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J. Lipid Res.
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Originally published In Press as doi:10.1194/jlr.M800625-JLR200 on January 9, 2009

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Journal of Lipid Research, Vol. 50, 908-914, May 2009
Copyright © 2009 by American Society for Biochemistry and Molecular Biology

Phenolic acids suppress adipocyte lipolysis via activation of the nicotinic acid receptor GPR109A (HM74a/PUMA-G)

Ning Ren, Rebecca Kaplan, Melba Hernandez, Kang Cheng, Lan Jin, Andrew K. P. Taggart, Amber Y. Zhu, Xiaodong Gan, Samuel D. Wright and Tian-Quan Cai1

Department of Cardiovascular Diseases, Merck Research Laboratories, Rahway, NJ 07065

Published, JLR Papers in Press, January 9, 2009.

1 To whom correspondence should be addressed. e-mail: tianquan_cai{at}merck.com

Phenolic acids are found in abundance throughout the plant kingdom. Consumption of wine or other rich sources of phenolic acids, such as the "Mediterranean diet," has been associated with a lower risk of cardiovascular disease. The underlying mechanism(s), however, has remained unclear. Here, we show that many phenolic acids, including those from the hydroxybenzoic and hydroxycinnamic acid classes, can bind and activate GPR109A (HM74a/PUMA-G), the receptor for the antidyslipidemic agent nicotinic acid. In keeping with this activity, treatment with a number of phenolic acids, including cinnamic acid, reduces lipolysis in cultured human adipocytes and in fat pats isolated from wild-type mice but not from mice deficient of GPR109A. Oral administration of cinnamic acid significantly reduces plasma levels of FFA in the wild type but not in mice deficient of GPR109A. Activation of GPR109A by phenolic acids may thus contribute to a cardiovascular benefit of these plant-derived products.

Supplementary key words GPCR • niacin • plant-derived product


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