthermore, 3T3-L1 cells failed to undergo typical mitotic clonal expansion in the presence of caffeine. Investigation of hormonal signaling revealed that caffeine inhibited the activation of AKT and glycogen synthase kinase (GSK) 3 in a dose-dependent manner, but not extracellular signal-regulated kinase (ERK). Our data show that caffeine is an anti-adipogenic bioactive compound involved in the modulation of mitotic clonal expansion during adipocyte differentiation through the AKT/GSK3 pathway.
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KEYWORD
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Adipogenesis, AKT, Caffeine, Glycogen synthase kinase, Mitotic clonal expansion
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