Article

Transcriptional activation of SHP by PPAR-γ in liver

Department of Biochemistry and Molecular Biology, Yonsei University College of Medicine, 134 Shinchon-dong, Seodaemoon-gu, Seoul 120-752, Republic of Korea; Center for Chronic Metabolic Disease Research, Yonsei University College of Medicine, 134 Shinchon-dong, Seodaemoon-gu, Seoul 120-752, Republic of Korea; Institute of Genetic Science, Yonsei University College of Medicine, 134 Shinchon-dong, Seodaemoon-gu, Seoul 120-752, Republic of Korea; Hormone Research Center, Chonnam National University, Kwangju 500-757, Republic of Korea
Biochemical and Biophysical Research Communications DOI:10.1016/j.bbrc.2007.05.171

ABSTRACT The mechanism of how PPARγ decrease gluconeogenic gene expressions in liver is still unclear. Since PPARγ 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 PPARγ. In the present study, we have identified and characterized the presence of functional PPRE in human SHP promoter. We show the binding of PPARγ/RXRα 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 PPARγ.

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Keywords

acute antigluconeogenic effect
 
antigluconeogenic effect
 
bile acid-dependent
 
decrease
 
functional PPRE
 
gluconeogenesis
 
gluconeogenic gene expression
 
gluconeogenic genes
 
human SHP promoter
 
PPARγ
 
PPARγ decrease gluconeogenic gene expressions
 
PPARγ/RXRα heterodimer
 
PPRE
 
primary rat hepatocytes
 
rosiglitazone
 
SHP
 
SHP expression
 
transcriptional activator