Lipoprotein particle metabolism can occur via the exogenous or link between higher serum vitamin D levels and lower cholesterol in children. Key words: High-density lipoproteins, reserve cholesterol transport, atherosclerosis, .. The inverse relationship between HDL-C blood concentrations and. Cholesterol Metabolism. Lipid and Lipoprotein Metabolism (Rosensen, ). Lipids = cholesterol and triglyceride - are insoluble in plasma and are transported .
Cholesterol, lipoproteins and the liver
An update for clinicians. Identification of scavenger-receptor SRB1 as high-density lipoprotein receptor. Apolipoprotein E and atherosclerosis. Moestrup SK, Kozyraki R. Cubilin, a high-density lipoprotein receptor.
Megalin acts in concert with cubilin to mediate endocytosis of high-density lipoprotein.
Obesity, Overweight, and Dyslipidemia in Children and Adolescents
High-density lipoprotein cholesterol in the cardiovascular equation: Does the "good" still count? High-density lipoprotein reverse inhibitory effect of oxidized low-density lipoprotein on endothelium dependent arterial relaxation. How high-density lipoprotein protects against the effects of lipid peroxidation.
Effects of lipids and lipoproteins on thrombosis and rheology. Inhibition of endothelial cell adhesion molecule expression by high-density lipoprotein. Clin Exp Pharmacol Physiol.
Stimulation of endothelin-1 release by low-density and very-low-density lipoproteins in cultured human endothelial cells. Stimulation of arterial endothelial cell prostacyclin synthesis by high-density lipoproteins. Lipoproteins regulated C-type natriuretic peptide secretion from cultured vascular endothelial cells. Arterioscler Thomb Vasc Biol. High-density lipoprotein increase the abundance of e NOS protein in human vascular endothelial cells by increasing its half-life.
J Am Coll Cardiol. Relation between high-density lipoprotein cholesterol and peripheral vasomotor function. Low- and high-density lipoproteins as mitogenic factors for vascular smooth muscle cells: J Vasc Res ; High-density lipoprotein and its apolipoproteins inhibit cytolytic activity of complement. Studies on the nature of inhibitory moiety. The scientific background to primary and secondary prevention of coronary heart disease.
Nutr Metab Cardiovasc Dis. Evidence-based guidelines for cardiovascular prevention in women. Bielicki JK, Oda M. Apolipoprotein AI RC Paris is defective in activation of lecithin-cholesterol acyl-transferase but not in initial lipid binding, formation of reconstituted lipoproteins, or promotion of cholesterol efflux.
Two novel molecular defects in the LCAT gene are associated with fish eye disease. Arterioscler Thromb Vasc Biol.
Mutations in ABC1 in Tangier disease and familial high-density lipoprotein deficiency. N Engl J Med. Cigarette smoking, high-density lipoprotein cholesterol subfractions, and lecitin-cholesterol acyltransferase in young women.
The effect of cessation from cigarette smoking on the lipid and lipoprotein profiles: Lipoproteins, nutrition and heart disease. Low-intensity endurance exercise training, plasma lipoproteins and the risk of coronary heart disease. Moderate alcohol intake and lower risk of coronary heart disease: Effects of post menopausal estrogen replacement on lipids concentration and metabolism of plasma lipoproteins.
Effects of phenytoin on plasma high-density lipoprotein cholesterol in men with low levels of high-density lipoprotein cholesterol. High-density lipoproteins and atherosclerosis: Low high-density lipoprotein as a risk factor in coronary heart disease: Assmann G, Schulte H.Physiology of Lipoproteins Cholesterol
Relation of high-density lipoprotein cholesterol and triglycerides to incidence of atherosclerotic coronary disease the PROCAM experience.
HDL-cholesterol as a marker of coronary heart disease: Factors associated with low and elevated plasma high-density lipoprotein cholesterol and apolipoprotein AI levels in the Framingham Offspring Study. Low-density lipoprotein size, triglycerides and high-density lipoprotein as a risk factor for coronary heart disease in older Japanese-American men.
Inhibition of early atherosclerosis in transgenic mice by human apolipoprotein AI. Regression of atherosclerotic lesions by high-density lipoprotein plasma fraction in the cholesterol-fed rabbit. Intravenous injection of rabbit apolipoprotein AI inhibits the progression af atherosclerosis in cholesterol-fed rabbits.
Recombinant apolipoprotein AI Milano reduces intimal thickening after balloon injury in hypercholesterolemic rabbits.
Apolipoprotein AI transgene corrects apolipoprotein E deficiency-induced atherosclerosis in mice. Human apolipoprotein AI gene expression increases high-density lipoprotein E deficient mouse. Interelations of lipids-lipoproteins with coronary artery disease mortality in 19 countries. Cholesterol and lipids in the risk of coronary heart disease: Multiple Risk Factor Intervention Trial: Risk factor changes and mortality results.
High-density lipoprotein cholesterol and coronary heart disease in hypercholesterolemic men. Predictive value of exercise test for mortality in North American men: High-density lipoprotein cholesterol and cardiovascular disease. Four prospective American studies.
Triglyceride concentration and ischemic heart disease. An eight-year follow-up in the Copenhagen Male Study. Epidemiologic aspects of high-density lipoprotein cholesterol.
Relation of the level of high-density lipoprotein subfraction to the presence and extent of coronay artery disease. Shah P, Amin J. Atherosclerosis is a cardiovascular disease in which lipids and inflammatory cells accumulate in plaques within the walls of blood vessels. As a result, vessel walls are narrowed and clots may form, impeding blood flow and oxygen delivery and causing tissue injury.
Heart disease occurs because the coronary arteries supplying the heart are a major site where atherosclerotic plaques form. The liver is central to the regulation of cholesterol levels in the body. Not only does it synthesize cholesterol for export to other cells, but it also removes cholesterol from the body by converting it to bile salts and putting it into the bile where it can be eliminated in the feces. Furthermore, the liver synthesizes the various lipoproteins involved in transporting cholesterol and other lipids throughout the body.
Cholesterol synthesis in the liver is under negative feedback regulation. Increased cholesterol in a hepatocyte leads to decreased activity of HMG-CoA reductase, the rate-limiting enzyme in cholesterol synthesis. Types of Lipoproteins Lipoproteins are particles that contain triacylglycerol TAGcholesterol, phospholipids and amphipathic proteins called apolipoproteins.
You can refresh your memory about the structure of lipoproteins by visiting the webpage Lipoproteins from fall quarter. Lipoproteins can be differentiated on the basis of their density, but also by the types of apolipoproteins they contain.
Cholesterol, Lipoproteins and the Liver
The degree of lipid in a lipoprotein affects its density—the lower the density of a lipoprotein, the more lipid it contains relative to protein. The figure below summarizes the fates of lipoproteins produced by the liver. Refer to it as you read about the different lipoproteins. Two types of lipoproteins are triglyceride-rich: Chylomicrons are synthesized by enterocytes from lipids absorbed in the small intestine.
VLDL is synthesized in the liver. The function of these lipoproteins is to deliver energy-rich triacylglycerol TAG to cells in the body pink pathway. TAG is stripped from chylomicrons and VLDL through the action of lipoprotein lipase, an enzyme that is found on the surface of endothelial cells. These factors in turn have been used for the clinical and biochemical classification of lipoprotein disorders. Schematically, lipoproteins have been described as globular or spherical units in which a nonpolar core lipid consisting mainly of cholesterol esters and triglycerides is surrounded by a layer containing phospholipids, apoproteins, and small amounts of unesterified cholesterol.
Apoproteins, in addition to serving as carrier proteins, have other important functions such as being co-factors for enzymes involved in lipoprotein metabolism, acting as specific ligands for binding of the particles to cellular receptor sites, and intervening in the exchange of lipid constituents between lipoprotein particles.
The fact that all the cholesterol required by the body can be produced by biosynthesis points to the essential nature of this substance. As an estimated loss of 1. Usually this replacement is obtained from dietary sources, but another portion is synthesized in multiple cells of the body.
Triglycerides are also obtained from the diet as well as synthesized by the liver. The origin of circulating lipoproteins is less understood than is their uptake, transport, and degradation. The lipid transport system in plasma has been described as involving two pathways: Exogenous and endogenous fat-transport pathways are diagrammed.
Dietary cholesterol is absorbed through the wall of the intestine and is packaged, along with triglyceride glycerol ester-linked to three fatty acid chainsin chylomicrons. In the capillaries more Exogenous Pathway The exogenous pathway starts with the intestinal absorption of triglycerides and cholesterol from dietary sources.
Its end result is the transfer of triglycerides to adipose and muscle tissue and of cholesterol to the liver.
Cholesterol, Triglycerides, and Associated Lipoproteins - Clinical Methods - NCBI Bookshelf
After absorption, triglycerides and cholesterol are re-esterified in the intestinal mucosal cells and then coupled with various apoproteins, phospholipids, and unesterified cholesterol into lipoprotein particles called chylomicrons. The chylomicrons in turn are secreted into intestinal lymph, enter the bloodstream through the thoracic: At these binding sites the chylomicrons interact with the enzyme lipoprotein lipase, which causes hydrolysis of the triglyceride core and liberation of free fatty acids.
These fatty acids then pass through the capillary endothelial cells and reach the adipocytes and skeletal muscle cells for storage or oxidation, respectively. After removal of the triglyceride core, remnant chylomicron particles are formed. These remnants are cleared from the circulation by binding of their E apoprotein to a receptor present only on the surface of hepatic cells. Subsequently, the bound remnants are taken to the inside of hepatic cells by endocytosis and then catabolized by lysosomes.
This process liberates cholesterol, which is then either converted into bile acids, excreted in bile, or incorporated into lipoproteins originated in the liver VLDL. Under normal physiologic conditions, chylomicrons are present in plasma for 1 to 5 hours after a meal and may give it a milky appearance. They are usually cleared from the circulation after a hour fast. Endogenous Pathway The liver constantly synthesizes triglycerides by utilizing as substrates free fatty acids and carbohydrates; these endogenous triglycerides are secreted into the circulation in the core of very-low-density lipoprotein particles VLDL.
The synthesis and secretion of VLDL at cellular level occur in a process similar to that of chylomicrons, except that a different B apoprotein B instead of B together with apoproteins C and E intervene in their secretion. Subsequent interaction of the VLDL particles with lipoprotein lipase in tissue capillaries leads to hydrolysis of the core triglycerides and production of smaller remnant VLDL particles rich in cholesterol esters intermediate-density lipoproteins, IDL and liberation of free fatty acids.
Around half of these remnant particles are removed from the circulation in 2 to 6 hours as they bind tightly to hepatic cells. The rest undergo modifications with detachment of the remaining triglycerides and its substitution by cholesterol esters and removal of all the apoproteins except apoprotein B.