Caffeine inhibits adipogenesis through modulation of mitotic clonal expansion and the AKT/GSK3 pathway in 3T3-L1 adipocytes

• Published in: BMB reports Vol. 49; no. 2; pp. 111 - 115
• Main Authors: Kim, Hyo Jung, Yoon, Bo Kyung, Park, Hyounkyoung, Seok, Jo Woon, Choi, Hyeonjin, Yu, Jung Hwan, Choi, Yoonjeong, Song, Su Jin, Kim, Ara, Kim, Jae-woo
• Format: Journal Article
• Language: English
• Published: Korea (South) Korean Society for Biochemistry and Molecular Biology 01.02.2016; 생화학분자생물학회
• Subjects: 3T3-L1 Cells; Adipocytes - cytology; Adipocytes - drug effects; Adipocytes - metabolism; Adipogenesis - drug effects; Animals; Caffeine - pharmacology; Cell Differentiation - drug effects; Cell Differentiation - genetics; Clone Cells; Gene Expression Regulation - drug effects; Glycogen Synthase Kinase 3 - metabolism; Glycogen Synthase Kinase 3 beta; Mice; Mitosis - drug effects; Proto-Oncogene Proteins c-akt - metabolism; Signal Transduction - drug effects; 화학
• ISSN: 1976-6696; 1976-670X
• DOI: 10.5483/BMBRep.2016.49.2.128

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 Krüppel-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. [BMB Reports 2016; 49(2): 111-115].