Abstract
Reverse cholesterol transport (RCT) is a physiological mechanism protecting cells from an excessive accumulation of cholesterol. When this process begins in vascular macrophages, it acquires antiatherogenic properties, as has been widely demonstrated in animal models. Dietary lipids, despite representing a fundamental source of energy and exerting multiple biological functions, may induce detrimental effects on cardiovascular health. In the present review we summarize the current knowledge on the mechanisms of action of the most relevant classes of dietary lipids, such as fatty acids, sterols and liposoluble vitamins, with effects on different steps of RCT. We also provide a critical analysis of data obtained from experimental models which can serve as a valuable tool to clarify the effects of dietary lipids on cardiovascular disease.
Highlights
Atherosclerotic cardiovascular disease (CVD) is the leading cause of mortality worldwide
C22:6 docosahexaenoic acid (DHA) on the rate of fecal macrophage-derived cholesterol excretion [30,161], these results would be consistent with the absence of effects when comparing low- and highsoybean oil-enriched diets in mice [30] or when evaluating the impact of alpha linoleic acid supplementation in a high-fat diet in cholesteryl ester transfer protein (CETP)-expressing apoE3 Leiden mice [165]
The evidence relating vitamin D and reverse cholesterol transport (RCT) in vivo is limited to a study on hypercholesterolemic swine, in which the authors reported that dietary supplementation with vitamin D 1000 and 3000 IU/day dose-dependently increased the expression of ABCA1 and ABCG1 in the aorta
Summary
Atherosclerotic cardiovascular disease (CVD) is the leading cause of mortality worldwide. By removing excess cholesterol from extrahepatic tissues for their final excretion into the feces, reverse cholesterol transport (RCT) represents a physiological, protective mechanism This process is mainly driven by high-density lipoproteins (HDL) and it is widely recognized as one of the main atheroprotective functions of these particles, especially when macrophage-derived cholesterol is involved [4]. Rader’s group, based on the evaluation of macrophage-specific RCT (m-RCT) upon an intraperitoneal injection of radiolabeled cholesterol-loaded macrophages in mice, very closely mimics the in vivo setting and tracks the most atherogenic pool of cholesterol in the body [26] The application of this method demonstrated that m-RCT in mice inversely correlates with atherosclerosis progression [27], providing for the first time the concept that this major HDL function, more than HDL plasma levels, is a milestone for atheroprotection. In this review we will critically analyze studies in which the impact of dietary lipids on RCT in animal models was evaluated
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