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J. Biol. Chem., Vol. 283, Issue 16, 10707-10715, April 18, 2008

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Suppression of Cardiac Myocyte Hypertrophy by Conjugated Linoleic Acid

ROLE OF PEROXISOME PROLIFERATOR-ACTIVATED RECEPTORS AND ^*

From the Faculty of Pharmacy, University of Manitoba and the Canadian Centre for Agri-Food Research in Health and Medicine, St. Boniface General Hospital Research Centre, Winnipeg, Manitoba R2H 2A6, Canada

Conjugated linoleic acid (CLA) refers to a naturally occurring mixture of positional and geometric isomers of linoleic acid. Evidence suggests that CLA is a dietary constituent and nutraceutical with anti-cancer, insulin-sensitizing, immunomodulatory, weight-partitioning, and cardioprotective properties. The aim of this study was to evaluate the effects of intervention with CLA on cardiac hypertrophy. In vitro, CLA prevented indicators of cardiomyocyte hypertrophy elicited by endothelin-1, including cell size augmentation, protein synthesis, and fetal gene activation. Similar anti-hypertrophic effects of CLA were observed in hypertrophy induced by angiotensin II, fibroblast growth factor, and mechanical strain. CLA may inhibit hypertrophy through activation of peroxisome proliferator-activated receptors (PPARs). CLA stimulated PPAR activity in cardiomyocytes, and the anti-hypertrophic effects of CLA were blocked by genetic and pharmacological inhibitors of PPAR isoforms and . CLA may disrupt hypertrophic signaling by stimulating diacylglycerol kinase , which decreases availability of diacylglycerol and thereby inhibits the protein kinase C pathway. In vivo, dietary CLA supplementation significantly reduced blood pressure and cardiac hypertrophy in spontaneously hypertensive heart failure rats. These data suggest that dietary supplementation with CLA may be a viable strategy to prevent pathological cardiac hypertrophy, a major risk factor for heart failure.

Received for publication, January 2, 2008 , and in revised form, February 13, 2008.

^* This work was supported by the Canadian Institutes of Health Research, the Heart and Stroke Foundation of Manitoba, Dairy Farmers of Canada, and the Manitoba Medical Service Foundation and a fellowship from the Manitoba Health Research Council (to C. P. A.). 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: CCARM, St. Boniface General Hospital Research Centre, 351 Taché Ave., Winnipeg, Manitoba R2H 2A6, Canada. Tel.: 204-235-3587; Fax: 204-237-4018; E-mail: handerson{at}sbrc.ca.

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