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Here we describe a simplified version of reverse cholesterol transport, how this has been modified by new research into HDL, and we explain the effect of raising or lowering insulin and insulin sensitivity on RCT. The role of HDL in reverse cholesterol transport and its disturbances in Tangier disease and HDL deficiency with xanthomas. Cells take up cholesterol from the LDL by means of LDL receptors in the outer cell membrane. Tag: reverse cholesterol transport Gray Baby syndrome and the role of Glucuronic acid Cholesterol is a major constituent of gallstones. A 70−75 kDa high-density lipoprotein (HDL) particle with pre-β-electrophoretic migration (pre-β1-HDL) has been identified in several studies as an early acceptor of cell-derived cholesterol. However, the further metabolism of this complex has not been determined. Reverse lipid transport is the movement of lipids, mainly cholesterol and phospholipids, from peripheral tissues, through the extracellular compartment, to the liver for catabolism. Besides LDL, high-density lipoproteins (HDLs) carry cholesterol from the peripheral tissues to the liver in a reverse transport mechanism to get rid of any excess cholesterol. Cholesterol Transport, Uptake, Control About 70 percent of the cholesterol molecules in LDL are esterified with a fatty acid (for example, palmitate) on the OH group (at Carbon 3; see Figure 1 ). Reverse cholesterol transport (RCT) is the term used for this extraction of unneeded cholesterol. Additionally, cholesteryl ester transfer protein (CETP) activity was increased in this group of patients. Free cholesterol is removed from tissues by plasma high-density lipoprotein (HDL) and transported to the liver, where it is eliminated from the body either unchanged or after conversion to bile acids in the process known as reverse cholesterol transport (see Chapter 25). High-density lipoprotein metabolism and reverse cholesterol transport: strategies for raising HDL cholesterol. tosheskatrajkovska@gmail.com. It is well established that cholesterol ester-enriched foam cells are the hallmark of atherosclerotic plaques. Lecithin:cholesterol acyltransferase (LCAT) activity, the driving force of reverse cholesterol transport, showed a tendency towards lower values in hypertriglyceridemic patients, but this difference was not statistically significant. Tosheska Trajkovska K(1), Topuzovska S. Author information: (1)Institute of Medical and Experimental Biochemistry, Medical Faculty-Skopje University, SS.Cyril and Methodius; Skopje-Republic of Macedonia. Cellular While all cells can synthesize cholesterol to a small extent, the liver is the major site of cholesterol synthesis. Reverse cholesterol transport is a multi-step process resulting in the net movement of cholesterol from peripheral tissues back to the liver first via entering the lymphatic system, then the bloodstream.. Cholesterol from non-hepatic peripheral tissues is transferred to HDL by the ABCA1 (ATP-binding cassette transporter). Eur Heart J.. 1990; 11:197-121. HDL functions as a cholesterol scavenger, extracting excess cholesterol from cell surfaces and transporting it back to the liver (“reverse cholesterol transport”). 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. Its concentration is inversely associated with cardiovascular disease (CVD), and thus it has been dubbed “good cholesterol.” However there are subtypes of HDLs.

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