All lipids are hydrophobic and not soluble in the blood for the most part, so they need to transport them hydrophilic, spherical structures called. Lipoproteins. Lipoproteins have (apoproteins or apolipoproteins) surface proteins, cofactors and ligands for lipidverstoffwechselnde enzymes (see Table: Major apoproteins and enzymes that are important for lipid metabolism). Lipoproteins are depending on the size and density (defined as the ratio of lipid to protein) classified and are important because high levels of low-density lipoproteins (LDL) and low levels of high-density lipoproteins (HDL) are important risk factors of coronary heart disease.

Lipids are fats that are either absorbed from the diet or synthesized by the liver. Triglycerides (TG) and cholesterol are the main contributors to the emergence of diseases, but ultimately all lipids are physiologically significant. The primary function of the triglycerides is the conservation of energy in adipocytes and muscle cells; Cholesterol is a ubiquitous component of cell membranes, steroids, bile acids and signaling molecules. All lipids are hydrophobic and not soluble in the blood for the most part, so they need to transport them hydrophilic, spherical structures called. Lipoproteins. Lipoproteins have (apoproteins or apolipoproteins) surface proteins, cofactors and ligands for lipidverstoffwechselnde enzymes (see Table: Major apoproteins and enzymes that are important for lipid metabolism). Lipoproteins are depending on the size and density (defined as the ratio of lipid to protein) classified and are important because high levels of low-density lipoproteins (LDL) and low levels of high-density lipoproteins (HDL) are important risk factors of coronary heart disease. Significant apoproteins and enzymes that are important for lipid metabolism ingredients place function apoproteins Apo A-I HDL main component of the HDL particle Apo A-II HDL component of the HDL particle Apo B-100 VLDL, IDL, LDL, Lp (a) LDL receptor ligand Apo B-48 chylomicrons main component of the chylomicron Apo C-II chylomicrons, VLDL, HDL LPL cofactor apo C-III chylomicrons, VLDL, HDL Inhibits LPL Apo E chylomicrons, remnants, VLDL, HDL LDL receptor ligand Apo (a) Lp (a) component of Lp (a) and left of the LDL particle enzymes ABCA1 involved in cell in the intracellular transport of cholesterol to the membrane CETP HDL mediates the transfer of cholesteryl esters from HDL to VLDL LPL endothelium Hydrolyses triglycerides of chylomicrons and VLDL to release free fatty acids LCAT HDL esterified free cholesterol for transport to HDL ABCA1 = ATP-binding cassette transporter A1; apo = apoprotein; CETP cholesteryl ester = protein; HDL = high-density lipoprotein; IDL = intermediate density lipoprotein; LCAT lecithin-cholesterol acyltransferase =; LDL = low-density lipoprotein; LPL = lipoprotein lipase, Lp (a) lipoprotein = (a); VLDL = very-low-density lipoprotein. Clinical Calculator: Framingham 10-year risk of general cardiovascular disease in men (Article 2008) clinical calculator: 10-year CHD risk prediction by Framingham basis of total cholesterol [1998: deprecated] Clinical Calculator: Framingham 10-year prediction of coronary risk than LDL physiology defects of the metabolic pathways in lipoprotein synthesis, processing and degradation can lead to the accumulation of atherogenic lipids in plasma and endothelium. Exogenous (food-related) lipid metabolism About 95% of the lipids contained in food are triglycerides, the rest are phospholipids, free fatty acids (FFA), cholesterol (in the diet as Cholesterinester included) and fat-soluble vitamins. The Nahrungstriglyceride be cleaved in the stomach and in the duodenum using the gastric lipase in monoglycerides (MG) and FFA and emulsified by the peristalsis of the stomach by using the pancreatic lipase. The Cholesterinester from the food are transferred through the same mechanism in free cholesterol. MG, FFA and free cholesterol are then dissolved in the intestine by Gallensäuremizellen and passed to the absorption to the intestinal villi. Once collected in enterocytes, they are reassembled to TGs and together with cholesterol in chylomicrons, the largest lipoproteins, packaged. Chylomicrons transport Nahrungstriglyceride and cholesterol of the enterocytes by lymphatic vessels in the bloodstream. In the capillaries of fat and muscle tissue apoprotein C-II (Apo C-II) activates the endothelial lipoprotein lipase chylomicrons (LPL) to 90% of TGs contained in the chylomicrons into free fatty acids and glycerol to convert. These are taken up by adipocytes and muscle cells for energy production or storage. Chylomicron remnants, which are rich in cholesterol, return to the liver where they werden.Endogener in a process (Apo E) is mediated by apoprotein E, reduced lipid metabolism lipoproteins which are synthesized in the liver, carry endogenous TGs and cholesterol. The lipoproteins circulate so long in circulation until the TGs they contain added in peripheral tissues or lipoproteins are rebuilt itself in the liver. Factors that stimulate hepatic lipoprotein, generally lead to elevated plasma cholesterol and triglyceride levels. Very-low-density lipoproteins (VLDL) contain apoprotein B-100 (Apo B), are synthesized in the liver and transported TGs and cholesterol into the peripheral tissues. VLDL is the form in which exports the liver in excess known TGs derived from plasma FFA and chylomicron remnants,; VLDL synthesis increases with the increase of the intrahepatic FFAs. This is done at a very high fat diet or if excessive fat tissue available, the FFAs directly emits in the bloodstream (z. B. in obesity, uncontrolled diabetes mellitus). Apo C-II on the surface of activated endothelial LPL VLDL, converts the TGs in FFAs and glycerol, which are then absorbed by the cells. IIntermediate density lipoproteins (IDL) arise then be further processed by LPL if VLDL and chylomicrons using. IDLs are cholesterol VLDL and chylomicron remnants, which are metabolized by hepatic lipase to LDL, retains the Apo B. Low-density lipoprotein (LDL), the product of the metabolism of VLDL and IDL, is the richest of all cholesterol lipoproteins. Approximately 40-60% of all LDLs are in the liver in a process that is mediated by Apo B and hepatic LDL receptors degraded. The remainder is either by hepatic LDL or non-hepatic non-LDL (scavenger) was added receptors. Hepatic LDL receptors are down-regulated by the delivery of cholesterol in the liver by chylomicrons or by a high proportion of saturated fatty acids in the dietary fat; they can be upregulated by reduced fat and cholesterol content of food again. Non-hepatic scavenger receptors, v. a. on macrophages, take excess oxidized, circulating LDL, which was not further processed by hepatic receptors on. Monocytes, which are rich in oxidized LDL, migrate into the subendothelial space and become macrophages; they then take on more oxidized LDL and form within atherosclerotic plaque foam cells (atherosclerosis: Pathophysiology). The size of the LDL particles varies from large and floatable towards small and dense. Small dense LDL are particularly rich in Cholesterinestern and with metabolic disorders such. brought as hypertriglyceridemia and insulin resistance in combination and are particularly atherogenic. The enhanced atherogenicity of small dense LDLs is due to a less effective binding to the hepatic LDL receptor forth, which in turn resulting in prolonged circulation and exposure to endothelial cells, and also to increased oxidation. High-density lipoproteins (HDL) are initial cholesterol-free lipoproteins that are synthesized in both the liver and in the enterocytes. The HDL metabolism is complex. One of the tasks of HDLs to absorb cholesterol from the peripheral tissues or from other lipoproteins and it to bring where it is needed most Р(other cells to other lipoproteins (using cholesteryl [CETP]) and liver to degradation). Its overall effect is antiatherogenic. The release of free cholesterol out of cells is the so-called. ATP-binding cassette transporter A1 (ABCA1) conveys that combines with the protein A1 (Apo A-I) to form nascent HDL. The free cholesterol in the nascent HDL is then esterified by the enzyme lecithin-cholesterol acyltransferase (LCAT). The result is mature HDL. The HDL levels in the blood do not represent the reverse cholesterol transport completely. Lipoprotein (a) [Lp (a)] is LDL, apolipoprotein (a), and is characterized by five cysteine-rich regions, the so-called. Kringles. One of these regions showing homology to plasminogen and it is believed that the fibrinolysis competitively inhibited and so thrombosis formation is promoted. Lp (a) may also directly promote the development of atherosclerosis. The pathway of Lp (a) synthesis and degradation is not well characterized, but we know that the Lp in patients with diabetic nephropathy (a) increase values.

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