LDL Cholesterol - The "Bad" Cholesterol Explained
Two types of lipoproteins carry cholesterol to and from cells. One is low-density lipoprotein, or LDL. The other is high-density lipoprotein, or HDL. The amount of. Two types of proteins called “lipoproteins” carry cholesterol in the blood: LDL and HDL. High LDL levels raise your risk for heart disease and. A lipoprotein is a biochemical assembly whose primary purpose is to transport hydrophobic lipid (a.k.a. fat) molecules in water, as in blood or extracellular fluid. They have a single-layer phospholipid and cholesterol outer shell, with the lipoproteins, according to density / size (an inverse relationship), compared with the.
Fats are insoluble in water and can therefore not be transported in blood on its own. These combinations of fats and protein are termed lipoproteins. The amount of cholesterol carried by different lipoproteins can provide valuable information about the risk of developing cardiovascular disease CVD.
Cholesterol, Triglycerides, and Associated Lipoproteins - Clinical Methods - NCBI Bookshelf
However, this association appears to become less prominent with increasing age, and some studies have suggested that low LDL-C may be associated with increased mortality in older adults. Cholesterol is the best-known sterol, mainly because of its proposed role in atherosclerosis and cardiovascular disease.
It is also a precursor molecule.
- LDL Cholesterol – The “Bad” Cholesterol Explained
- HDL (Good), LDL (Bad) Cholesterol and Triglycerides
- LDL and HDL Cholesterol: "Bad" and "Good" Cholesterol
Cholesterol is also a precursor of important hormones such as progesterones, glucocorticoids cortisolmineralocorticoids aldosteroneandrogens testosterone and estrogens. Cholesterol occurs only in foods of animal origin. Because the body can synthesize cholesterol, it is not needed in the diet.
The Role of Lipoproteins A standard lipid panel provides information about the amount of cholesterol carried by different lipoproteins. The main role of lipoprotein particles is to transport fats such as triglycerides and cholesterol in the blood between the organs of the body.
Diet, cholesterol and lipoproteins explained
A lack of LDL-receptors may reduce the uptake of cholesterol by the cells, forcing it to remain in the circulation thereby raising blood levels. In familial hypercholesterolemiawhich is a genetic disorder, the body is unable to remove LDL from the blood. This leads to high levels of LDL-C in the blood, which may severely increase the risk of cardiovascular disease, even at a young age. Blood tests typically report LDL-C. This equation relies on the assumption that the ratio of triglyceride to cholesterol is constant, which is not always the case.
Direct LDL -C measurements are also available, but are less often done due to higher costs. Quantitative determination of apoproteins is performed in sophisticated laboratories utilizing radioimmunoassays for apoprotein AI and apoprotein B and isoelectric focusing for apoproteins C and E.
Other specialized tests are: Basic Science Plasma lipoprotein particles contain variable proportions of four major elements: The varying composition of these elements determines the density, size, and electrophoretic mobility of each particle. 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.Physiology of Lipoproteins Cholesterol
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. 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.
All about diet, cholesterol and lipoproteins
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.
Their predominant function is to supply cholesterol to cells with LDL receptors, like those in the adrenal glands, skeletal muscle, lymphocytes, gonads, and kidneys. The quantity of cholesterol freed from LDL is said to control cholesterol metabolism in the cell through the following mechanisms: Besides the above described route for LDL degradation in extrahepatic sites, a so-called scavenger cell pathway has been described. This consists of cells in the reticuloendothelial system which, by phagocytosis, dispose of the excess concentrations of this lipoprotein in plasma.
Transport of High-Density Lipoprotein Cholesterol High-density lipoproteins are a heterogeneous group of macromolecules with different physical properties and chemical components; two subclasses of HDL have been identified HDL2 and HDL3 within which several subspecies have also been demonstrated. The predomination function of HDL seems to be the reverse transport of cholesterol from different tissues into the liver, where it is eventually removed.
Subclass HDL2 has been reported to have a better correlation with coronary artery disease protection than total HDL cholesterol. The serum concentration of HDL and its components derives from various complex intravascular and cellular metabolic events.
These events include secretion of precursor HDL particles from the liver and small intestine, interaction of these particles with lipids and proteins released during the catabolism of triglyceride-rich lipoproteins, and production of cholesteryl esters the core substance in HDL from the action of lecithin—cholesterol acyltransferase LCATan enzyme that originates in the liver.
This enzyme acts on unesterified cholesterol released into plasma from cellular turnover. The end result is a system that allows the transfer of cholesterol through LDL to peripheral cells and its return to the liver through HDL, and that prevents excessive accumulation of cholesterol in the body.