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

Authors
 Hyo Jung Kim  ;  Bo Kyung Yoon  ;  Hyounkyoung Park  ;  Jo Woon Seok  ;  Hyeonjin Choi  ;  Jung Hwan Yu  ;  Yoonjeong Choi  ;  Su Jin Song  ;  Ara Kim  ;  Jae-woo Kim 
Citation
 BMB Reports, Vol.49(2) : 111-115, 2016 
Journal Title
 BMB Reports 
ISSN
 1976-6696 
Issue Date
2016
MeSH
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*
Keywords
Adipogenesis ; AKT ; Caffeine ; Glycogen synthase kinase ; Mitotic clonal expansion
Abstract
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].
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DOI
10.5483/BMBRep.2016.49.2.128
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Biochemistry and Molecular Biology (생화학-분자생물학교실) > 1. Journal Papers
Yonsei Authors
김재우(Kim, Jae Woo) ORCID logo https://orcid.org/0000-0001-5456-9495
김효정(Kim, Hyo Jung) ORCID logo https://orcid.org/0000-0002-3514-1247
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URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/146603
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