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Article: Effects of an AMP-activated protein kinase inhibitor, compound C, on adipogenic differentiation of 3T3-L1 cells

TitleEffects of an AMP-activated protein kinase inhibitor, compound C, on adipogenic differentiation of 3T3-L1 cells
Authors
Issue Date2008
PublisherPharmaceutical Society of Japan. The Journal's web site is located at http://bpb.pharm.or.jp/index.html
Citation
Biological And Pharmaceutical Bulletin, 2008, v. 31 n. 9, p. 1716-1722 How to Cite?
AbstractThe role of AMP-activated protein kinase (AMPK) in adipocyte differentiation is not completely understood. Here we reported that an AMPK inhibitor, compound C, significantly inhibited adipogenic differentiation of 3T3-L1 cells in a dose dependent manner, and this inhibitory effect was primarily effective in the initial stage of differentiation. Compound C prevented the mitotic clonal expansion (MCE) of preadipocytes, probably by inhibiting expression of CCAAT/enhancer-binding protein (C/EBP)β and δ, and subsequently blocked the expression of C/EBP α and peroxisome proliferator-activated receptor (PPAR)γ and transcriptional activation of genes that produce the adipocyte phenotype. AMPK activity was also suppressed by compound C treatment during the early phase of adipogenic differentiation, which indicated that suppressed activation of AMPK by compound C may inhibit the MCE process of preadipocytes. Our results suggest that compound C might serve as a useful molecule in both basic and clinical research on adipogenesis and as a potential lead compound for the treatment of obesity. © 2008 Pharmaceutical Society of Japan.
Persistent Identifierhttp://hdl.handle.net/10722/76399
ISSN
2015 Impact Factor: 1.574
2015 SCImago Journal Rankings: 0.644
ISI Accession Number ID
Funding AgencyGrant Number
National Natural Science Foundation of China30670457
Guangzhou Administration of Science and Technology2007Z2-E4021
Guangzhou Economic and Technological Development District matching funds2007Ss-P059
National 973 program of China2006CB503908
2004CB720102
Funding Information:

This work was supported in part by funds From the National Natural Science Foundation of China (30670457), Guangzhou Administration of Science and Technology (2007Z2-E4021), Guangzhou Economic and Technological Development District matching funds (2007Ss-P059) and the National 973 program of China (2006CB503908 and 2004CB720102).

References

 

DC FieldValueLanguage
dc.contributor.authorGao, Yen_HK
dc.contributor.authorZhou, Yen_HK
dc.contributor.authorXu, Aen_HK
dc.contributor.authorWu, Den_HK
dc.date.accessioned2010-09-06T07:20:48Z-
dc.date.available2010-09-06T07:20:48Z-
dc.date.issued2008en_HK
dc.identifier.citationBiological And Pharmaceutical Bulletin, 2008, v. 31 n. 9, p. 1716-1722en_HK
dc.identifier.issn0918-6158en_HK
dc.identifier.urihttp://hdl.handle.net/10722/76399-
dc.description.abstractThe role of AMP-activated protein kinase (AMPK) in adipocyte differentiation is not completely understood. Here we reported that an AMPK inhibitor, compound C, significantly inhibited adipogenic differentiation of 3T3-L1 cells in a dose dependent manner, and this inhibitory effect was primarily effective in the initial stage of differentiation. Compound C prevented the mitotic clonal expansion (MCE) of preadipocytes, probably by inhibiting expression of CCAAT/enhancer-binding protein (C/EBP)β and δ, and subsequently blocked the expression of C/EBP α and peroxisome proliferator-activated receptor (PPAR)γ and transcriptional activation of genes that produce the adipocyte phenotype. AMPK activity was also suppressed by compound C treatment during the early phase of adipogenic differentiation, which indicated that suppressed activation of AMPK by compound C may inhibit the MCE process of preadipocytes. Our results suggest that compound C might serve as a useful molecule in both basic and clinical research on adipogenesis and as a potential lead compound for the treatment of obesity. © 2008 Pharmaceutical Society of Japan.en_HK
dc.languageengen_HK
dc.publisherPharmaceutical Society of Japan. The Journal's web site is located at http://bpb.pharm.or.jp/index.htmlen_HK
dc.relation.ispartofBiological and Pharmaceutical Bulletinen_HK
dc.subject.mesh3T3 Cellsen_HK
dc.subject.meshAdipocytes - drug effectsen_HK
dc.subject.meshAdipogenesis - drug effectsen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshAzo Compoundsen_HK
dc.subject.meshBlotting, Westernen_HK
dc.subject.meshCCAAT-Enhancer-Binding Proteins - metabolismen_HK
dc.subject.meshCell Differentiation - drug effectsen_HK
dc.subject.meshClone Cells - drug effectsen_HK
dc.subject.meshColoring Agentsen_HK
dc.subject.meshCyclic AMP-Dependent Protein Kinases - antagonists & inhibitorsen_HK
dc.subject.meshDNA, Complementary - biosynthesis - isolation & purificationen_HK
dc.subject.meshEnzyme Inhibitors - pharmacologyen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMitosis - drug effectsen_HK
dc.subject.meshPyrazoles - pharmacologyen_HK
dc.subject.meshPyrimidines - pharmacologyen_HK
dc.subject.meshRNA - biosynthesis - isolation & purificationen_HK
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_HK
dc.subject.meshTranscription Factors - metabolismen_HK
dc.titleEffects of an AMP-activated protein kinase inhibitor, compound C, on adipogenic differentiation of 3T3-L1 cellsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0918-6158&volume=31&spage=1716&epage=22&date=2009&atitle=Effects+of+an+AMP-activated+protein+kinase+inhibitor,+compound+C,+on+adipogenic+differentiation+of+3T3-L1+cells.en_HK
dc.identifier.emailXu, A:amxu@hkucc.hku.hken_HK
dc.identifier.authorityXu, A=rp00485en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1248/bpb.31.1716en_HK
dc.identifier.pmid18758065-
dc.identifier.scopuseid_2-s2.0-51449094922en_HK
dc.identifier.hkuros158002en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-51449094922&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume31en_HK
dc.identifier.issue9en_HK
dc.identifier.spage1716en_HK
dc.identifier.epage1722en_HK
dc.identifier.isiWOS:000259061700015-
dc.publisher.placeJapanen_HK
dc.identifier.scopusauthoridGao, Y=36463367100en_HK
dc.identifier.scopusauthoridZhou, Y=25654258200en_HK
dc.identifier.scopusauthoridXu, A=7202655409en_HK
dc.identifier.scopusauthoridWu, D=7404297751en_HK

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