"binding. Portions of the cytosolic sequence have been found in other lipoprotein receptors, as well as in more distant receptor relatives. Mutations in the gene encoding the LDL receptor are known to cause familial hypercholesterolaemia. There are 5 broad classes of mutation of the LDL receptor: LDL receptor mediates the endocytosis of cholesterol-rich LDL and thus maintains the plasma level of LDL. This occurs in all nucleated cells, but mainly in the liver which removes ~70% of LDL from the circulation. LDL receptors are clustered in clathrin-coated pits, and coated pits pinch off from the surface to form coated endocytic"
"are not conclusive. Low-density lipoprotein Low-density lipoprotein (LDL) is one of the five major groups of lipoprotein which transport all fat molecules around the body in the extracellular water. These groups, from least dense, compared to surrounding water (largest particles) to most dense (smallest particles), are chylomicrons (aka ULDL by the overall density naming convention), very low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), low-density lipoprotein and high-density lipoprotein (HDL). LDL delivers fat molecules to the cells and can drive the progression of atherosclerosis if they become oxidized within the walls of arteries. Lipoproteins transfer lipids (fats) around the body in the"
"plasma lipoprotein particles classified as HDL, LDL, IDL, VLDL and ULDL (a.k.a. chylomicrons) lipoproteins, according to density / size (an inverse relationship), compared with the surrounding plasma water. These complex protein capsules enable fats to be carried in all extracellular water, including the blood stream (an example of emulsification), subgroups of which are primary drivers / modulators of atherosclerosis, the transmembrane proteins of mitochondrion, chloroplast, and bacterial lipoproteins. Proteolipids are a different kind of protein-lipid combination that are insoluble in water. Proteolipids are abundant in brain tissue, and are also present in many other animal and plant tissues. The lipids"
"Low-density lipoprotein Low-density lipoprotein (LDL) is one of the five major groups of lipoprotein which transport all fat molecules around the body in the extracellular water. These groups, from least dense, compared to surrounding water (largest particles) to most dense (smallest particles), are chylomicrons (aka ULDL by the overall density naming convention), very low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), low-density lipoprotein and high-density lipoprotein (HDL). LDL delivers fat molecules to the cells and can drive the progression of atherosclerosis if they become oxidized within the walls of arteries. Lipoproteins transfer lipids (fats) around the body in the extracellular fluid, making"
"They are classified on the basis of electrophoresis, ultracentrifugation and nuclear magnetic resonance spectroscopy via the Vantera Analyzer. For young healthy research subjects, ~70 kg (154 lb), this data represents averages across individuals studied, percentages represent % dry weight: It is also possible to classify lipoproteins as ""alpha"" and ""beta"", according to the classification of proteins in serum protein electrophoresis. This terminology is sometimes used in describing lipid disorders such as abetalipoproteinemia. Lipoproteins, such as LDL and HDL, can be further subdivided into subspecies isolated through a variety of methods . These subspecies are subdivided by density or by the"
"that has been shown to have beneficial anti-inflammatory properties), and an increase in Serum amyloid A. This altered composition of HDL is commonly referred to as acute-phase HDL in an acute-phase inflammatory response, during which time HDL can lose its ability to inhibit the oxidation of LDL. In fact, this altered composition of HDL is associated with increased mortality and worse clinical outcomes in patients with sepsis. Lipoproteins may be classified as five major groups follows, listed from larger and less dense to smaller and denser. Lipoproteins are larger and less dense when the fat to protein ratio is increased."
"High-density lipoprotein HDL particles have long been divided into 5 subgroups, by density/size (an inverse relationship), which also correlates with function and incidence of cardiovascular events. Unlike the larger lipoprotein particles which deliver fat molecules to cells, HDL particles remove fat molecules from cells which need to export fat molecules. The lipids carried include cholesterol, phospholipids, and triglycerides, amounts of each are quite variable. Increasing concentrations of HDL particles are strongly associated with decreasing accumulation of atherosclerosis within the walls of arteries. This is important because atherosclerosis eventually results in sudden plaque ruptures, cardiovascular disease, stroke and other vascular diseases."
"ULDL Ultra Low Density Lipoproteins (ULDL), historically commonly called chylomicrons (dating to before these particles were better characterized and understood) are one of the five major groups of lipoprotein, as divided by density or size [an inherently inverse relationship because the larger particles (higher ratio of fat molecules inside compared with the outer emulsifying protein molecules in the shell) and fats are always lower density than either protein or water molecules, i.e. fats float in water.]. Specifically they are the largest and only lipoprotein particles (which transport fat molecules around the body in the water outside cells) which can sometimes"
"measure all lipoprotein subfractions ( VLDL, IDL, LDL, and HDL) when assessing hypercholesterolemia and measurement of apolipoproteins and lipoprotein (a) can also be of value. Genetic screening is now advised if a form of familial hypercholesterolemia is suspected. Classically, hypercholesterolemia was categorized by lipoprotein electrophoresis and the Fredrickson classification. Newer methods, such as ""lipoprotein subclass analysis"", have offered significant improvements in understanding the connection with atherosclerosis progression and clinical consequences. If the hypercholesterolemia is hereditary (familial hypercholesterolemia), more often a family history of premature, earlier onset atherosclerosis is found. The U.S. Preventive Services Task Force in 2008 strongly recommends routine"
"Very low-density lipoprotein Very-low-density lipoprotein (VLDL), density relative to extracellular water, is a type of lipoprotein made by the liver. VLDL is one of the five major groups of lipoproteins (chylomicrons, VLDL, intermediate-density lipoprotein, low-density lipoprotein, high-density lipoprotein) that enable fats and cholesterol to move within the water-based solution of the bloodstream. VLDL is assembled in the liver from triglycerides, cholesterol, and apolipoproteins. VLDL is converted in the bloodstream to low-density lipoprotein (LDL) and intermediate-density lipoprotein (IDL). VLDL particles have a diameter of 30–80 nm. VLDL transports endogenous products, whereas chylomicrons transport exogenous (dietary) products. Recently both the lipid composition"
"widely available and increasingly regarded as important for assessing individual risk for progressive arterial disease and treatment methods. Since the HDL particles have a net negative charge and vary by density & size, ultracentrifugation combined with electrophoresis have been utilized since before 1950 to enumerate the concentration of HDL particles and sort them by size with a specific volume of blood plasma. Larger HDL particles are carrying more cholesterol. Concentration and sizes of lipoprotein particles can be estimated using nuclear magnetic resonance fingerprinting. The HDL particle concentrations are typically categorized by event rate percentiles based on the people participating and"
"including subtypes), and each are classified from both the altered lipid profile and by the genetic abnormality. For example, high LDL (often due to LDL receptor defect) is type 2. Others include defects in chylomicron metabolism, triglyceride metabolism, and metabolism of other cholesterol-containing particles, such as VLDL and IDL. About 1 in 300 to 500 people have mutations in the ""LDLR"" gene that encodes the LDL receptor protein, which normally removes LDL from the circulation, or apolipoprotein B (ApoB), which is the part of LDL that binds with the receptor; mutations in other genes are rare. People who have one"
"maintaining electron transport chain in mitochondria. They participate in the reverse cholesterol transport and thus help in the removal of cholesterol from the body. They are involved in signal transmission across membranes and they act as detergents and help in solubilization of cholesterol. Lipoprotein: These consist of a central core of a hydrophobic lipid (including TGs and cholesteryl esters) encased in a hydrophilic coat of polar phospholipid, free cholesterol and apolipoprotein. There are six main classes of lipoprotein, differing in the relative proportion of the core lipids and in the type of apoprotein. Men tend to have noticeably lower HDL"
"VLDL will come in contact with lipoprotein lipase (LPL) in the capillary beds in the body (adipose, cardiac, and skeletal muscle). LPL will remove triglycerides from VLDL for storage or energy production. VLDL now meets back up with HDL where apoC-II is transferred back to HDL (but keeps apoE). HDL also transfers cholesteryl esters to the VLDL in exchange for phospholipids and triglycerides via cholesterylester transfer protein (CETP). As more and more triglycerides are removed from the VLDL because of the action of LPL and CETP enzymes, the composition of the molecule changes, and it becomes intermediate-density lipoprotein (IDL). Fifty"
"(if large enough, at close to about 1,000 microns or more) be seen using only a light microscope, at maximum magnification. All the other classes are submicroscopic, one of the reasons these particles were long difficult to identify and better understand. ULDL Ultra Low Density Lipoproteins (ULDL), historically commonly called chylomicrons (dating to before these particles were better characterized and understood) are one of the five major groups of lipoprotein, as divided by density or size [an inherently inverse relationship because the larger particles (higher ratio of fat molecules inside compared with the outer emulsifying protein molecules in the shell)"
"Lipoprotein such as HDL. When HDL takes up free fatty acids from cells to prevent plaque build-up, it begins to increase its overall negative charge and instead stimulates HL to catalysis the triacylglycerides inside of VLDL (very low density lipoprotein). This is because the build-up of negative charge in HDL inhibits binding, but will allow HL to catalyze other lipoproteins. Other lipoproteins, such as ApoE, works in a similar way by inhibiting binding of HL and HDL but will allow HL to catalyze other lipoproteins. Other factors that contribute the regulation of HL are due to sex differences between women"
"that is hypercholesterolemia, hypertriglyceridemia or both in combined hyperlipidemia. Elevated levels of Lipoprotein(a) may also be classified as a form of hyperlipidemia. Familial hyperlipidemias are classified according to the Fredrickson classification, which is based on the pattern of lipoproteins on electrophoresis or ultracentrifugation. It was later adopted by the World Health Organization (WHO). It does not directly account for HDL, and it does not distinguish among the different genes that may be partially responsible for some of these conditions. Type I hyperlipoproteinemia exists in several forms: Type I hyperlipoproteinemia usually presents in childhood with eruptive xanthomata and abdominal colic. Complications"
"for primary or secondary prevention of cardiovascular disease. Though it has not yet been FDA-approved, the PPAR modulator (sometimes referred to as a SARM) GW501516, currently a research chemical (not for human consumption), has shown a positive effect on HDL-C and an antiatherogenic where LDL is an issue. High-density lipoprotein HDL particles have long been divided into 5 subgroups, by density/size (an inverse relationship), which also correlates with function and incidence of cardiovascular events. Unlike the larger lipoprotein particles which deliver fat molecules to cells, HDL particles remove fat molecules from cells which need to export fat molecules. The lipids"
"known as ""multiple-type hyperlipoproteinemia"") is a commonly occurring form of hypercholesterolemia (elevated cholesterol levels) characterized by increased LDL and triglyceride concentrations, often accompanied by decreased HDL. On lipoprotein electrophoresis (a test now rarely performed) it shows as a hyperlipoproteinemia type IIB. It is the most common inherited lipid disorder, occurring in about one in 200 persons. In fact, almost one in five individuals who develop coronary heart disease before the age of 60 has this disorder. The elevated triglyceride levels (>5 mmol/l) are generally due to an increase in very low density lipoprotein (VLDL), a class of lipoprotein prone to"
"HDL has the ability to bind LPS and LTA, creating HDL-LPS complexes to neutralize the harmful effects in the body and clear the LPS from the body. HDL also has significant roles interacting with cells of the immune system to modulate the availability of cholesterol and modulate the immune response itself. Under certain abnormal physiological conditions such as system infection or sepsis, the major components of HDL become altered, The composition and quantity of lipids and apolipoproteins are altered as compared to normal physiological conditions, such as a decrease in HDL cholesterol (HDL-C), phospholipids, apoA-I (a major lipoprotein in HDL"
"LDL receptor-binding domain of apoE indicates that the protein forms an unusually elongated four-helix bundle that may be stabilised by a tightly packed hydrophobic core that includes leucine zipper-type interactions and by numerous salt bridges on the mostly charged surface. Basic amino acids important for LDL receptor binding are clustered into a surface patch on one long helix. There are two major types of apolipoproteins. Apolipoproteins B form low-density lipoprotein (sometimes referred to as ""bad cholesterol"") particles. These proteins have mostly beta-sheet structure and associate with lipid droplets irreversibly. Most of the other apolipoproteins form high-density lipoprotein (""good cholesterol"") particles."
"relevance to human phenotypes. The G1 is a pair of two non-synonymous single nucleotide polymorphisms (SNPs) in almost complete linkage disequilibrium. G2 is an in-frame deletion of the two amino acid residues, N388 and Y389. Apolipoprotein L1 (apoL1) is a minor apoprotein component of HDL (High-density lipoprotein) or 'good cholesterol' which is synthesized in the liver and also in many other tissues, including pancreas, kidney, and brain. APOL1 is found in vascular endothelium, liver, heart, lung, placenta, podocytes, proximal tubules, and arterial cells. The protein has a secreted form that allows it to circulate in the blood. It forms a"
"Lipoprotein lipase Lipoprotein lipase (LPL) () is a member of the lipase gene family, which includes pancreatic lipase, hepatic lipase, and endothelial lipase. It is a water-soluble enzyme that hydrolyzes triglycerides in lipoproteins, such as those found in chylomicrons and very low-density lipoproteins (VLDL), into two free fatty acids and one monoacylglycerol molecule. It is also involved in promoting the cellular uptake of chylomicron remnants, cholesterol-rich lipoproteins, and free fatty acids. LPL requires ApoC-II as a cofactor. LPL is attached to the luminal surface of endothelial cells in capillaries by the protein glycosylphosphatidylinositol HDL-binding protein 1 (GPIHBP1) and by heparan"
"with 80 to 100 additional ancillary proteins. Each LDL has a highly hydrophobic core consisting of polyunsaturated fatty acid known as linoleate and hundreds to thousands (about 1500 commonly cited as an average) esterified and unesterified cholesterol molecules. This core also carries varying numbers of triglycerides and other fats and is surrounded by a shell of phospholipids and unesterified cholesterol, as well as the single copy of Apo B-100. LDL particles are approximately 22 nm (0.00000087 in.) to 27.5 nm in diameter and have a mass of about 3 million daltons. Since LDL particles contain a variable and changing number"
"percent of IDLs are recognized by receptors in the liver cells because of the apolipoprotein B-100 (apoB-100) and apoE they contain and are endocytosed. The other 50% of IDL lose apoE; when their cholesterol content becomes greater than the content of triglyceride, they become LDL, with apoB-100 as the primary apolipoprotein. The LDL is taken into a cell via the LDL receptor via endocytosis, where the contents are either stored, used for cell membrane structure, or converted into other products such as steroid hormones or bile acids. Very low-density lipoprotein Very-low-density lipoprotein (VLDL), density relative to extracellular water, is a"
"fats available to body cells for receptor-mediated endocytosis. Lipoproteins are complex particles composed of multiple proteins, typically 80–100 proteins/particle (organized by a single apolipoprotein B for LDL and the larger particles). A single LDL particle is about 220–275 angstroms in diameter, typically transporting 3,000 to 6,000 fat molecules/particle, and varying in size according to the number and mix of fat molecules contained within. The lipids carried include all fat molecules with cholesterol, phospholipids, and triglycerides dominant; amounts of each varying considerably. LDL particles pose a risk for cardiovascular disease when they invade the endothelium and become oxidized, since the oxidized"
"YWTD domain of low-density lipoprotein receptor The low-density lipoprotein receptor (LDLR) regulates cholesterol homeostasis in mammalian cells. LDLR binds cholesterol-carrying LDL, associates with clathrin-coated pits, and is internalized into acidic endosomes where it separates from its ligand. The ligand is degraded in lysosomes, while the receptor returns to the cell surface. The LDLR has several domains. The ligand-binding domain contains seven LDL receptor class A repeats, each with three disulphide bonds and a coordinated Ca ion. The second conserved region contains two EGF repeats, followed by six YWTD or LDL receptor class B repeats and another EGF repeat. This conserved"
"intermediate-density lipoprotein (IDL), which is capable of scavenging cholesterol from the blood. This converts IDL into low-density lipoprotein (LDL), which is taken up by cells that require cholesterol for incorporation into their cell membranes or for synthetic purposes (e.g. the formation of the steroid hormones). The remainder of the LDLs is removed by the liver. Adipose tissue and lactating mammary glands also take up glucose from the blood for conversion into triglycerides. This occurs in the same way as it does in the liver, except that these tissues do not release the triglycerides thus produced as VLDL into the blood."
"protein contents/ proteins they carry . While the research is currently ongoing and there are still many details to be uncovered, researchers are learning that different subspecies contain different apolipoproteins, proteins, and lipid contents between species which have different physiological roles . For example, within the HDL lipoprotein subspecies, a large number of proteins are involved in general lipid metabolism . However, it is being elucidated that HDL subspecies also contain proteins involved in the following functions: homeostasis, fibrinogen, clotting cascade, inflammatory and immune responses, including the complement system, proteolysis inhibitors, acute-phase response proteins, and the LPS-binding protein, heme and"
"often found bound to HSPG, heparan sulfate proteoglycans (HSPG), keeping HL inactive and unable to bind to HDL (high density lipoprotein) or IDL (intermediate density lipoprotein). When it is free in the bloodstream, however, it is found associated with HDL to maintain it inactive. This is because the triacylglycerides in HDL serve as a substrate, but the lipoprotein contains proteins around the triacylglycerides that can prevent the triacylglycerides from being broken down by HL. One of the principal functions of hepatic lipase is to convert intermediate-density lipoprotein (IDL) to low-density lipoprotein (LDL). Hepatic lipase thus plays an important role in"
"the receptor ligand ApoE in addition to a single copy of ApoB-100. The multiple copies of ApoE allow IDL to bind to the LDL receptor with a very high affinity. When IDL is converted to LDL, the ApoE leaves the particle and only the ApoB-100 remains. Thereafter, the affinity for the LDL receptor is much reduced. Intermediate-density lipoprotein Intermediate-density lipoproteins (IDLs) belong to the lipoprotein particle family and are formed from the degradation of very low-density lipoproteins as well as high-density lipoproteins. IDL is one of the five major groups of lipoproteins (chylomicrons, VLDL, IDL, LDL, HDL) that enable fats"
"by the liver that transports triglyceride to adipose tissue and muscle. The triglycerides in VLDL are removed in capillaries by the enzyme lipoprotein lipase, and the VLDL returns to the circulation as a smaller particle with a new name, intermediate-density lipoprotein (IDL). The IDL particles have lost most of their triglyceride, but they retain cholesteryl esters. Some of the IDL particles are rapidly taken up by the liver; others remain in circulation, where they undergo further triglyceride hydrolysis by hepatic lipase and are converted to LDL. A distinguishing feature of the IDL particle is their content of multiple copies of"
"cytokines (interleukin 1, interleukin 6), and cortisol produced in the adrenal cortex and carried to the damaged tissue incorporated into HDL particles. At the inflammation site, it attracts and activates leukocytes. In chronic inflammations, its deposition in the tissues manifests itself as amyloidosis. It has been postulated that the concentration of large HDL particles more accurately reflects protective action, as opposed to the concentration of total HDL particles. This ratio of large HDL to total HDL particles varies widely and is measured only by more sophisticated lipoprotein assays using either electrophoresis (the original method developed in the 1970s) or newer"