HDL is synthesized and secreted from both liver and intestine (Figure 1). However, apo C and apo E are synthesized in the liver and transferred from liver HDL to intestinal HDL when the latter enters the plasma. A major function of HDL is to act as a repository for the apo C and apo E required in the metabolism of chylomicrons and VLDL. Nascent HDL consists of discoid phospholipid bilayers containing apo A and free cholesterol. These lipoproteins are similar to the particles found in the plasma of patients with a deficiency of the plasma enzyme LCAT and in the plasma of patients with obstructive jaundice. LCAT—and the LCAT activator apo A-I—bind to the discoidal particles, and the surface phospholipid and free cholesterol are converted into cholesteryl esters and lysolecithin. The nonpolar cholesteryl esters move into the hydrophobic interior of the bilayer, whereas lysolecithin is transferred to plasma albumin. Thus, a nonpolar core is generated, forming a spherical, pseudomicellar HDL covered by a surface film of polar lipids and apolipoproteins. This aids the removal of excess unesterified cholesterol from lipoproteins and tissues as described in the following discussion.

Fig1. Metabolism of high-density lipoprotein (HDL) in reverse cholesterol transport. A-I, apolipoprotein A-I; ABCA1, ATP binding cassette transporter A1; ABCG1, ATP-binding cassette transporter G1; C, cholesterol; CE, cholesteryl ester; LCAT, lecithin:cholesterol acyl transferase; PL, phospholipid; SR-B1, scavenger receptor B1. Preβ-HDL, HDL2 , HDL3 . Surplus surface constituents from the action of lipoprotein lipase on chylomicrons and VLDL are another source of preβ-HDL.

Reverse Cholesterol Transport Is a Major Function of HDL

The removal of cholesterol from the tissues and its return to the liver for excretion is termed reverse cholesterol transport. The class B scavenger receptor B1 (SR-B1) is an HDL receptor with a dual role in this process. In the liver, it binds HDL via apo A-I, and cholesteryl ester is selectively delivered to the cells, although the particle itself, including apo A-I, is not taken up. In the extrahepatic tissues, on the other hand, SR-B1 mediates the acceptance of cholesterol effluxed from the cells by HDL, which then transports it to the liver where it is excreted in the bile either as cholesterol or after conversion to bile acids (see Figure 1). HDL3 , generated from discoidal HDL by the action of LCAT, accepts cholesterol from the tissues via the SR-B1 and the cholesterol is then esterified by LCAT, increasing the size of the particles to form the less dense HDL2 . HDL3 is then reformed, either after selective delivery of cholesteryl ester to the liver via the SR-B1 or by hydrolysis of HDL2 phospholipid and triacylglycerol by hepatic lipase and endothelial lipase. This interchange of HDL2 and HDL3 is called the HDL cycle (see Figure1). Free apo A-I is released by these processes and forms preβ-HDL after associating with a minimum amount of phospholipid and cholesterol. Surplus apo A-I is destroyed in the kidney. A second important mechanism for reverse cholesterol transport involves the ATP-binding cassette transporters A1 (ABCA1) (also called cholesterol efflux regulatory protein) and G1 (ABCG1). These transporters are members of a family of transporter proteins that couple the hydrolysis of ATP to the binding of a substrate, enabling it to be transported across the membrane. ABCG1 mediates the transport of cholesterol from cells to HDL, while ABCA1 preferentially promotes efflux to poorly lipidated particles such as preβ-HDL or apo A-1, which are then converted to HDL3 via discoidal HDL (see Figure 1). Preβ-HDL is the most potent form of HDL inducing cholesterol efflux from the tissues.

HDL concentrations vary reciprocally with plasma tri acylglycerol concentrations and directly with the activity of lipoprotein lipase. This may be due to surplus surface constituents, for example, phospholipid and apo A-I, being released during hydrolysis of chylomicrons and VLDL and contributing toward the formation of preβ-HDL and discoidal HDL. HDL2 concentrations are inversely related to the incidence of atherosclerosis, possibly because they reflect the efficiency of reverse cholesterol transport. HDLc (HDL1 ) is found in the blood of diet-induced hypercholesterolemic animals. It is rich in cholesterol, and its sole apolipoprotein is apo E. It appears that all plasma lipoproteins are interrelated components of one or more metabolic cycles that together are responsible for the complex process of plasma lipid transport.

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مواضيع ذات صلة

Brown Adipose Tissue Promotes Thermogenesis

Hormones Regulate Fat Mobilization

Adipose Tissue is The Main Store of Triacylglycerol in The Body

Classification of Proteins

Precipitation Reactions of Proteins

Study of Protein Structure

Imbalance in the Rate of Triacylglycerol Formation & Export Causes Fatty Liver

The Liver Plays A Central Role in Lipid Transport & Metabolism

Tertiary Structure of Proteins

Secondary Structure of Proteins

Primary Structure of Proteins

Chylomicrons & Very-low Density Lipoproteins are Rapidly Catabolized