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Piperine, a Component of Black Pepper, Inhibits Adipogenesis by Antagonizing PPARγ Activity in 3T3-L1 Cells

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† Department of Bioscience and Biotechnology, BK21 Graduate Program, Sejong University, Seoul 143-747, Korea
§ Department of Biochemistry, Molecular Biology and Internal Medicine, College of Oriental Medicine, Dongguk University, Kyungpook 780-714, Korea
# Department of Food and Nutrition, Brain Korea 21 Project, Yonsei University, Seoul 120-749, Korea
⊗ Department of Internal Medicine, The Catholic University of Korea, Seoul 137-701, Korea
⊥ Department of Molecular Biology, BK21 Graduate Program, Dankook University, 126 Jukjeon-dong, Suji-gu, Yongin-si, Gyeonggi-do 448-701, Korea
*(S.-J.U.) Phone: +82-2-3408-3641. Fax: +82-2-3408-4334. E-mail: [email protected]. (J.-C.J.) E-mail: [email protected]
Cite this: J. Agric. Food Chem. 2012, 60, 15, 3853–3860
Publication Date (Web):April 2, 2012
https://doi.org/10.1021/jf204514a
Copyright © 2012 American Chemical Society
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    Abstract

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    This study investigated the antiadipogenic activity of black pepper extract and its constituent piperine in 3T3-L1 preadipocytes as well as the underlying molecular mechanisms. Both black pepper extract and piperine, without affecting cytotoxicity, strongly inhibited the adipocyte differentiation of 3T3-L1 cells. The mRNA expression of the master adipogenic transcription factors, PPARγ, SREBP-1c, and C/EBPβ, was markedly decreased. Intriguingly, mRNA levels of PPARγ target genes were also down-regulated. Moreover, a luciferase reporter assay indicated that pipierine significantly represses the rosiglitazone-induced PPARγ transcriptional activity. Finally, GST-pull down assays demonstrated that piperine disrupts the rosiglitazone-dependent interaction between PPARγ and coactivator CBP. Genome-wide analysis using microarray further supports the role of piperine in regulating genes associated with lipid metabolism. Overall, these results suggest that piperine, a major component of black pepper, attenuates fat cell differentiation by down-regulating PPARγ activity as well as suppressing PPARγ expression, thus leading to potential treatment for obesity-related diseases.

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