Journal
BRITISH JOURNAL OF CLINICAL PHARMACOLOGY
Volume 83, Issue 1, Pages 46-53Publisher
WILEY
DOI: 10.1111/bcp.12948
Keywords
atherosclerosis; conjugated linoleic acid; inflammation; resolution
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Atherosclerosis, the underlying cause of heart attack and strokes, is a progressive dyslipidaemic and inflammatory disease where monocyte-derived macrophage cells play a pivotal role. Although most of the mechanisms that contribute to the progression of atherosclerosis have been identified, there is limited information on those governing regression. Conjugated linoleic acid (CLA) is a generic term denoting a group of naturally occurring isomers of linoleic acid (18: 2, n6) that differ in the position or geometry (i.e. cis or trans) of their double bonds. The most predominant isomers in ruminant fats are cis-9, trans-11 CLA (c9, t11-CLA), which accounts for more than 80% of CLA isomers in dairy products and trans-10, cis-12 CLA (t10, c12-CLA). Dietary administration of a blend of the two most abundant isomers of CLA has been shown to inhibit the progression and induce the regression of preestablished atherosclerosis. Studies investigating the mechanisms involved in CLA-induced atheroprotective effects are continually emerging. The purpose of this review is to discuss comprehensively the effects of CLA on monocyte/macrophage function in atherosclerosis and to identify possible mechanisms through which CLA mediates its atheroprotective effects.
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