Caffeine inhibits adipogenesis through modulation of mitotic clonal expansion and the AKT/GSK3 pathway in 3T3-L1 adipocytes
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 exp...
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| Published in | BMB reports Vol. 49; no. 2; pp. 111 - 115 |
|---|---|
| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Korea (South)
Korean Society for Biochemistry and Molecular Biology
01.02.2016
생화학분자생물학회 |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1976-6696 1976-670X |
| DOI | 10.5483/BMBRep.2016.49.2.128 |
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| 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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| AbstractList | 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 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. KCI Citation Count: 19 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] |
| Author | Choi, Hyeonjin Seok, Jo Woon Park, Hyounkyoung Yu, Jung Hwan Kim, Jae-woo Kim, Hyo Jung Song, Su Jin Choi, Yoonjeong Yoon, Bo Kyung Kim, Ara |
| AuthorAffiliation | 3 Brain Korea 21 PLUS Project for Medical Science, Yonsei University 2 Yonsei University College of Medicine 1 Department of Biochemistry and Molecular Biology, Integrated Genomic Research Center for Metabolic Regulation, Institute of Genetic Science, Yonsei University College of Medicine 4 Severance Biomedical Science Institute, Yonsei University College of Medicine, Seoul 03722, Korea |
| AuthorAffiliation_xml | – name: 1 Department of Biochemistry and Molecular Biology, Integrated Genomic Research Center for Metabolic Regulation, Institute of Genetic Science, Yonsei University College of Medicine – name: 3 Brain Korea 21 PLUS Project for Medical Science, Yonsei University – name: 4 Severance Biomedical Science Institute, Yonsei University College of Medicine, Seoul 03722, Korea – name: 2 Yonsei University College of Medicine |
| Author_xml | – sequence: 1 givenname: Hyo Jung surname: Kim fullname: Kim, Hyo Jung – sequence: 2 givenname: Bo Kyung surname: Yoon fullname: Yoon, Bo Kyung – sequence: 3 givenname: Hyounkyoung surname: Park fullname: Park, Hyounkyoung – sequence: 4 givenname: Jo Woon surname: Seok fullname: Seok, Jo Woon – sequence: 5 givenname: Hyeonjin surname: Choi fullname: Choi, Hyeonjin – sequence: 6 givenname: Jung Hwan surname: Yu fullname: Yu, Jung Hwan – sequence: 7 givenname: Yoonjeong surname: Choi fullname: Choi, Yoonjeong – sequence: 8 givenname: Su Jin surname: Song fullname: Song, Su Jin – sequence: 9 givenname: Ara surname: Kim fullname: Kim, Ara – sequence: 10 givenname: Jae-woo surname: Kim fullname: Kim, Jae-woo |
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| SubjectTerms | 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 |
| Title | Caffeine inhibits adipogenesis through modulation of mitotic clonal expansion and the AKT/GSK3 pathway in 3T3-L1 adipocytes |
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