Journal
BMB REPORTS
Volume 49, Issue 2, Pages 111-115Publisher
KOREAN SOCIETY BIOCHEMISTRY & MOLECULAR BIOLOGY
DOI: 10.5483/BMBRep.2016.49.2.128
Keywords
Adipogenesis; AKT; Caffeine; Glycogen synthase kinase; Mitotic clonal expansion
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Funding
- National Research Foundation of Korea (NRF) [2011-0030086, 2015R1A2A2A01004345, 2013R1A1A1059527]
- Korea government, Ministry of Science, ICT and Future Planning (MSIP)
- National Research Foundation of Korea [2013R1A1A1059527, 2015R1A2A2A01004345, 2011-0030086] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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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). and peroxisome proliferator-activated receptor (PPAR)., two main adipogenic transcription factors. Anti-adipogenic markers, such as preadipocyte secreted factor (Pref)-1 and Kruppel-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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