Because, GW501516 increases ABCA1 expression, promotes cholesterol efflux from peripheral cell types, and raises HDLc in primates, it appears that activation of PPARδ provides a novel mechanism for promoting reverse cholesterol transport . Increased risk of CHD has been found in people with increased levels of Lp (a). Our study and the re- Elevation of nonfasting triglyceride (TG) levels above 1.8 g/L (2 mmol/L) is associated with increased risk of cardiovascular diseases. reverse cholesterol transport, that is, the ability of HDL to accept excess cholesterol from tissues and return it to the liver either directly or via other lipoproteins. 1979), as was found in the present study. It is well established that cholesterol ester-enriched foam cells are the hallmark of atherosclerotic plaques. Exacerbated postprandial hypertriglyceridemia (PP–HTG) and metabolic context both modulate the overall efficacy of the reverse cholesterol transport (RCT) pathway, but the specific contribution of exaggerated PP–HTG on RCT efficacy remains indeterminate. Reverse cholesterol transport is a term that comprises all the different steps in cholesterol metabolism between cholesterol efflux from macrophage foam cells and the * Correspondence: 1Department of Pediatrics, Center for Liver, Digestive and Metabolic Diseases, Reverse cholesterol transport (RCT) is a pivotal pathway involved in the return of excess cholesterol from peripheral tissues to the liver for excretion in the bile and eventually the feces. pates in the 'reverse cholesterol transport' of excess cholesterol from the extrahepatic tissues to the liver for catabolism. Multiple lines of evidence support that enhancing foam cell cholesterol efflux by HDL (high-density lipoprotein) particles, the first step of reverse cholesterol transport (RCT), is a promising antiatherogenic strategy. Reverse Cholesterol Transport (RCT) Reverse cholesterol transport is a mechanism by which the body removes excess cholesterol from peripheral tissues and delivers them to the liver, where it will be redistributed to other tissues or removed from the body by the gallbladder. CEPT is also involved in this process. This entire transport process is called reverse cholesterol transport (RCT), and macrophage RCT refers specif-ically to the removal of cholesterol from macrophage cholesterol ester stores (9). Smoking is known to depress levels of HDL-cholesterol and apo A-I (Berg et al. The fraction of cholesterol disposed of through macrophages is small overall compared with the amounts in the pathway (7, 8). Reverse Cholesterol Transport. Fortunately our gut and liver cells make a protein called ApoA1, which the liver turns into something called a nascent HDL particle. RCT from macrophages in atherosclerotic plaques (macrophage RCT) is a critical mechanism of antiatherogenicity of high-density lipoproteins (HDL). worldwide. Lp (a) is a LDL particle to which an additional large protein termed apo (a) is attached. The main lipoprotein involved in this process is the HDL-c. tion such as reverse cholesterol transport are being extensively investigated. In this chapter, we summarize recent advances in the critical role of HDL in reverse cholesterol transport … Based on these findings, many new concepts and mechanisms regarding the physiologi-cal functions of HDL have been proposed. Farnesoid X Receptor Activation Increases Reverse Cholesterol Transport by Modulating Bile Acid Composition and Cholesterol Absorption in Mice Yang Xu,1 Fei Li, 2Munaf Zalzala,1,3 Jiesi Xu, 1Frank J. Gonzalez, Luciano Adorini,4 Yoon-Kwang Lee, Liya Yin, and Yanqiao Zhang1 Activation of farnesoid X receptor (FXR) markedly attenuates development of atherosclerosis in animal models.
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