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J. Biol. Chem., Vol. 283, Issue 50, 34896-34906, December 12, 2008

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Lipin1 Is a Key Factor for the Maturation and Maintenance of Adipocytes in the Regulatory Network with CCAAT/Enhancer-binding Protein and Peroxisome Proliferator-activated Receptor ₂^*

From the Department of Biochemistry and Molecular Biology, Brain Korea 21 Project for Medical Science, Institute of Genetic Science, Center for Chronic Metabolic Disease Research, Yonsei University College of Medicine, Seoul 120-752, Korea

Lipin1 expression was induced at a late stage of differentiation of 3T3-L1 preadipocytes and maintained at high levels in mature adipocytes. Knockdown of expression of lipin1 by small interfering RNA in 3T3-L1 preadipocytes almost completely inhibited differentiation into adipocytes, whereas overexpression of lipin1 accelerated adipocyte differentiation, demonstrating that lipin1 is required for adipocyte differentiation. In mature adipocytes, transfection of lipin1-small interfering RNA decreased the expression of adipocyte functional genes, indicating the involvement of lipin1 in the maintenance of adipocyte function. Lipin1 increases the transcription-activating function of peroxisome proliferator-activated receptor ₂ (PPAR₂) via direct physical interaction, whereas lipin1 did not affect the function of other adipocyte-related transcription factors such as C/EBP, liver X-activated receptor , or sterol regulatory element binding protein 1c. In mature adipocytes, lipin1 was specifically recruited to the PPAR-response elements of the phosphoenolpyruvate carboxykinase gene, an adipocyte-specific gene. C/EBP up-regulates lipin1 transcription by directly binding to the lipin1 promoter. Based on the existence of a positive feedback loop between C/EBP and PPAR₂, we propose that lipin1 functions as an amplifier of the network between these factors, resulting in the maintenance of high levels of the specific gene expression that are required for adipogenesis and mature adipocyte functions.

Received for publication, May 26, 2008 , and in revised form, October 16, 2008.

^* This work was supported by Korea Science and Engineering Foundation Grant R13-2002-054-03001-0. 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 To whom correspondence should be addressed: 134 Shinchon-dong, Seodaemun-gu, Seoul 120-752, Korea. Tel.: 822-2228-1676; Fax: 822-312-5041; E-mail: kyungsup59{at}yuhs.ac.

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