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J. Biol. Chem., Vol. 283, Issue 14, 8788-8795, April 4, 2008

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Transcriptional Regulation of Fatty Acid Translocase/CD36 Expression by CCAAT/Enhancer-binding Protein ^*

Liping Qiao, Chenhui Zou, Peng Shao¹, Jerome Schaack, Peter F. Johnson^¶2, and Jianhua Shao³

From the Graduate Center for Nutritional Sciences, University of Kentucky, Lexington, Kentucky 40536, Department of Microbiology, University of Colorado at Denver and Health Sciences Center, Aurora, Colorado 80045, and ^¶Laboratory of Protein Dynamics and Signaling, NCI-Frederick, National Institutes of Health, Frederick, Maryland 21702

Fatty acid translocase (FAT/CD36) plays an important role in facilitating long chain fatty acid transport. FAT/CD36 gene deletion protects mice from high fat diet-induced obesity. In this study we have investigated the regulatory mechanism of FAT/CD36 expression at the transcription level. FAT/CD36 expression was activated during 3T3-L1 adipocyte differentiation, and FAT/CD36 protein levels were positively correlated with CCAAT/enhancer-binding protein (C/EBP) and peroxisome proliferator-activated receptor . However, a negative correlation was detected between FAT/CD36 and C/EBPβ. Overexpression of C/EBP or C/EBPβ increased FAT/CD36 mRNA and protein levels in several types of cells. Restoration of C/EBP or C/EBPβ expression in C/EBP- or C/EBPβ-deficient mouse embryonic fibroblasts increased FAT/CD36 expression. However, in mouse embryonic fibroblasts C/EBP was a more potent activator of FAT/CD36 expression than was C/EBPβ. Expression of C/EBP robustly increased FAT/CD36 proximal promoter-directed luciferase expression in human embryonic kidney 293 cells. A C/EBP-responsive element was identified in the FAT/CD36 promoter by using 5' and specific site mutations. The binding of C/EBP in the FAT/CD36 promoter was detected by chromatin immunoprecipitation in 3T3-L1 adipocytes. These results demonstrated that C/EBP regulates FAT/CD36 gene expression at the transcriptional level.

Received for publication, January 3, 2008 , and in revised form, February 8, 2008.

^* This work was supported in part by National Institutes of Health Grant RDK077643A (to J. S.), American Diabetes Association Grant 7-07-CD-23 (to J. S.), and American Heart Association Grant 0665289B (to J. S.) and by the Intramural Research Program of the Center for Cancer Research, NCI, National Institutes of Health (to P. F. J.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ Recipient of the William C. Parker Scholarship.

² Present address: Basic Research Laboratory, NCI-Frederick, National Institutes of Health.

³ To whom correspondence should be addressed: Graduate Center for Nutritional Sciences, University of Kentucky, 900 S. Limestone, Lexington, KY 40536-0200. Tel.: 859-323-4933 (ext. 81801); Fax: 859-257-3565; E-mail: JianhuaShao{at}uky.edu.

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