Abstract:
:The mechanism of how PPARgamma decrease gluconeogenic gene expressions in liver is still unclear. Since PPARgamma is a transcriptional activator, it requires a mediator to decrease the transcription of gluconeogenic genes. Recently, SHP has been shown to mediate the bile acid-dependent down regulation of gluconeogenic gene expression in liver. This led us to explore the possibility that SHP may mediate the antigluconeogenic effect of PPARgamma. In the present study, we have identified and characterized the presence of functional PPRE in human SHP promoter. We show the binding of PPARgamma/RXRalpha heterodimer to the PPRE and increased SHP expression by rosiglitazone in primary rat hepatocytes. Taken together with the previous reports about the function of SHP on gluconeogenesis, our results indicate that SHP can mediate the acute antigluconeogenic effect of PPARgamma.
journal_name
Biochem Biophys Res Communjournal_title
Biochemical and biophysical research communicationsauthors
Kim HI,Koh YK,Kim TH,Kwon SK,Im SS,Choi HS,Kim KS,Ahn YHdoi
10.1016/j.bbrc.2007.05.171subject
Has Abstractpub_date
2007-08-24 00:00:00pages
301-6issue
2eissn
0006-291Xissn
1090-2104pii
S0006-291X(07)01098-4journal_volume
360pub_type
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