VLDL vs. LDL: What’s the Difference?
This study offers information on the relationship between some lipoprotein . tion of LDL-C between groups while behaviour of VLDL-C, VLDL-TG, HDL-C. The main difference between VLDL and LDL is that they have different percentages of the cholesterol, protein, and triglycerides that make up each lipoprotein. In fact, the VLDL and LDL exhibit a continuum of decreasing size and density. exchange between lipoprotein classes and acquire lipids during circulation. .. of lipoproteins in the metabolism of triacylglycerol and cholesterol in relation to.
The amphipathic surface monolayer has a single copy of apo B together with about phospholipid and free cholesterol molecules. Phosphatidylcholine, about molecules, and sphingomyelin, about molecules, are the main phospholipids, together with smaller numbers of lysophosphatidylcholine, phosphatidylethanolamine and other lipid molecules.
The structure and physical functions of LDLs depend mainly on the core—lipid composition and the conformation of the apoB, which is able to interact with extracellular membranes such as blood vessel intima where the LDL lipids are susceptible to modification, e. In contrast, HDL are highly heterogeneous in terms of their size, lipid and protein contents, and their functional properties, and they can be separated by various means into subclasses, HDL1, HDL2, HDL3, etc, that reflect the differences in composition.
Discoidal nascent HDL particles are believed to consist of a small unilamellar bilayer, containing approximately molecules of phospholipid, which is surrounded by four apoprotein molecules, including at least two apo A1 monomers. Although most HDL particles in human plasma are spherical, the structures are poorly characterized in comparison to discoidal HDL.
It is believed that the apoA-I molecule changes conformation from the discoidal state and adopts a helical structure with the C-terminal domain binding to the phospholipids. Lipoproteins can be categorized simplistically according to their main metabolic functions. While these functions are considered separately for convenience in the discussion that follows, it should be recognized that the processes are highly complex and inter-related, and they involve transfer of apoproteins, enzymes and lipid constituents among the heterogeneous mix of all the lipoprotein fractions.
In addition to the apoproteins, lipoproteins carry a number of enzymes with important functions, including lipases, acyltransferases, transport proteins and some with anti-oxidative or anti-inflammatory properties; some are concerned with metabolic processes that do not involve lipids.
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- Definition of HDL, LDL & VLDL
- Cholesterol, Lipoproteins and the Liver
As birds, amphibians, fishes and even round worms have lipoprotein systems comparable to those in mammals, it is evident that these must have developed early in evolution. The equivalent protein in these species is vitellogin, which is closely related to mammalian apo B. Lipoprotein a Lp a is structurally and metabolically distinct from the other lipoproteins, and it consists of an LDL-like particle containing a specific highly polymorphic glycoprotein named apolipoprotein a apo awhich is covalently bound via a disulfide bond to the apo B of the LDL-like particle.
Cholesterol, lipoproteins and the liver
While its physiological function is uncertain, it is of particular interest in that there is an appreciable homology between apo a and the fibrinolytic proenzyme plasminogen and because it is a risk factor for cardiovascular disease see below. Apo a should not be confused with apo A.
Lipoprotein and Triacylglycerol Metabolism Triacylglycerols are the most energy-dense molecules available to the body as a source of fuel but are highly hydrophobic. For efficient transport from the intestine and the liver to other organs of the body, it is essential that they be packaged in a form compatible with the aqueous environment in plasma, i.
Chylomicrons and VLDL are mainly involved, although some proteins that are shared with HDL are essential for the process to function normally. For example, exchangeable apoproteins protect triacylglycerol-rich particles from non-specific interactions in plasma and ensure that they have the correct configuration to be acted upon by lipases. Dietary fatty acids and monoacylglycerols are absorbed by the enterocytes in the intestines, where they must cross the cytoplasm to the endoplasmic reticulum with the aid of fatty acid binding proteins.
These are immediately utilized to form new triacylglycerols, and are thus detoxified see our web page on triacylglycerol biosynthesismainly by the monoacylglycerol pathway. The triacylglycerols are incorporated together with dietary cholesterol, much of which is in cholesterol ester form, into spherical chylomicron particles.
These have a surface layer of phospholipids to which is attached a single molecule of the truncated form of apo B, apo B48, which is diagnostic for triacylglycerol-rich lipoproteins of intestinal origin. The synthesis of apo B and its truncated form, and the accumulation of lipids to form chylomicrons or VLDL in intestinal cells and liver, respectively, are complex processes that are still only partly understood.HDL and LDL Explained (Made Easy to Understand, Updated Version)
Simplistically, secretory proteins such as apo B are synthesised on ribosomes on the surface of the endoplasmic reticulum and translocated through the membrane to the lumen of the endoplasmic reticulum.
VLDL are then assembled by accretion of lipids, for example with the aid of a microsomal triacylglycerol transfer protein MTTPan essential protein that transfers phospholipids and triacylglycerols to nascent apo B for the assembly of lipoproteins.
This occurs in three stages - pre-VLDL pre-chylomicrons - nascent lipoproteinsVLDL2, a triacylglycerol-poor form of VLDL that is assembled in the Golgi and is transported to the basolateral membrane, where the final triacylglycerol-rich VLDL1 or chylomicrons with the assistance of apo B48 and apo A4, are secreted by a process of reverse exocytosis into the intestinal lamina propria.
Apo A1 is generated separately in the endoplasmic reticulum of enterocytes, and it is transported to the Golgi and added to the chylomicrons just before the mature particle is secreted into the lymph. The chylomicrons are transported via the intestinal lymphatic system and enter the blood stream at the left subclavian vein. During circulation throughout the body, triacylglycerols are removed by the peripheral tissues by endothelial-bound lipoprotein lipase with entry of fatty acids into muscle for energy production and adipocytes for storage.
However, the apo B48 remains with the residual particle. The chylomicrons also contain some apo A1, which is synthesised in the intestines and liver, but this is transferred spontaneously to the HDL as soon as the chylomicrons reach the circulation, while transfer of apo E and apo C in the reverse direction from the HDL to the surface of the chylomicrons, displacing apo A4, occurs at the same time.
The main LDL receptor in liver is a polypeptide of amino acids to which complex carbohydrate moieties are linked that spans the plasma membrane and has an extracellular domain, which is responsible for binding to apo B and apo E. After binding of the LDL and some of the VLDL remnants to the receptor, the LDL-receptor complexes are internalized by endocytosis of the coated pit and then dissociated by means of an ATP-dependent proton pump, which lowers the pH in the endosomes, enabling the receptors to be recycled to the plasma membrane.
The LDL-containing endosomes fuse with lysosomes, and lipolytic enzymes, especially a lysosomal acid lipase LALrelease free fatty acids and cholesterol from triacylglycerols and cholesterol esters, while acid hydrolases degrade the apoproteins. However, much of the apo E is believed to escape this process and is returned to the circulation and the HDL.
An additional receptor, the LDL-receptor-related-protein, assists in the removal of chylomicron remnants. After their release from lysosomes, the fatty acids and other lipid components serve as precursors for the synthesis of new lipid species and may also function in the regulation of many metabolic processes. Secretion from the liver: The triacylglycerols of the remnant chylomicrons, together with cholesterol and cholesterol esters, are secreted by the liver into the circulation in the form of VLDL, which contain one molecule of the full-length form of apo B, apo B In addition, an appreciable amount of triacylglycerol in VLDL is synthesised in the liver from free fatty acids reaching it from adipose tissue via the plasma in the post-absorptive and fasted states, and stored in triacylglycerol form in lipid droplets for mobilization upon demand.
In effect, liver lipid droplets and VLDL serve to buffer the plasma free fatty acids released following lipolysis in adipose tissue in excess of the requirements of muscle and liver. Within the liver, the nascent VLDLs consisting largely of triacylglycerol droplets with the apo B are synthesised in the endoplasmic reticulum, and they are transported to the Golgi in a complex multistep process, involving a specific VLDL transport vesicle.
In the lumen of the cis-Golgi lumen, VLDLs undergo a number of essential modifications before they are transported to the plasma membrane and secreted into the circulatory system.
Definition of HDL, LDL & VLDL | Healthy Eating | SF Gate
The surface layer of the newly synthesised VLDL is enriched in phosphatidylethanolamine, which rapidly exchanges with the phosphatidylcholine of other lipoproteins. The newly synthesised VLDL contain a little apo C3, apo E and apo A5, which may have a role in the assembly process, but they rapidly take up apo C2 molecules and apo E from HDL after a few minutes in the circulation while the small amount of apo A1 of intestinal origin is transferred to HDL.
Lipoprotein lipase, the key enzyme in the peripheral tissues that is responsible for the hydrolysis of triacylglycerols from the chylomicrons and VLDL, is bound to the vascular surface of the endothelial cells of the capillaries of adipose tissue, heart and skeletal muscle, and lactating mammary gland primarily.
The enzyme is synthesised in the endoplasmic reticulum where it is activated by lipase maturation factor 1 LMF1before the complex is stabilized by a chaperone so that it attains a proper tertiary fold before its assembly into homodimers, arranged in a head-to-tail orientation, for transport to the luminal surface of endothelial cells.
A small glycosylphosphatidylinositol-anchored protein designated GPIHBP1 facilitates the transfer of lipoprotein lipase across the cell, and in concert with heparin sulfate-proteoglycans HSPG on the capillary wall anchors the enzyme to the endothelial cell surface.
Apo C2 is an absolute requirement for activation of the enzyme, and there is evidence that this opens a lid-like region of the enzyme to enable the active site to hydrolyse the fatty acid ester bonds of the triacylglycerols; apo A5 is also stimulatory. However, monoacylglycerols can be taken up directly by cells and are not found in the remnant lipoproteins or bound to circulating albumin. As the transport of VLDL particles progresses, the core of triacylglycerols is reduced and the proteins, including apo C2, and phospholipids on the surface are transferred away to the HDL.
However, sufficient apo C2 remains to ensure that most of the triacylglycerols are removed. As partially delipidated lipoproteins are detected in the circulation, it is believed that there is a process of dissociation and rebinding to the enzyme, during each step of which triacylglycerols are hydrolysed and apo C2 is gradually released with formation of remnant particles.
Lipoprotein lipase is also involved in the non-hydrolytic uptake of esters of cholesterol and retinol, possibly by facilitating transport. Some of the unesterified fatty acids resulting from the action of lipoprotein lipase are taken up immediately by the cells by both receptor-mediated and receptor-independent pathways, where they can be used for energy purposes or for the synthesis of other lipids. The remainder is bound to circulating albumin from which it is released slowly to meet the cellular requirements of peripheral tissues.
The glycerol produced is transported back to the liver and kidneys, where it can be converted to the glycolytic intermediate dihydroxyacetone phosphate. In muscle tissue, much of the fatty acids taken up are oxidized to two-carbon units, but in adipose tissue triacylglycerols are formed for storage purposes while in lactating mammary gland they are used for milk fat synthesis.
During fasting, hormone-sensitive lipase releases fatty acids from the triacylglycerols stores and they are transported back into the circulation. Apo C1 and apo C3 inhibit lipoprotein lipase by competing for binding to lipoproteins rather than by deactivating the enzyme.
Apo C3 inhibits the hepatic uptake of VLDL remnants also and so has a controlling influence on the turnover of triacylglycerols; high levels have been correlated with elevated levels of blood lipids hypertriglyceridemia.
In addition, angiopoietin-like proteins are key regulators of plasma lipid metabolism by serving as potent inhibitors of lipoprotein lipase. Improper regulation of the enzyme has been associated with the pathologies of atherosclerosis, coronary heart disease, cerebrovascular accidents, Alzheimer disease and chronic lymphocytic leukemia. VLDL, LDL and Cholesterol Metabolism Cholesterol has a vital role in life and is essential for the normal functioning of cells both as a cell membrane constituent and as a precursor of steroid hormones and other key metabolites.
In the lumen of the small intestine, free cholesterol from the diet and from biliary secretion is solubilized in mixed micelles containing bile acids and phospholipids before it is absorbed by the enterocytes by a mechanism for which the apical protein Niemann-Pick C1-like 1 NPC1L1 is crucial.
Within the enterocyte, the metabolic fate of the absorbed cholesterol involves an integrated network of many different proteins. Over time, the extra wear and tear on your heart makes your heart muscle weak, elevating your risk of heart disease. Your low-density lipoprotein needs to stay below milligrams per deciliter, reports the National Heart, Lung, and Blood Institute. Diet and exercise can help bring your low-density lipoprotein into a normal range if it gets too high.
However, in severe cases, your doctor may have to prescribe a cholesterol-lowering medication. VLDL Very-low-density lipoprotein is especially harmful because is made up of even more triglycerides, a type of fat, than low-density lipoprotein and thus further increases your risk of heart disease whenever levels get too high.
A healthy range of very-low-density lipoprotein falls between 2 and 30 milligrams per deciliter. Typical blood cholesterol panels, however, may not include very-low-density lipoprotein, so you may need to specifically request this test. HDL is involved in reverse cholesterol transport. Excess cholesterol is eliminated from the body via the liver, which secretes cholesterol in bile or converts it to bile salts.
The liver removes LDL and other lipoproteins from the circulation by receptor-mediated endocytosis. Additionally, excess cholesterol from cells is brought back to the liver by HDL in a process known as reverse cholesterol transport green pathway.
It travels in the circulation where it gathers cholesterol to form mature HDL, which then returns the cholesterol to the liver via various pathways. Disorders and Drug Treatments The link between cholesterol and heart disease was recognized through the study of individuals with familial hypercholesterolemia. Individuals with this disorder have several-fold higher levels of circulating LDL due to a defect in the function of their LDL receptors. As well, because cholesterol cannot get into cells efficiently, there is no negative feedback suppression of cholesterol synthesis in the liver.
Individuals with familial hypercholesterolemia may have strokes and heart attacks starting in their 30's. More common in the general population is dyslipidemia, which is the term that is used if lipid levels are outside the normal range. In a typical lipid profile, the fasting levels of total cholesterol, LDL cholesterol, HDL cholesterol, and triglycerides are determined.
Low levels of HDL cholesterol the so-called "good cholesterol" are an independent risk factor, because reverse cholesterol transport works to prevent plaque formation, or may even cause regression of plaques once they have formed. HDL may also have anti-inflammatory properties that help reduce the risk of atherosclerosis. Fasting triglyceride levels are used to estimate the level of VLDL. High levels of triglycerides are also associated with an increased risk for atherosclerosis, although the mechanism is not entirely clear.
The most important drugs for the treatment of dyslipidemia are by far, the statins. Statins have been shown in multiple clinical trials to reduce cardiovascular events and mortality. Inhibition of cholesterol synthesis further decreases circulating LDL because reduced levels of cholesterol in the hepatocyte cause it to upregulate expression of LDL receptors. In the past, several different drugs have been used to treat dyslipidemia, however the most recent treatment guidelines recommend mainly statin therapy at different intensities according to the patient's risk for cardiovascular disease.