Apolipoproteins. Medical search

Protein components on the surface of LIPOPROTEINS. They form a layer surrounding the hydrophobic lipid core. There are several classes of apolipoproteins with each playing a different role in lipid transport and LIPID METABOLISM. These proteins are synthesized mainly in the LIVER and the INTESTINES.

Structural proteins of the alpha-lipoproteins (HIGH DENSITY LIPOPROTEINS), including APOLIPOPROTEIN A-I and APOLIPOPROTEIN A-II. They can modulate the activity of LECITHIN CHOLESTEROL ACYLTRANSFERASE. These apolipoproteins are low in atherosclerotic patients. They are either absent or present in extremely low plasma concentration in TANGIER DISEASE.

A group of apolipoproteins that can readily exchange among the various classes of lipoproteins (HDL; VLDL; CHYLOMICRONS). After lipolysis of TRIGLYCERIDES on VLDL and chylomicrons, Apo-C proteins are normally transferred to HDL. The subtypes can modulate remnant binding to receptors, LECITHIN CHOLESTEROL ACYLTRANSFERASE, or LIPOPROTEIN LIPASE.

Major structural proteins of triacylglycerol-rich LIPOPROTEINS. There are two forms, apolipoprotein B-100 and apolipoprotein B-48, both derived from a single gene. ApoB-100 expressed in the liver is found in low-density lipoproteins (LIPOPROTEINS, LDL; LIPOPROTEINS, VLDL). ApoB-48 expressed in the intestine is found in CHYLOMICRONS. They are important in the biosynthesis, transport, and metabolism of triacylglycerol-rich lipoproteins. Plasma Apo-B levels are high in atherosclerotic patients but non-detectable in ABETALIPOPROTEINEMIA.

The most abundant protein component of HIGH DENSITY LIPOPROTEINS or HDL. This protein serves as an acceptor for CHOLESTEROL released from cells thus promoting efflux of cholesterol to HDL then to the LIVER for excretion from the body (reverse cholesterol transport). It also acts as a cofactor for LECITHIN CHOLESTEROL ACYLTRANSFERASE that forms CHOLESTEROL ESTERS on the HDL particles. Mutations of this gene APOA1 cause HDL deficiency, such as in FAMILIAL ALPHA LIPOPROTEIN DEFICIENCY DISEASE and in some patients with TANGIER DISEASE.

The second most abundant protein component of HIGH DENSITY LIPOPROTEINS or HDL. It has a high lipid affinity and is known to displace APOLIPOPROTEIN A-I from HDL particles and generates a stable HDL complex. ApoA-II can modulate the activation of LECITHIN CHOLESTEROL ACYLTRANSFERASE in the presence of APOLIPOPROTEIN A-I, thus affecting HDL metabolism.

A class of protein components which can be found in several lipoproteins including HIGH-DENSITY LIPOPROTEINS; VERY-LOW-DENSITY LIPOPROTEINS; and CHYLOMICRONS. Synthesized in most organs, Apo E is important in the global transport of lipids and cholesterol throughout the body. Apo E is also a ligand for LDL receptors (RECEPTORS, LDL) that mediates the binding, internalization, and catabolism of lipoprotein particles in cells. There are several allelic isoforms (such as E2, E3, and E4). Deficiency or defects in Apo E are causes of HYPERLIPOPROTEINEMIA TYPE III.

A 9-kDa protein component of VERY-LOW-DENSITY LIPOPROTEINS. It contains a cofactor for LIPOPROTEIN LIPASE and activates several triacylglycerol lipases. The association of Apo C-II with plasma CHYLOMICRONS; VLDL, and HIGH-DENSITY LIPOPROTEINS is reversible and changes rapidly as a function of triglyceride metabolism. Clinically, Apo C-II deficiency is similar to lipoprotein lipase deficiency (HYPERLIPOPROTEINEMIA TYPE I) and is therefore called hyperlipoproteinemia type IB.

A 9-kDa protein component of VERY-LOW-DENSITY LIPOPROTEINS and CHYLOMICRON REMNANTS. Apo C-III, synthesized in the liver, is an inhibitor of LIPOPROTEIN LIPASE. Apo C-III modulates the binding of chylomicron remnants and VLDL to receptors (RECEPTORS, LDL) thus decreases the uptake of triglyceride-rich particles by the liver cells and subsequent degradation. The normal Apo C-III is glycosylated. There are several polymorphic forms with varying amounts of SIALIC ACID (Apo C-III-0, Apo C-III-1, and Apo C-III-2).

A class of lipoproteins of small size (4-13 nm) and dense (greater than 1.063 g/ml) particles. HDL lipoproteins, synthesized in the liver without a lipid core, accumulate cholesterol esters from peripheral tissues and transport them to the liver for re-utilization or elimination from the body (the reverse cholesterol transport). Their major protein component is APOLIPOPROTEIN A-I. HDL also shuttle APOLIPOPROTEINS C and APOLIPOPROTEINS E to and from triglyceride-rich lipoproteins during their catabolism. HDL plasma level has been inversely correlated with the risk of cardiovascular diseases.

A glycoprotein component of HIGH-DENSITY LIPOPROTEINS that transports small hydrophobic ligands including CHOLESTEROL and STEROLS. It occurs in the macromolecular complex with LECITHIN CHOLESTEROL ACYLTRANSFERASE. Apo D is expressed in and secreted from a variety of tissues such as liver, placenta, brain tissue and others.

Lipid-protein complexes involved in the transportation and metabolism of lipids in the body. They are spherical particles consisting of a hydrophobic core of TRIGLYCERIDES and CHOLESTEROL ESTERS surrounded by a layer of hydrophilic free CHOLESTEROL; PHOSPHOLIPIDS; and APOLIPOPROTEINS. Lipoproteins are classified by their varying buoyant density and sizes.

A 6.6-kDa protein component of VERY-LOW-DENSITY LIPOPROTEINS; INTERMEDIATE-DENSITY LIPOPROTEINS; and HIGH-DENSITY LIPOPROTEINS. Apo C-I displaces APO E from lipoproteins, modulate their binding to receptors (RECEPTORS, LDL), and thereby decrease their clearance from plasma. Elevated Apo C-I levels are associated with HYPERLIPOPROTEINEMIA and ATHEROSCLEROSIS.

The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils.

A class of lipoproteins of very light (0.93-1.006 g/ml) large size (30-80 nm) particles with a core composed mainly of TRIGLYCERIDES and a surface monolayer of PHOSPHOLIPIDS and CHOLESTEROL into which are imbedded the apolipoproteins B, E, and C. VLDL facilitates the transport of endogenously made triglycerides to extrahepatic tissues. As triglycerides and Apo C are removed, VLDL is converted to INTERMEDIATE-DENSITY LIPOPROTEINS, then to LOW-DENSITY LIPOPROTEINS from which cholesterol is delivered to the extrahepatic tissues.

A generic term for fats and lipoids, the alcohol-ether-soluble constituents of protoplasm, which are insoluble in water. They comprise the fats, fatty oils, essential oils, waxes, phospholipids, glycolipids, sulfolipids, aminolipids, chromolipids (lipochromes), and fatty acids. (Grant & Hackh's Chemical Dictionary, 5th ed)

A 513-kDa protein synthesized in the LIVER. It serves as the major structural protein of low-density lipoproteins (LIPOPROTEINS, LDL; LIPOPROTEINS, VLDL). It is the ligand for the LDL receptor (RECEPTORS, LDL) that promotes cellular binding and internalization of LDL particles.

A 241-kDa protein synthesized only in the INTESTINES. It serves as a structural protein of CHYLOMICRONS. Its exclusive association with chylomicron particles provides an indicator of intestinally derived lipoproteins in circulation. Apo B-48 is a shortened form of apo B-100 and lacks the LDL-receptor region.

Cholesterol which is contained in or bound to high-density lipoproteins (HDL), including CHOLESTEROL ESTERS and free cholesterol.

Intermediate-density subclass of the high-density lipoproteins, with particle sizes between 7 to 8 nm. As the larger lighter HDL2 lipoprotein, HDL3 lipoprotein is lipid-rich.

An autosomal recessively inherited disorder caused by mutation of ATP-BINDING CASSETTE TRANSPORTERS involved in cellular cholesterol removal (reverse-cholesterol transport). It is characterized by near absence of ALPHA-LIPOPROTEINS (high-density lipoproteins) in blood. The massive tissue deposition of cholesterol esters results in HEPATOMEGALY; SPLENOMEGALY; RETINITIS PIGMENTOSA; large orange tonsils; and often sensory POLYNEUROPATHY. The disorder was first found among inhabitants of Tangier Island in the Chesapeake Bay, MD.

An enzyme secreted from the liver into the plasma of many mammalian species. It catalyzes the esterification of the hydroxyl group of lipoprotein cholesterol by the transfer of a fatty acid from the C-2 position of lecithin. In familial lecithin:cholesterol acyltransferase deficiency disease, the absence of the enzyme results in an excess of unesterified cholesterol in plasma. EC 2.3.1.43.

A class of lipoproteins of small size (18-25 nm) and light (1.019-1.063 g/ml) particles with a core composed mainly of CHOLESTEROL ESTERS and smaller amounts of TRIGLYCERIDES. The surface monolayer consists mostly of PHOSPHOLIPIDS, a single copy of APOLIPOPROTEIN B-100, and free cholesterol molecules. The main LDL function is to transport cholesterol and cholesterol esters to extrahepatic tissues.

Chemical analysis based on the phenomenon whereby light, passing through a medium with dispersed particles of a different refractive index from that of the medium, is attenuated in intensity by scattering. In turbidimetry, the intensity of light transmitted through the medium, the unscattered light, is measured. In nephelometry, the intensity of the scattered light is measured, usually, but not necessarily, at right angles to the incident light beam.

A superfamily of large integral ATP-binding cassette membrane proteins whose expression pattern is consistent with a role in lipid (cholesterol) efflux. It is implicated in TANGIER DISEASE characterized by accumulation of cholesteryl ester in various tissues.

Fatty acid esters of cholesterol which constitute about two-thirds of the cholesterol in the plasma. The accumulation of cholesterol esters in the arterial intima is a characteristic feature of atherosclerosis.

Electrophoresis in which a pH gradient is established in a gel medium and proteins migrate until they reach the site (or focus) at which the pH is equal to their isoelectric point.

Cell surface proteins that bind lipoproteins with high affinity. Lipoprotein receptors in the liver and peripheral tissues mediate the regulation of plasma and cellular cholesterol metabolism and concentration. The receptors generally recognize the apolipoproteins of the lipoprotein complex, and binding is often a trigger for endocytosis.

Physiological processes in biosynthesis (anabolism) and degradation (catabolism) of LIPIDS.

A class of lipoproteins that carry dietary CHOLESTEROL and TRIGLYCERIDES from the SMALL INTESTINE to the tissues. Their density (0.93-1.006 g/ml) is the same as that of VERY-LOW-DENSITY LIPOPROTEINS.

Cholesterol which is contained in or bound to low density lipoproteins (LDL), including CHOLESTEROL ESTERS and free cholesterol.

Lipids containing one or more phosphate groups, particularly those derived from either glycerol (phosphoglycerides see GLYCEROPHOSPHOLIPIDS) or sphingosine (SPHINGOLIPIDS). They are polar lipids that are of great importance for the structure and function of cell membranes and are the most abundant of membrane lipids, although not stored in large amounts in the system.

Centrifugation with a centrifuge that develops centrifugal fields of more than 100,000 times gravity. (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)

Conditions with abnormally low levels of LIPOPROTEINS in the blood. This may involve any of the lipoprotein subclasses, including ALPHA-LIPOPROTEINS (high-density lipoproteins); BETA-LIPOPROTEINS (low-density lipoproteins); and PREBETA-LIPOPROTEINS (very-low-density lipoproteins).

Low-density subclass of the high-density lipoproteins, with particle sizes between 8 to 13 nm.

A lipoprotein that resembles the LOW-DENSITY LIPOPROTEINS but with an extra protein moiety, APOPROTEIN (A) also known as APOLIPOPROTEIN (A), linked to APOLIPOPROTEIN B-100 on the LDL by one or two disulfide bonds. High plasma level of lipoprotein (a) is associated with increased risk of atherosclerotic cardiovascular disease.

The interstitial fluid that is in the LYMPHATIC SYSTEM.

Electrophoresis in which a polyacrylamide gel is used as the diffusion medium.

The protein components of a number of complexes, such as enzymes (APOENZYMES), ferritin (APOFERRITINS), or lipoproteins (APOLIPOPROTEINS).

Conditions with excess LIPIDS in the blood.

A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.

Technique involving the diffusion of antigen or antibody through a semisolid medium, usually agar or agarose gel, with the result being a precipitin reaction.

An enzyme of the hydrolase class that catalyzes the reaction of triacylglycerol and water to yield diacylglycerol and a fatty acid anion. The enzyme hydrolyzes triacylglycerols in chylomicrons, very-low-density lipoproteins, low-density lipoproteins, and diacylglycerols. It occurs on capillary endothelial surfaces, especially in mammary, muscle, and adipose tissue. Genetic deficiency of the enzyme causes familial hyperlipoproteinemia Type I. (Dorland, 27th ed) EC 3.1.1.34.

(Z)-9-Octadecenoic acid 1,2,3-propanetriyl ester.

A hypertriglyceridemia disorder, often with autosomal dominant inheritance. It is characterized by the persistent elevations of plasma TRIGLYCERIDES, endogenously synthesized and contained predominantly in VERY-LOW-DENSITY LIPOPROTEINS (pre-beta lipoproteins). In contrast, the plasma CHOLESTEROL and PHOSPHOLIPIDS usually remain within normal limits.

Derivatives of phosphatidic acids in which the phosphoric acid is bound in ester linkage to a choline moiety. Complete hydrolysis yields 1 mole of glycerol, phosphoric acid and choline and 2 moles of fatty acids.

The rate dynamics in chemical or physical systems.

A family of MEMBRANE TRANSPORT PROTEINS that require ATP hydrolysis for the transport of substrates across membranes. The protein family derives its name from the ATP-binding domain found on the protein.

Conditions with abnormally elevated levels of LIPOPROTEINS in the blood. They may be inherited, acquired, primary, or secondary. Hyperlipoproteinemias are classified according to the pattern of lipoproteins on electrophoresis or ultracentrifugation.

A 34-kDa glycosylated protein. A major and most common isoform of apolipoprotein E. Therefore, it is also known as apolipoprotein E (ApoE). In human, Apo E3 is a 299-amino acid protein with a cysteine at the 112 and an arginine at the 158 position. It is involved with the transport of TRIGLYCERIDES; PHOSPHOLIPIDS; CHOLESTEROL; and CHOLESTERYL ESTERS in and out of the cells.

The specialty of ANALYTIC CHEMISTRY applied to assays of physiologically important substances found in blood, urine, tissues, and other biological fluids for the purpose of aiding the physician in making a diagnosis or following therapy.

Cholesterol which is contained in or bound to very low density lipoproteins (VLDL). High circulating levels of VLDL cholesterol are found in HYPERLIPOPROTEINEMIA TYPE IIB. The cholesterol on the VLDL is eventually delivered by LOW-DENSITY LIPOPROTEINS to the tissues after the catabolism of VLDL to INTERMEDIATE-DENSITY LIPOPROTEINS, then to LDL.

A condition of elevated levels of TRIGLYCERIDES in the blood.

Proteins that bind to and transfer CHOLESTEROL ESTERS between LIPOPROTEINS such as LOW-DENSITY LIPOPROTEINS and HIGH-DENSITY LIPOPROTEINS.

A mixture of very-low-density lipoproteins (VLDL), particularly the triglyceride-poor VLDL, with slow diffuse electrophoretic mobilities in the beta and alpha2 regions which are similar to that of beta-lipoproteins (LDL) or alpha-lipoproteins (HDL). They can be intermediate (remnant) lipoproteins in the de-lipidation process, or remnants of mutant CHYLOMICRONS and VERY-LOW-DENSITY LIPOPROTEINS which cannot be metabolized completely as seen in FAMILIAL DYSBETALIPOPROTEINEMIA.

The range or frequency distribution of a measurement in a population (of organisms, organs or things) that has not been selected for the presence of disease or abnormality.

A family of scavenger receptors that are predominately localized to CAVEOLAE of the PLASMA MEMBRANE and bind HIGH DENSITY LIPOPROTEINS.

Method of tissue preparation in which the tissue specimen is frozen and then dehydrated at low temperature in a high vacuum. This method is also used for dehydrating pharmaceutical and food products.

A semisynthetic alkylated ESTRADIOL with a 17-alpha-ethinyl substitution. It has high estrogenic potency when administered orally, and is often used as the estrogenic component in ORAL CONTRACEPTIVES.

Relating to the size of solids.

A technique using antibodies for identifying or quantifying a substance. Usually the substance being studied serves as antigen both in antibody production and in measurement of antibody by the test substance.

An ACUTE PHASE REACTION protein present in low concentrations in normal sera, but found at higher concentrations in sera of older persons and in patients with AMYLOIDOSIS. It is the circulating precusor of amyloid A protein, which is found deposited in AA type AMYLOID FIBRILS.

Fats present in food, especially in animal products such as meat, meat products, butter, ghee. They are present in lower amounts in nuts, seeds, and avocados.

Microscopy using an electron beam, instead of light, to visualize the sample, thereby allowing much greater magnification. The interactions of ELECTRONS with specimens are used to provide information about the fine structure of that specimen. In TRANSMISSION ELECTRON MICROSCOPY the reactions of the electrons that are transmitted through the specimen are imaged. In SCANNING ELECTRON MICROSCOPY an electron beam falls at a non-normal angle on the specimen and the image is derived from the reactions occurring above the plane of the specimen.

A technique that combines protein electrophoresis and double immunodiffusion. In this procedure proteins are first separated by gel electrophoresis (usually agarose), then made visible by immunodiffusion of specific antibodies. A distinct elliptical precipitin arc results for each protein detectable by the antisera.

A severe type of hyperlipidemia, sometimes familial, that is characterized by the elevation of both plasma CHYLOMICRONS and TRIGLYCERIDES contained in VERY-LOW-DENSITY LIPOPROTEINS. Type V hyperlipoproteinemia is often associated with DIABETES MELLITUS and is not caused by reduced LIPOPROTEIN LIPASE activity as in HYPERLIPOPROTEINEMIA TYPE I .

An autosomal recessive disorder of lipid metabolism. It is caused by mutation of the microsomal triglyceride transfer protein that catalyzes the transport of lipids (TRIGLYCERIDES; CHOLESTEROL ESTERS; PHOSPHOLIPIDS) and is required in the secretion of BETA-LIPOPROTEINS (low density lipoproteins or LDL). Features include defective intestinal lipid absorption, very low serum cholesterol level, and near absent LDL.

A synthetic phospholipid used in liposomes and lipid bilayers for the study of biological membranes.

A large group of structurally diverse cell surface receptors that mediate endocytic uptake of modified LIPOPROTEINS. Scavenger receptors are expressed by MYELOID CELLS and some ENDOTHELIAL CELLS, and were originally characterized based on their ability to bind acetylated LOW-DENSITY LIPOPROTEINS. They can also bind a variety of other polyanionic ligand. Certain scavenger receptors can internalize micro-organisms as well as apoptotic cells.

The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.

An unsaturated fatty acid that is the most widely distributed and abundant fatty acid in nature. It is used commercially in the preparation of oleates and lotions, and as a pharmaceutical solvent. (Stedman, 26th ed)

Chromatography on non-ionic gels without regard to the mechanism of solute discrimination.

The sum of the weight of all the atoms in a molecule.

Thickening and loss of elasticity of the walls of ARTERIES of all sizes. There are many forms classified by the types of lesions and arteries involved, such as ATHEROSCLEROSIS with fatty lesions in the ARTERIAL INTIMA of medium and large muscular arteries.

The movement of materials (including biochemical substances and drugs) through a biological system at the cellular level. The transport can be across cell membranes and epithelial layers. It also can occur within intracellular compartments and extracellular compartments.

The metabolic process of breaking down LIPIDS to release FREE FATTY ACIDS, the major oxidative fuel for the body. Lipolysis may involve dietary lipids in the DIGESTIVE TRACT, circulating lipids in the BLOOD, and stored lipids in the ADIPOSE TISSUE or the LIVER. A number of enzymes are involved in such lipid hydrolysis, such as LIPASE and LIPOPROTEIN LIPASE from various tissues.

An enzyme that catalyzes the formation of cholesterol esters by the direct transfer of the fatty acid group from a fatty acyl CoA derivative. This enzyme has been found in the adrenal gland, gonads, liver, intestinal mucosa, and aorta of many mammalian species. EC 2.3.1.26.

Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations or by parent x offspring matings carried out with certain restrictions. This also includes animals with a long history of closed colony breeding.

A subfamily in the family CEBIDAE that consists of four genera: CALLITHRIX (marmosets), CALLIMICO (Goeldi's monkey), LEONTOPITHECUS (lion tamarins), and SAGUINUS (long-tusked tamarins). The members of this family inhabit the tropical forests of South and Central America.

A highly dense subclass of the high-density lipoproteins, with particle sizes below 7 nm. They are also known as nascent HDL, composed of a few APOLIPOPROTEIN A-I molecules which are complexed with PHOSPHOLIPIDS. The lipid-poor pre-beta-HDL particles serve as progenitors of HDL3 and then HDL2 after absorption of free cholesterol from cell membranes, cholesterol esterification, and acquisition of apolipoproteins A-II, Cs, and E. Pre-beta-HDL initiate the reverse cholesterol transport process from cells to liver.

An enzyme of the hydrolase class that catalyzes the reaction of triacylglycerol and water to yield diacylglycerol and a fatty acid anion. It is produced by glands on the tongue and by the pancreas and initiates the digestion of dietary fats. (From Dorland, 27th ed) EC 3.1.1.3.

Artificial, single or multilaminar vesicles (made from lecithins or other lipids) that are used for the delivery of a variety of biological molecules or molecular complexes to cells, for example, drug delivery and gene transfer. They are also used to study membranes and membrane proteins.

Receptors on the plasma membrane of nonhepatic cells that specifically bind LDL. The receptors are localized in specialized regions called coated pits. Hypercholesteremia is caused by an allelic genetic defect of three types: 1, receptors do not bind to LDL; 2, there is reduced binding of LDL; and 3, there is normal binding but no internalization of LDL. In consequence, entry of cholesterol esters into the cell is impaired and the intracellular feedback by cholesterol on 3-hydroxy-3-methylglutaryl CoA reductase is lacking.

A group of fatty acids that contain 18 carbon atoms and a double bond at the omega 9 carbon.

Transport proteins that carry specific substances in the blood or across cell membranes.

Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.

An autosomal recessively inherited disorder caused by mutation of LECITHIN CHOLESTEROL ACYLTRANSFERASE that facilitates the esterification of lipoprotein cholesterol and subsequent removal from peripheral tissues to the liver. This defect results in low HDL-cholesterol level in blood and accumulation of free cholesterol in tissue leading to a triad of CORNEAL OPACITY, hemolytic anemia (ANEMIA, HEMOLYTIC), and PROTEINURIA.

A type of familial lipid metabolism disorder characterized by a variable pattern of elevated plasma CHOLESTEROL and/or TRIGLYCERIDES. Multiple genes on different chromosomes may be involved, such as the major late transcription factor (UPSTREAM STIMULATORY FACTORS) on CHROMOSOME 1.

The process in which substances, either endogenous or exogenous, bind to proteins, peptides, enzymes, protein precursors, or allied compounds. Specific protein-binding measures are often used as assays in diagnostic assessments.

Leukocyte differentiation antigens and major platelet membrane glycoproteins present on MONOCYTES; ENDOTHELIAL CELLS; PLATELETS; and mammary EPITHELIAL CELLS. They play major roles in CELL ADHESION; SIGNAL TRANSDUCTION; and regulation of angiogenesis. CD36 is a receptor for THROMBOSPONDINS and can act as a scavenger receptor that recognizes and transports oxidized LIPOPROTEINS and FATTY ACIDS.

The fatty portion of milk, separated as a soft yellowish solid when milk or cream is churned. It is processed for cooking and table use. (Random House Unabridged Dictionary, 2d ed)

A group of familial disorders characterized by elevated circulating cholesterol contained in either LOW-DENSITY LIPOPROTEINS alone or also in VERY-LOW-DENSITY LIPOPROTEINS (pre-beta lipoproteins).

The process of converting an acid into an alkyl or aryl derivative. Most frequently the process consists of the reaction of an acid with an alcohol in the presence of a trace of mineral acid as catalyst or the reaction of an acyl chloride with an alcohol. Esterification can also be accomplished by enzymatic processes.

Conjugated protein-carbohydrate compounds including mucins, mucoid, and amyloid glycoproteins.

Colloids formed by the combination of two immiscible liquids such as oil and water. Lipid-in-water emulsions are usually liquid, like milk or lotion. Water-in-lipid emulsions tend to be creams. The formation of emulsions may be aided by amphiphatic molecules that surround one component of the system to form MICELLES.

A family of anadromous fish comprising SALMON; TROUT; whitefish; and graylings. They are the most important food and game fishes. Their habitat is the northern Atlantic and Pacific, both marine and inland, and the Great Lakes. (Nelson: Fishes of the World, 1976, p97)

The interaction of two or more substrates or ligands with the same binding site. The displacement of one by the other is used in quantitative and selective affinity measurements.

Cholesterol present in food, especially in animal products.

A basis of value established for the measure of quantity, weight, extent or quality, e.g. weight standards, standard solutions, methods, techniques, and procedures used in diagnosis and therapy.

Unstable isotopes of iodine that decay or disintegrate emitting radiation. I atoms with atomic weights 117-139, except I 127, are radioactive iodine isotopes.

Electrophoresis in which agar or agarose gel is used as the diffusion medium.

Unctuous combustible substances that are liquid or easily liquefiable on warming, and are soluble in ether but insoluble in water. Such substances, depending on their origin, are classified as animal, mineral, or vegetable oils. Depending on their behavior on heating, they are volatile or fixed. (Dorland, 28th ed)

A thickening and loss of elasticity of the walls of ARTERIES that occurs with formation of ATHEROSCLEROTIC PLAQUES within the ARTERIAL INTIMA.

A method of gel filtration chromatography using agarose, the non-ionic component of agar, for the separation of compounds with molecular weights up to several million.

Substances that lower the levels of certain LIPIDS in the BLOOD. They are used to treat HYPERLIPIDEMIAS.

Separation of particles according to density by employing a gradient of varying densities. At equilibrium each particle settles in the gradient at a point equal to its density. (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)

Conditions with abnormally low levels of BETA-LIPOPROTEINS (low density lipoproteins or LDL) in the blood. It is defined as LDL values equal to or less than the 5th percentile for the population. They include the autosomal dominant form involving mutation of the APOLIPOPROTEINS B gene, and the autosomal recessive form involving mutation of the microsomal triglyceride transfer protein. All are characterized by low LDL and dietary fat malabsorption.

Classic quantitative assay for detection of antigen-antibody reactions using a radioactively labeled substance (radioligand) either directly or indirectly to measure the binding of the unlabeled substance to a specific antibody or other receptor system. Non-immunogenic substances (e.g., haptens) can be measured if coupled to larger carrier proteins (e.g., bovine gamma-globulin or human serum albumin) capable of inducing antibody formation.

A change from planar to elliptic polarization when an initially plane-polarized light wave traverses an optically active medium. (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)

An electrochemical process in which macromolecules or colloidal particles with a net electric charge migrate in a solution under the influence of an electric current.

The level of protein structure in which regular hydrogen-bond interactions within contiguous stretches of polypeptide chain give rise to alpha helices, beta strands (which align to form beta sheets) or other types of coils. This is the first folding level of protein conformation.

Elements of limited time intervals, contributing to particular results or situations.

Compounds that contain a 1-dimethylaminonaphthalene-5-sulfonyl group.

The regular and simultaneous occurrence in a single interbreeding population of two or more discontinuous genotypes. The concept includes differences in genotypes ranging in size from a single nucleotide site (POLYMORPHISM, SINGLE NUCLEOTIDE) to large nucleotide sequences visible at a chromosomal level.

Abnormalities in the serum levels of LIPIDS, including overproduction or deficiency. Abnormal serum lipid profiles may include high total CHOLESTEROL, high TRIGLYCERIDES, low HIGH DENSITY LIPOPROTEIN CHOLESTEROL, and elevated LOW DENSITY LIPOPROTEIN CHOLESTEROL.

A 44-kDa highly glycosylated plasma protein that binds phospholipids including CARDIOLIPIN; APOLIPOPROTEIN E RECEPTOR; membrane phospholipids, and other anionic phospholipid-containing moieties. It plays a role in coagulation and apoptotic processes. Formerly known as apolipoprotein H, it is an autoantigen in patients with ANTIPHOSPHOLIPID ANTIBODIES.

Measurable and quantifiable biological parameters (e.g., specific enzyme concentration, specific hormone concentration, specific gene phenotype distribution in a population, presence of biological substances) which serve as indices for health- and physiology-related assessments, such as disease risk, psychiatric disorders, environmental exposure and its effects, disease diagnosis, metabolic processes, substance abuse, pregnancy, cell line development, epidemiologic studies, etc.

Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.

An imbalance between myocardial functional requirements and the capacity of the CORONARY VESSELS to supply sufficient blood flow. It is a form of MYOCARDIAL ISCHEMIA (insufficient blood supply to the heart muscle) caused by a decreased capacity of the coronary vessels.

An early local inflammatory reaction to insult or injury that consists of fever, an increase in inflammatory humoral factors, and an increased synthesis by hepatocytes of a number of proteins or glycoproteins usually found in the plasma.

A condition with abnormally high levels of CHOLESTEROL in the blood. It is defined as a cholesterol value exceeding the 95th percentile for the population.

A ubiquitous family of proteins that transport PHOSPHOLIPIDS such as PHOSPHATIDYLINOSITOL and PHOSPHATIDYLCHOLINE between membranes. They play an important role in phospholipid metabolism during vesicular transport and SIGNAL TRANSDUCTION.

A highly conserved heterodimeric glycoprotein that is differentially expressed during many severe physiological disturbance states such as CANCER; APOPTOSIS; and various NEUROLOGICAL DISORDERS. Clusterin is ubiquitously expressed and appears to function as a secreted MOLECULAR CHAPERONE.

The characteristic 3-dimensional shape of a protein, including the secondary, supersecondary (motifs), tertiary (domains) and quaternary structure of the peptide chain. PROTEIN STRUCTURE, QUATERNARY describes the conformation assumed by multimeric proteins (aggregates of more than one polypeptide chain).

A polypeptide hormone of approximately 25 kDa that is produced by the SYNCYTIOTROPHOBLASTS of the PLACENTA, also known as chorionic somatomammotropin. It has both GROWTH HORMONE and PROLACTIN activities on growth, lactation, and luteal steroid production. In women, placental lactogen secretion begins soon after implantation and increases to 1 g or more a day in late pregnancy. Placental lactogen is also an insulin antagonist.

Organic, monobasic acids derived from hydrocarbons by the equivalent of oxidation of a methyl group to an alcohol, aldehyde, and then acid. Fatty acids are saturated and unsaturated (FATTY ACIDS, UNSATURATED). (Grant & Hackh's Chemical Dictionary, 5th ed)

Organic compounds that generally contain an amino (-NH2) and a carboxyl (-COOH) group. Twenty alpha-amino acids are the subunits which are polymerized to form proteins.

Method for assessing flow through a system by injection of a known quantity of radionuclide into the system and monitoring its concentration over time at a specific point in the system. (From Dorland, 28th ed)

Treatment process involving the injection of fluid into an organ or tissue.

An aspect of personal behavior or lifestyle, environmental exposure, or inborn or inherited characteristic, which, on the basis of epidemiologic evidence, is known to be associated with a health-related condition considered important to prevent.

An autosomal recessively inherited disorder characterized by the accumulation of intermediate-density lipoprotein (IDL or broad-beta-lipoprotein). IDL has a CHOLESTEROL to TRIGLYCERIDES ratio greater than that of VERY-LOW-DENSITY LIPOPROTEINS. This disorder is due to mutation of APOLIPOPROTEINS E, a receptor-binding component of VLDL and CHYLOMICRONS, resulting in their reduced clearance and high plasma levels of both cholesterol and triglycerides.

The isolation and partial characterization of the serum lipoproteins and apolipoproteins of the rainbow trout. (1/2216)

1. VLD (very-low-density), LD (low-density) and HD (high-density) lipoproteins were isolated from the serum of trout (Salmo gairdneri Richardson). 2. Each lipoprotein class resembled that of the human in immunological reactivity, electrophoretic behaviour and appearance in the electron microscope. Trout LD lipoprotein, however, was of greater density than human LD lipoprotein. 3. The trout lipoproteins have lipid compositions which are similar to those of the corresponding human components, except for their high contents of long-chain unsaturated fatty acids. 4. HD and LD lipoproteins were immunologically non-identical, whereas LD lipoproteins possessed antigenic determinants in common with VLD lipoproteins. 5. VLD and HD lipoproteins each contained at least seven different apoproteins, whereas LD liprotein was composed largely of a single apoprotein which resembled human apolipoprotein B. 6. At least one, and possibly three, apoprotein of trout HD lipoprotein showed features which resemble human apoprotein A-1.7. The broad similarity between the trout and human lipoprotein systems suggests that both arose from common ancestral genes early in evolutionary history. (+info)

Transgenic rabbits as models for atherosclerosis research. (2/2216)

Several characteristics of the rabbit make it an excellent model for the study of lipoprotein metabolism and atherosclerosis. New Zealand White (NZW) rabbits have low plasma total cholesterol concentrations, high cholesteryl ester transfer protein activity, low hepatic lipase (HL) activity, and lack an analogue of human apolipoprotein (apo) A-II, providing a unique system in which to assess the effects of human transgenes on plasma lipoproteins and atherosclerosis susceptibility. Additionally, rabbit models of human lipoprotein disorders, such as the Watanabe Heritable Hyperlipidemic (WHHL) and St. Thomas' Hospital strains, models of familial hypercholesterolemia and familial combined hyperlipidemia, respectively, allow for the assessment of candidate genes for potential use in the treatment of dyslipoproteinemic patients. To date, transgenes for human apo(a), apoA-I, apoB, apoE2, apoE3, HL, and lecithin:cholesterol acyltransferase (LCAT), as well as for rabbit apolipoprotein B mRNA-editing enzyme catalytic poly-peptide 1 (APOBEC-1), have been expressed in NZW rabbits, whereas only those for human apoA-I and LCAT have been introduced into the WHHL background. All of these transgenes have been shown to have significant effects on plasma lipoprotein concentrations. In both NZW and WHHL rabbits, human apoA-I expression was associated with a significant reduction in the extent of aortic atherosclerosis, which was similarly the case for LCAT in rabbits having at least one functional LDL receptor allele. Conversely, expression of apoE2 in NZW rabbits caused increased susceptibility to atherosclerosis. These studies provide new insights into the mechanisms responsible for the development of atherosclerosis, emphasizing the strength of the rabbit model in cardiovascular disease research. (+info)

The heparin/heparan sulfate-binding site on apo-serum amyloid A. Implications for the therapeutic intervention of amyloidosis. (3/2216)

Serum amyloid A isoforms, apoSAA1 and apoSAA2, are apolipoproteins of unknown function that become major components of high density lipoprotein (HDL) during the acute phase of an inflammatory response. ApoSAA is also the precursor of inflammation-associated amyloid, and there is strong evidence that the formation of inflammation-associated and other types of amyloid is promoted by heparan sulfate (HS). Data presented herein demonstrate that both mouse and human apoSAA contain binding sites that are specific for heparin and HS, with no binding for the other major glycosaminoglycans detected. Cyanogen bromide-generated peptides of mouse apoSAA1 and apoSAA2 were screened for heparin binding activity. Two peptides, an apoSAA1-derived 80-mer (residues 24-103) and a smaller carboxyl-terminal 27-mer peptide of apoSAA2 (residues 77-103), were retained by a heparin column. A synthetic peptide corresponding to the CNBr-generated 27-mer also bound heparin, and by substituting or deleting one or more of its six basic residues (Arg-83, His-84, Arg-86, Lys-89, Arg-95, and Lys-102), their relative importance for heparin and HS binding was determined. The Lys-102 residue appeared to be required only for HS binding. The residues Arg-86, Lys-89, Arg-95, and Lys-102 are phylogenetically conserved suggesting that the heparin/HS binding activity may be an important aspect of the function of apoSAA. HS linked by its carboxyl groups to an Affi-Gel column or treated with carbodiimide to block its carboxyl groups lost the ability to bind apoSAA. HDL-apoSAA did not bind to heparin; however, it did bind to HS, an interaction to which apoA-I contributed. Results from binding experiments with Congo Red-Sepharose 4B columns support the conclusions of a recent structural study which found that heparin binding domains have a common spatial distance of about 20 A between their two outer basic residues. Our present work provides direct evidence that apoSAA can associate with HS (and heparin) and that the occupation of its binding site by HS, and HS analogs, likely caused the previously reported increase in amyloidogenic conformation (beta-sheet) of apoSAA2 (McCubbin, W. D., Kay, C. M., Narindrasorasak, S., and Kisilevsky, R. (1988) Biochem. J. 256, 775-783) and their amyloid-suppressing effects in vivo (Kisilevsky, R., Lemieux, L. J., Fraser, P. E., Kong, X., Hultin, P. G., and Szarek, W. A. (1995) Nat. Med. 1, 143-147), respectively. (+info)

Potent inhibition of CD4/TCR-mediated T cell apoptosis by a CD4-binding glycoprotein secreted from breast tumor and seminal vesicle cells. (4/2216)

We previously isolated a CD4 ligand glycoprotein, gp17, from human seminal plasma; this glycoprotein is identical with gross cystic disease fluid protein-15 (GCDFP-15), a factor specifically secreted from primary and secondary breast tumors. The function of gp17/GCDFP-15 in physiological as well as in pathological conditions has remained elusive thus far. As a follow up to our previous findings that gp17 binds to CD4 with high affinity and interferes with both HIV-1 gp120 binding to CD4 and syncytium formation, we investigated whether gp17 could affect the T lymphocyte apoptosis induced by a separate ligation of CD4 and TCR. We show here that gp17/GCDFP-15 is in fact a strong and specific inhibitor of the T lymphocyte programmed cell death induced by CD4 cross-linking and subsequent TCR activation. The antiapoptotic effect observed in the presence of gp17 correlates with a moderate up-regulation of Bcl-2 expression in treated cells. The presence of gp17 also prevents the down-modulation of Bcl-2 expression in Bcl-2bright CD4+ T cells that is caused by the triggering of apoptosis. Our results suggest that gp17 may represent a new immunomodulatory CD4 binding factor playing a role in host defense against infections and tumors. (+info)

Effects of alcohol and cholesterol feeding on lipoprotein metabolism and cholesterol absorption in rabbits. (5/2216)

Alcohol fed to rabbits in a liquid formula at 30% of calories increased plasma cholesterol by 36% in the absence of dietary cholesterol and by 40% in the presence of a 0.5% cholesterol diet. The increase was caused almost entirely by VLDL, IDL, and LDL. Cholesterol feeding decreased the fractional catabolic rate for VLDL and LDL apoprotein by 80% and 57%, respectively, and increased the production rate of VLDL and LDL apoprotein by 75% and 15%, respectively. Alcohol feeding had no effect on VLDL apoprotein production but increased LDL production rate by 55%. The efficiency of intestinal cholesterol absorption was increased by alcohol. In the presence of dietary cholesterol, percent cholesterol absorption rose from 34.4+/-2.6% to 44.9+/-2.5% and in the absence of dietary cholesterol, from 84.3+/-1.4% to 88.9+/-1.0%. Increased cholesterol absorption and increased LDL production rate may be important mechanisms for exacerbation by alcohol of hypercholesterolemia in the cholesterol-fed rabbit model. (+info)

Lipid transfer inhibitor protein defines the participation of lipoproteins in lipid transfer reactions: CETP has no preference for cholesteryl esters in HDL versus LDL. (6/2216)

Cholesteryl ester transfer protein (CETP) catalyzes the net transfer of cholesteryl ester (CE) between lipoproteins in exchange for triglyceride (heteroexchange). It is generally held that CETP primarily associates with HDL and preferentially transfers lipids from this lipoprotein fraction. This is illustrated in normal plasma where HDL is the primary donor of the CE transferred to VLDL by CETP. However, in plasma deficient in lipid transfer inhibitor protein (LTIP) activity, HDL and LDL are equivalent donors of CE to VLDL (Arterioscler Thromb Vasc Biol. 1997;17:1716-1724). Thus, we have hypothesized that the preferential transfer of CE from HDL in normal plasma is a consequence of LTIP activity and not caused by a preferential CETP-HDL interaction. We have tested this hypothesis in lipid mass transfer assays with partially purified CETP and LTIP, and isolated lipoproteins. With a physiological mixture of lipoproteins, the preference ratio (PR, ratio of CE mass transferred from a lipoprotein to VLDL versus its CE content) for HDL and LDL in the presence of CETP alone was approximately 1 (ie, no preference). Fourfold variations in the LDL/HDL ratio or in the levels of HDL in the assay did not result in significant preferential transfer from any lipoprotein. On addition of LTIP, the PR for HDL was increased up to 2-fold and that for LDL decreased in a concentration-dependent manner. Under all conditions where LDL and HDL levels were varied, LTIP consistently resulted in a PR >1 for CE transfer from HDL. Short-term experiments with radiolabeled lipoproteins and either partially purified or homogenous CETP confirmed these observations and further demonstrated that CETP has a strong predilection to mediate homoexchange (bidirectional transfer of the same lipid) rather than heteroexchange (CE for TG); LTIP had no effect on the selection of CE or TG by CETP or its mechanism of action. We conclude, in contrast to current opinion, that CETP has no preference for CE in HDL versus LDL, suggesting that the previously reported stable binding of CETP to HDL does not result in selective transfer from this lipoprotein. These data suggest that LTIP is responsible for the preferential transfer of CE from HDL that occurs in plasma. CETP and LTIP cooperatively determine the extent of CETP-mediated remodeling of individual lipoprotein fractions. (+info)

Levels of soluble cell adhesion molecules in patients with angiographically defined coronary atherosclerosis. (7/2216)

Adhesion molecules on the endothelial cell membrane play an important role in the pathogenesis of atherosclerosis. Levels of soluble forms of cell adhesion molecules are reportedly elevated in patients with peripheral artery vessel disease and in patients with an atherosclerotic aorta. The present study investigated the association of serum levels of soluble vascular cell adhesion molecule 1 (sVCAM-1), soluble intercellular adhesion molecule 1 (sICAM-1), and soluble P-selectin (sP-selectin) with coronary heart disease (CHD) and the extent of coronary atherosclerosis, and examined the influence of serum levels of lipids, lipoproteins and apolipoproteins (apo) in subjects with (n=52, M/F:43/9) and without (controls, n=40, M/F:25/15) angiographically proven coronary atherosclerosis. After controlling for age and gender, levels of sVCAM-1 (least squares mean +/- std error: 565+/-36 ng/ml vs 540+/-41 ng/ml, ns), sICAM-1 (261+/-17ng/ml vs 247+/-19ng/ml, ns), and sP-selectin (142+/-8ng/ml vs 149+/-10 ng/ml, ns) in patients with coronary atherosclerosis were not different from those in controls, as assessed by an analysis of covariance. After also adjusting for body mass index, hypertension, diabetes mellitus, and smoking by a multiple logistic function analysis, the association of sVCAM-1, sICAM-1, and sP-selectin with CHD was still not significant. Levels of sVCAM-1, sICAM-1, and sP-selectin were also not related to the extent of coronary atherosclerosis as judged by the number of stenosed vessels. However, inverse (p<0.05) relationships were observed between sVCAMs and serum levels of HDL3-cholesterol, apo A-II, and lipoprotein containing apo A-I and A-II, between sICAMs and levels of apo A-II and Lp A-I/A-II (Lp A-I/A-II), and between sP-selectin and lipoprotein containing only apo A-I. In conclusion, serum levels of soluble VCAM-1, ICAM-1, and P-selectin were not related to CHD or the extent of coronary atherosclerosis, but were inversely related to serum levels of high-density lipoprotein-related lipoproteins. (+info)

CREB-binding protein is a transcriptional coactivator for hepatocyte nuclear factor-4 and enhances apolipoprotein gene expression. (8/2216)

Hepatocyte nuclear factor-4 (HNF-4) is a liver-enriched transcription factor that is crucial in the regulation of a large number of genes involved in glucose, cholesterol, and fatty acid metabolism and in determining the hepatic phenotype. We have previously shown that HNF-4 contains transcription activation functions at the N terminus (AF-1) and the C terminus (AF-2) which work synergistically to confer full HNF-4 activity. Here, we show that HNF-4 recruits the CREB-binding protein (CBP) coactivator on promoters of genes that contain functional HNF-4 sites. HNF-4 interacts with the N-terminal region of CBP (amino acids 1-771) and the C-terminal region of CBP (amino acids 1812-2441). The two activating functions of HNF-4, AF-1 and AF-2, interact with the N terminus and the N and C terminus of CBP, respectively. In addition, we show that in contrast to the other nuclear hormone receptors the interaction between HNF-4 and CBP is ligand-independent. Recruitment of CBP by HNF-4 results in an enhancement of the transcriptional activity of the latter. CBP does not activate gene expression in the absence of HNF-4, and dominant negative forms of HNF-4 prevent transcriptional activation by CBP, suggesting that the mere recruitment of CBP by HNF-4 is not sufficient for enhancement of gene expression. These findings demonstrate that CBP acts as a transcriptional coactivator for HNF-4 and provide new insights into the regulatory function of HNF-4. (+info)

People with Tangier disease often have extremely high levels of low-density lipoprotein (LDL) cholesterol, which can lead to the development of cardiovascular disease at an early age. The disorder is caused by mutations in the gene that codes for a protein called ATP-binding cassette transporter 1 (ABC1), which plays a critical role in the transport of cholesterol and other lipids in the body.

The symptoms of Tangier disease can vary depending on the severity of the disorder, but may include:

* High levels of LDL cholesterol
* Low levels of HDL cholesterol
* Abnormal liver function tests
* Yellowing of the skin and eyes (jaundice)
* Fatigue
* Weakness
* Muscle cramps
* Heart disease
* Stroke

Tangier disease is usually diagnosed through a combination of clinical evaluation, laboratory tests, and genetic analysis. Treatment for the disorder typically involves a combination of dietary modifications, medications, and lipid-lowering therapy to reduce the levels of LDL cholesterol and increase the levels of HDL cholesterol. In some cases, a liver transplant may be necessary to treat the liver damage that can occur as a result of the disorder.

The most common form of hypolipoproteinemia is familial hypobetalipoproteinemia (FHBL), which is caused by mutations in the gene encoding apoB, a protein component of low-density lipoproteins (LDL). People with FHBL have extremely low levels of LDL cholesterol and often develop symptoms such as fatty liver disease, liver cirrhosis, and cardiovascular disease.

Another form of hypolipoproteinemia is familial hypoalphalipoproteinemia (FHAL), which is caused by mutations in the gene encoding apoA-I, a protein component of high-density lipoproteins (HDL). People with FHAL have low levels of HDL cholesterol and often develop symptoms such as cardiovascular disease and premature coronary artery disease.

Hypolipoproteinemia can be diagnosed through a combination of clinical evaluation, laboratory tests, and genetic analysis. Treatment for the disorder typically involves managing associated symptoms and reducing lipid levels through diet, exercise, and medication. In some cases, liver transplantation may be necessary.

Prevention of hypolipoproteinemia is challenging, as it is often inherited in an autosomal recessive pattern, meaning that both parents must be carriers of the mutated gene to pass it on to their children. However, genetic counseling and testing can help identify carriers and allow for informed family planning.

Overall, hypolipoproteinemia is a rare and complex group of disorders that affect lipid metabolism and transport. While treatment and management options are available, prevention and early diagnosis are key to reducing the risk of complications associated with these disorders.

There are several types of hyperlipidemia, including:

1. High cholesterol: This is the most common type of hyperlipidemia and is characterized by elevated levels of low-density lipoprotein (LDL) cholesterol, also known as "bad" cholesterol.
2. High triglycerides: This type of hyperlipidemia is characterized by elevated levels of triglycerides in the blood. Triglycerides are a type of fat found in the blood that is used for energy.
3. Low high-density lipoprotein (HDL) cholesterol: HDL cholesterol is known as "good" cholesterol because it helps remove excess cholesterol from the bloodstream and transport it to the liver for excretion. Low levels of HDL cholesterol can contribute to hyperlipidemia.

Symptoms of hyperlipidemia may include xanthomas (fatty deposits on the skin), corneal arcus (a cloudy ring around the iris of the eye), and tendon xanthomas (tender lumps under the skin). However, many people with hyperlipidemia have no symptoms at all.

Hyperlipidemia can be diagnosed through a series of blood tests that measure the levels of different types of cholesterol and triglycerides in the blood. Treatment for hyperlipidemia typically involves dietary changes, such as reducing intake of saturated fats and cholesterol, and increasing physical activity. Medications such as statins, fibric acid derivatives, and bile acid sequestrants may also be prescribed to lower cholesterol levels.

In severe cases of hyperlipidemia, atherosclerosis (hardening of the arteries) can occur, which can lead to cardiovascular disease, including heart attacks and strokes. Therefore, it is important to diagnose and treat hyperlipidemia early on to prevent these complications.

The condition is caused by mutations in genes that code for enzymes involved in lipid metabolism, such as ACY1 and APOB100. These mutations lead to a deficiency in the breakdown and transport of lipids in the body, resulting in the accumulation of chylomicrons and other lipoproteins in the blood.

Symptoms of hyperlipoproteinemia Type IV can include abdominal pain, fatigue, and joint pain, as well as an increased risk of pancreatitis and cardiovascular disease. Treatment typically involves a combination of dietary modifications, such as reducing intake of saturated fats and cholesterol, and medications to lower lipid levels. In severe cases, liver transplantation may be necessary.

Hyperlipoproteinemia Type IV is a rare disorder, and the prevalence is not well-defined. However, it is estimated to affect approximately 1 in 100,000 individuals worldwide. The condition can be diagnosed through a combination of clinical evaluation, laboratory tests, and genetic analysis.

In summary, hyperlipoproteinemia Type IV is a rare genetic disorder that affects the metabolism of lipids and lipoproteins in the body, leading to elevated levels of chylomicrons and other lipoproteins in the blood, as well as low levels of HDL. The condition can cause a range of symptoms and is typically treated with dietary modifications and medications.

There are several types of hyperlipoproteinemias, each with distinct clinical features and laboratory findings. The most common forms include:

1. Familial hypercholesterolemia (FH): This is the most common type of hyperlipoproteinemia, caused by mutations in the LDLR gene that codes for the low-density lipoprotein receptor. FH is characterized by extremely high levels of low-density lipoprotein (LDL) cholesterol in the blood, which can lead to premature cardiovascular disease, including heart attacks and strokes.
2. Familial hypobetalipoproteinemia (FHBL): This rare disorder is caused by mutations in the APOB100 gene that codes for a protein involved in lipid metabolism. FHBL is characterized by very low levels of low-density lipoprotein (LDL) and high-density lipoprotein (HDL) cholesterol, as well as a deficiency of Apolipoprotein B-100, a protein that helps transport lipids in the blood.
3. Hypertriglyceridemia: This condition is caused by mutations in genes that regulate triglyceride metabolism, leading to extremely high levels of triglycerides in the blood. Hypertriglyceridemia can increase the risk of pancreatitis and other health problems.
4. Lipoprotein lipase deficiency: This rare disorder is caused by mutations in the LPL gene that codes for the enzyme lipoprotein lipase, which helps break down triglycerides in the blood. Lipoprotein lipase deficiency can lead to very high levels of triglycerides and cholesterol in the blood, increasing the risk of pancreatitis and other health problems.
5. Familial dyslipidemia: This is a group of rare inherited disorders that affect lipid metabolism and can cause extremely high or low levels of various types of cholesterol and triglycerides in the blood. Some forms of familial dyslipidemia are caused by mutations in genes that code for enzymes involved in lipid metabolism, while others may be caused by unknown factors.
6. Chylomicronemia: This rare disorder is characterized by extremely high levels of chylomicrons (type of triglyceride-rich lipoprotein) in the blood, which can increase the risk of pancreatitis and other health problems. The exact cause of chylomicronemia is not fully understood, but it may be related to genetic mutations or other factors that affect lipid metabolism.
7. Hyperchylomicronemia: This rare disorder is similar to chylomicronemia, but it is characterized by extremely high levels of chylomicrons in the blood, as well as very low levels of HDL (good) cholesterol. Hyperchylomicronemia can increase the risk of pancreatitis and other health problems.
8. Hypoalphalipoproteinemia: This rare disorder is characterized by extremely low levels of apolipoprotein A-I (ApoA-I), a protein that plays a key role in lipid metabolism and helps to regulate the levels of various types of cholesterol and triglycerides in the blood. Hypoalphalipoproteinemia can increase the risk of pancreatitis and other health problems.
9. Hypobetalipoproteinemia: This rare disorder is characterized by extremely low levels of apolipoprotein B (ApoB), a protein that helps to regulate the levels of various types of cholesterol and triglycerides in the blood. Hypobetalipoproteinemia can increase the risk of pancreatitis and other health problems.
10. Sitosterolemia: This rare genetic disorder is caused by mutations in the gene that codes for sterol-CoA-desmethylase (SCD), an enzyme involved in the metabolism of plant sterols. Sitosterolemia can cause elevated levels of plant sterols and sitosterol in the blood, which can increase the risk of pancreatitis and other health problems.
11. Familial hyperchylomicronemia type 1 (FHMC1): This rare genetic disorder is caused by mutations in the gene that codes for apolipoprotein C-II (APOC2), a protein that helps to regulate the levels of various types of cholesterol and triglycerides in the blood. FHMC1 can cause elevated levels of chylomicrons and other lipids in the blood, which can increase the risk of pancreatitis and other health problems.
12. Familial hyperchylomicronemia type 2 (FHMC2): This rare genetic disorder is caused by mutations in the gene that codes for apolipoprotein A-IV (APOA4), a protein that helps to regulate the levels of various types of cholesterol and triglycerides in the blood. FHMC2 can cause elevated levels of chylomicrons and other lipids in the blood, which can increase the risk of pancreatitis and other health problems.
13. Lipoprotein (a) deficiency: This rare genetic disorder is caused by mutations in the gene that codes for apolipoprotein (a), a protein that helps to regulate the levels of lipoproteins in the blood. Lipoprotein (a) deficiency can cause low levels of lipoprotein (a) and other lipids in the blood, which can increase the risk of pancreatitis and other health problems.
14. Chylomicron retention disease: This rare genetic disorder is caused by mutations in the gene that codes for apolipoprotein C-II (APOC2), a protein that helps to regulate the levels of chylomicrons in the blood. Chylomicron retention disease can cause elevated levels of chylomicrons and other lipids in the blood, which can increase the risk of pancreatitis and other health problems.
15. Hypertriglyceridemia-apolipoprotein C-II deficiency: This rare genetic disorder is caused by mutations in the gene that codes for apolipoprotein C-II (APOC2), a protein that helps to regulate the levels of triglycerides in the blood. Hypertriglyceridemia-apolipoprotein C-II deficiency can cause elevated levels of triglycerides and other lipids in the blood, which can increase the risk of pancreatitis and other health problems.
16. Familial partial lipodystrophy (FPLD): This rare genetic disorder is characterized by the loss of fat tissue in certain areas of the body, such as the arms, legs, and buttocks. FPLD can cause elevated levels of lipids in the blood, which can increase the risk of pancreatitis and other health problems.
17. Lipodystrophy: This rare genetic disorder is characterized by the loss of fat tissue in certain areas of the body, such as the face, arms, and legs. Lipodystrophy can cause elevated levels of lipids in the blood, which can increase the risk of pancreatitis and other health problems.
18. Abetalipoproteinemia: This rare genetic disorder is caused by mutations in the gene that codes for apolipoprotein B, a protein that helps to regulate the levels of lipids in the blood. Abetalipoproteinemia can cause elevated levels of triglycerides and other lipids in the blood, which can increase the risk of pancreatitis and other health problems.
19. Chylomicronemia: This rare genetic disorder is characterized by the presence of excessively large amounts of chylomicrons (type of lipid particles) in the blood. Chylomicronemia can cause elevated levels of triglycerides and other lipids in the blood, which can increase the risk of pancreatitis and other health problems.
20. Hyperlipidemia due to medications: Certain medications, such as corticosteroids and some anticonvulsants, can cause elevated levels of lipids in the blood.

It's important to note that many of these disorders are rare and may not be common causes of high triglycerides. Additionally, there may be other causes of high triglycerides that are not listed here. It's important to talk to a healthcare provider for proper evaluation and diagnosis if you have concerns about your triglyceride levels.

There are several causes of hypertriglyceridemia, including:

* Genetics: Some people may inherit a tendency to have high triglyceride levels due to genetic mutations that affect the genes involved in triglyceride metabolism.
* Obesity: Excess body weight is associated with higher triglyceride levels, as there is more fat available for energy.
* Diabetes: Both type 1 and type 2 diabetes can lead to high triglyceride levels due to insulin resistance and altered glucose metabolism.
* High-carbohydrate diet: Consuming high amounts of carbohydrates, particularly refined or simple carbohydrates, can cause a spike in blood triglycerides.
* Alcohol consumption: Drinking too much alcohol can increase triglyceride levels in the blood.
* Certain medications: Some drugs, such as anabolic steroids and some antidepressants, can raise triglyceride levels.
* Underlying medical conditions: Certain medical conditions, such as hypothyroidism, kidney disease, and polycystic ovary syndrome (PCOS), can also contribute to high triglyceride levels.

Hypertriglyceridemia is typically diagnosed with a blood test that measures the level of triglycerides in the blood. Treatment options for hypertriglyceridemia depend on the underlying cause of the condition, but may include lifestyle modifications such as weight loss, dietary changes, and medications to lower triglyceride levels.

People with hyperlipoproteinemia type V often have a history of low birth weight and growth retardation, and may experience a range of health problems including fatigue, muscle weakness, and liver disease. The disorder is usually inherited in an autosomal recessive pattern, meaning that a person must inherit two copies of the mutated gene - one from each parent - to develop the condition.

Treatment for hyperlipoproteinemia type V typically involves a combination of dietary changes and medication. Dietary recommendations may include avoiding foods high in saturated fats and cholesterol, and increasing intake of unsaturated fats, such as those found in nuts and vegetable oils. Medications may include drugs that raise HDL levels or lower LDL levels, such as niacin or statins. In severe cases, liver transplantation may be necessary.

In summary, hyperlipoproteinemia type V is a rare genetic disorder that affects the metabolism of lipids and lipoproteins in the body, leading to extremely low levels of LDL cholesterol and high levels of HDL cholesterol. Treatment typically involves a combination of dietary changes and medication, and may include liver transplantation in severe cases.

The main symptom of abetalipoproteinemia is a complete absence of chylomicrons, which are small particles that carry triglycerides and other lipids in the bloodstream. This results in low levels of triglycerides and other lipids in the blood, as well as an impaired ability to absorb vitamins and other nutrients from food.

Abetalipoproteinemia is usually diagnosed during infancy or early childhood, when symptoms such as fatigue, weakness, and poor growth become apparent. The disorder can be identified through blood tests that measure lipid levels and genetic analysis.

Treatment for abetalipoproteinemia typically involves a combination of dietary changes and supplements to ensure adequate nutrition and prevent complications such as malnutrition and liver disease. In some cases, medications may be prescribed to lower triglyceride levels or improve the absorption of fat-soluble vitamins.

The prognosis for abetalipoproteinemia varies depending on the severity of the disorder and the presence of any complications. In general, early diagnosis and appropriate treatment can help to manage symptoms and prevent long-term health problems. However, some individuals with abetalipoproteinemia may experience ongoing health issues throughout their lives.

Arteriosclerosis can affect any artery in the body, but it is most commonly seen in the arteries of the heart, brain, and legs. It is a common condition that affects millions of people worldwide and is often associated with aging and other factors such as high blood pressure, high cholesterol, diabetes, and smoking.

There are several types of arteriosclerosis, including:

1. Atherosclerosis: This is the most common type of arteriosclerosis and occurs when plaque builds up inside the arteries.
2. Arteriolosclerosis: This type affects the small arteries in the body and can cause decreased blood flow to organs such as the kidneys and brain.
3. Medial sclerosis: This type affects the middle layer of the artery wall and can cause stiffness and narrowing of the arteries.
4. Intimal sclerosis: This type occurs when plaque builds up inside the innermost layer of the artery wall, causing it to become thick and less flexible.

Symptoms of arteriosclerosis can include chest pain, shortness of breath, leg pain or cramping during exercise, and numbness or weakness in the limbs. Treatment for arteriosclerosis may include lifestyle changes such as a healthy diet and regular exercise, as well as medications to lower blood pressure and cholesterol levels. In severe cases, surgery may be necessary to open up or bypass blocked arteries.

The primary symptom of LCAT deficiency is a high level of low-density lipoprotein (LDL) cholesterol, also known as "bad" cholesterol, in the blood. This can lead to the development of cholesterol deposits in the skin, eyes, and other tissues, which can cause a range of health problems including xanthomas (yellowish patches on the skin), corneal arcus (a cloudy ring around the cornea of the eye), and xanthelasma (yellowish patches on the eyelids).

Treatment for LCAT deficiency typically involves a combination of dietary changes, such as reducing intake of saturated fats and cholesterol, and medication to lower cholesterol levels. In some cases, liver transplantation may be necessary.

Prevention of LCAT deficiency is not possible, as it is a genetic disorder that is inherited in an autosomal recessive pattern. This means that a child must inherit two copies of the mutated LCAT gene, one from each parent, to develop the condition. However, early detection and treatment can help manage the symptoms and prevent complications.

The diagnosis of LCAT deficiency is based on a combination of clinical features, laboratory tests, and genetic analysis. Laboratory tests may include measurements of lipid levels in the blood, as well as assays for LCAT enzyme activity. Genetic testing can identify the presence of mutations in the LCAT gene that cause the condition.

Overall, LCAT deficiency is a rare and potentially serious genetic disorder that affects the body's ability to metabolize cholesterol and other fats. Early diagnosis and treatment can help manage the symptoms and prevent complications, but there is currently no cure for the condition.

The condition is caused by mutations in genes that code for proteins involved in lipid metabolism, such as the low-density lipoprotein receptor gene (LDLR), apolipoprotein A-1 gene (APOA1), and proprotein convertase subtilisin/kexin type 9 (PCSK9) genes. These mutations can lead to the overproduction or underexpression of certain lipids, leading to the characteristic lipid abnormalities seen in HeFH.

HeFH is usually inherited in an autosomal dominant manner, meaning that a single copy of the mutated gene is enough to cause the condition. However, some cases may be caused by recessive inheritance or de novo mutations. The condition can affect both children and adults, and it is important for individuals with HeFH to be monitored closely by a healthcare provider to manage their lipid levels and reduce the risk of cardiovascular disease.

Treatment for HeFH typically involves a combination of dietary modifications, such as reducing saturated fat intake and increasing fiber and omega-3 fatty acid intake, and medications, such as statins, to lower cholesterol levels. In some cases, apheresis or liver transplantation may be necessary to reduce lipid levels. Early detection and management of HeFH can help prevent or delay the development of cardiovascular disease, which is the leading cause of death worldwide.

The condition is caused by mutations in the genes that code for proteins involved in cholesterol transport and metabolism, such as the low-density lipoprotein receptor gene (LDLR) or the PCSK9 gene. These mutations lead to a decrease in the ability of the liver to remove excess cholesterol from the bloodstream, resulting in high levels of LDL cholesterol and low levels of HDL cholesterol.

Hyperlipoproteinemia type II is usually inherited in an autosomal dominant pattern, meaning that a single copy of the mutated gene is enough to cause the condition. However, some cases can be caused by spontaneous mutations or incomplete penetrance, where not all individuals with the mutated gene develop the condition.

Symptoms of hyperlipoproteinemia type II can include xanthomas (yellowish deposits of cholesterol in the skin), corneal arcus (a white, waxy deposit on the iris of the eye), and tendon xanthomas (small, soft deposits of cholesterol under the skin). Treatment typically involves a combination of dietary changes and medication to lower LDL cholesterol levels and increase HDL cholesterol levels. In severe cases, liver transplantation may be necessary.

Hyperlipoproteinemia type II is a serious condition that can lead to cardiovascular disease, including heart attacks, strokes, and peripheral artery disease. Early diagnosis and treatment are important to prevent or delay the progression of the disease and reduce the risk of complications.

The disease begins with endothelial dysfunction, which allows lipid accumulation in the artery wall. Macrophages take up oxidized lipids and become foam cells, which die and release their contents, including inflammatory cytokines, leading to further inflammation and recruitment of more immune cells.

The atherosclerotic plaque can rupture or ulcerate, leading to the formation of a thrombus that can occlude the blood vessel, causing ischemia or infarction of downstream tissues. This can lead to various cardiovascular diseases such as myocardial infarction (heart attack), stroke, and peripheral artery disease.

Atherosclerosis is a multifactorial disease that is influenced by genetic and environmental factors such as smoking, hypertension, diabetes, high cholesterol levels, and obesity. It is diagnosed by imaging techniques such as angiography, ultrasound, or computed tomography (CT) scans.

Treatment options for atherosclerosis include lifestyle modifications such as smoking cessation, dietary changes, and exercise, as well as medications such as statins, beta blockers, and angiotensin-converting enzyme (ACE) inhibitors. In severe cases, surgical interventions such as bypass surgery or angioplasty may be necessary.

In conclusion, atherosclerosis is a complex and multifactorial disease that affects the arteries and can lead to various cardiovascular diseases. Early detection and treatment can help prevent or slow down its progression, reducing the risk of complications and improving patient outcomes.

The symptoms of hypobetalipoproteinemia usually become apparent during childhood or adolescence and can include:

* Poor growth and development
* Delayed puberty
* Abnormal fat distribution (e.g., accumulation of fat in the face, neck, and abdomen)
* Elevated levels of HDL cholesterol
* Low levels of LDL cholesterol
* Increased risk of bleeding due to low levels of clotting factors
* Abnormal liver function tests

Hypobetalipoproteinemia is caused by mutations in the genes that code for apolipoprotein B-100 or other proteins involved in lipid metabolism. These mutations can be inherited from one or both parents, or they can occur spontaneously.

The diagnosis of hypobetalipoproteinemia is based on a combination of clinical findings, laboratory tests, and genetic analysis. Laboratory tests may include measurements of lipids and lipoproteins, as well as genetic testing to identify mutations in the apolipoprotein B-100 gene or other genes involved in lipid metabolism.

Treatment for hypobetalipoproteinemia typically involves a combination of dietary changes and medication. Dietary changes may include increasing the intake of healthy fats, such as nuts and avocados, while avoiding foods high in saturated and trans fats. Medications may be used to raise HDL cholesterol levels or lower LDL cholesterol levels. In some cases, liver transplantation may be necessary if the condition is caused by a genetic mutation that leads to liver dysfunction.

The prognosis for hypobetalipoproteinemia varies depending on the underlying cause of the condition and the severity of the symptoms. In general, early diagnosis and treatment can improve outcomes and reduce the risk of complications such as cardiovascular disease. However, some individuals with severe forms of the condition may have a poor prognosis if left untreated.

In conclusion, hypobetalipoproteinemia is a rare genetic disorder characterized by very low levels of apolipoprotein B-100 and other lipid abnormalities. The diagnosis is based on laboratory tests and genetic analysis, and treatment typically involves a combination of dietary changes and medication. Early diagnosis and treatment can improve outcomes and reduce the risk of complications such as cardiovascular disease.

There are several types of dyslipidemias, including:

1. Hyperlipidemia: Elevated levels of lipids and lipoproteins in the blood, which can increase the risk of CVD.
2. Hypolipidemia: Low levels of lipids and lipoproteins in the blood, which can also increase the risk of CVD.
3. Mixed dyslipidemia: A combination of hyperlipidemia and hypolipidemia.
4. Familial dyslipidemia: An inherited condition that affects the levels of lipids and lipoproteins in the blood.
5. Acquired dyslipidemia: A condition caused by other factors, such as poor diet or medication side effects.

Dyslipidemias can be diagnosed through a variety of tests, including fasting blood sugar (FBS), lipid profile, and apolipoprotein testing. Treatment for dyslipidemias often involves lifestyle changes, such as dietary modifications and increased physical activity, as well as medications to lower cholesterol and triglycerides.

In conclusion, dyslipidemias are abnormalities in the levels or composition of lipids and lipoproteins in the blood that can increase the risk of CVD. They can be caused by a variety of factors and diagnosed through several tests. Treatment often involves lifestyle changes and medications to lower cholesterol and triglycerides.

Coronary disease is often caused by a combination of genetic and lifestyle factors, such as high blood pressure, high cholesterol levels, smoking, obesity, and a lack of physical activity. It can also be triggered by other medical conditions, such as diabetes and kidney disease.

The symptoms of coronary disease can vary depending on the severity of the condition, but may include:

* Chest pain or discomfort (angina)
* Shortness of breath
* Fatigue
* Swelling of the legs and feet
* Pain in the arms and back

Coronary disease is typically diagnosed through a combination of physical examination, medical history, and diagnostic tests such as electrocardiograms (ECGs), stress tests, and cardiac imaging. Treatment for coronary disease may include lifestyle changes, medications to control symptoms, and surgical procedures such as angioplasty or bypass surgery to improve blood flow to the heart.

Preventative measures for coronary disease include:

* Maintaining a healthy diet and exercise routine
* Quitting smoking and limiting alcohol consumption
* Managing high blood pressure, high cholesterol levels, and other underlying medical conditions
* Reducing stress through relaxation techniques or therapy.

The term "acute-phase" describes the rapid onset and short duration of this reaction, which typically lasts for hours to days before resolving as the body's inflammatory response subsides. APR is characterized by a series of molecular events that result in altered expression of genes involved in inflammation, immune response, and tissue repair.

Some key components of an acute-phase reaction include:

1. Cytokine production: Cytokines are signaling molecules released by immune cells, such as white blood cells, that coordinate the immune response. During an APR, cytokine levels increase, triggering a cascade of downstream effects.
2. Leukocyte trafficking: White blood cells migrate towards sites of inflammation or infection, where they phagocytose (engulf and digest) pathogens and cellular debris. This process helps to limit the spread of infection and initiate tissue repair.
3. Coagulation cascade: The APR triggers a complex series of events involving blood coagulation factors, leading to the formation of blood clots and preventing excessive bleeding.
4. Anti-inflammatory response: As the APR progresses, anti-inflammatory cytokines, such as interleukin-10 (IL-10), are produced to dampen the inflammatory response and promote tissue repair.
5. Cellular proliferation: To replace damaged cells and tissues, the APR stimulates cellular proliferation and tissue regeneration.
6. Nutrient mobilization: The APR enhances nutrient uptake and utilization by immune cells, allowing them to mount an effective response to the stress.
7. Hormonal changes: The APR is accompanied by changes in hormone levels, such as the increase in corticotropin-releasing factor (CRF) and cortisol, which help to mobilize energy resources and regulate metabolism.
8. Immune tolerance: The APR helps to establish immune tolerance, preventing excessive or inappropriate immune responses that can lead to autoimmune diseases or allergies.
9. Tissue remodeling: The APR stimulates the remodeling of damaged tissues, allowing for the restoration of normal tissue function.
10. Memory formation: The APR sets the stage for the formation of immunological memory, which enables the immune system to mount a more effective response to future infections or stressors.

There are several types of hypercholesterolemia, including:

1. Familial hypercholesterolemia: This is an inherited condition that causes high levels of low-density lipoprotein (LDL) cholesterol, also known as "bad" cholesterol, in the blood.
2. Non-familial hypercholesterolemia: This type of hypercholesterolemia is not inherited and can be caused by a variety of factors, such as a high-fat diet, lack of exercise, obesity, and certain medical conditions, such as hypothyroidism or polycystic ovary syndrome (PCOS).
3. Mixed hypercholesterolemia: This type of hypercholesterolemia is characterized by high levels of both LDL and high-density lipoprotein (HDL) cholesterol in the blood.

The diagnosis of hypercholesterolemia is typically made based on a physical examination, medical history, and laboratory tests, such as a lipid profile, which measures the levels of different types of cholesterol and triglycerides in the blood. Treatment for hypercholesterolemia usually involves lifestyle changes, such as a healthy diet and regular exercise, and may also include medication, such as statins, to lower cholesterol levels.

The condition is caused by mutations in the genes that code for proteins involved in lipid metabolism, such as the LDL receptor gene or the apoB100 gene. These mutations lead to a deficiency of functional LDL receptors on the surface of liver cells, which results in reduced clearance of LDL cholesterol from the blood and increased levels of LDL-C.

The main symptom of hyperlipoproteinemia type III is very high levels of LDL-C (>500 mg/dL) and low levels of HDL-C (<20 mg/dL). Other signs and symptoms may include xanthomas (fatty deposits in the skin), corneal arcus (a cloudy ring around the cornea of the eye), and an increased risk of cardiovascular disease.

Treatment for hyperlipoproteinemia type III typically involves a combination of dietary changes, such as reducing intake of saturated fats and cholesterol, and medications, such as statins or other lipid-lowering drugs, to lower LDL-C levels. In severe cases, a liver transplant may be necessary.

Hyperlipoproteinemia type III is an autosomal dominant disorder, meaning that a single copy of the mutated gene is enough to cause the condition. It is important to identify and treat individuals with this condition early to prevent or delay the development of cardiovascular disease.

... D Apolipoprotein E Apolipoprotein F Apolipoprotein H - a misnomer Apolipoprotein L Apolipoprotein M ... Apolipoprotein A (Apo-AI, Apo-A2, Apo-A4, and Apo-A5) Apolipoprotein B (Apo-B48 and Apo B-100) Apolipoprotein C (ApoC-I, apo ... Apolipoprotein F (apoF) is one of the minor apolipoprotein in blood plasma and it is a lipid transfer inhibit protein to ... Apolipoprotein synthesis in the intestine is regulated principally by the fat content of the diet. Apolipoprotein synthesis in ...

https://en.wikipedia.org/wiki/Apolipoprotein

... is a protein that in humans is encoded by the APOL1 gene. Two transcript variants encoding two different ... APOL1 is a member of a family of apolipoproteins which also includes six other proteins and it is a member of bcl2 genes which ... G2 is an in-frame deletion of the two amino acid residues, N388 and Y389.[citation needed] Apolipoprotein L1 (apoL1) is a minor ... particles that also contain apolipoprotein A1 (APOA1) and the hemoglobin-binding, haptoglobin-related protein (HPR). The APOL1 ...

https://en.wikipedia.org/wiki/Apolipoprotein_L1

Identification of apolipoprotein D, apolipoprotein A-IV, apolipoprotein E, and apolipoprotein A-I". The Journal of Biological ... Apolipoprotein D (ApoD) is a component of HDL that has no marked similarity to other apolipoprotein sequences. It has a high ... "Entrez Gene: APOD apolipoprotein D". Muffat J, Walker DW (January 2010). "Apolipoprotein D: an overview of its role in aging ... Apolipoproteins+D at the US National Library of Medicine Medical Subject Headings (MeSH) Applied Research on Apolipoproteins ...

https://en.wikipedia.org/wiki/Apolipoprotein_D

Apolipoprotein+H at the US National Library of Medicine Medical Subject Headings (MeSH) Apolipoprotein H and Applied Research ... The first four domains found in Apolipoprotein H resemble each other, however the fifth one appears to be different. This ... PDBe-KB provides an overview of all the structure information available in the PDB for Human Apolipoprotein H (B2G1) (Articles ... β2-glycoprotein 1, also known as beta-2 glycoprotein 1 and Apolipoprotein H (Apo-H), is a 38 kDa multifunctional plasma protein ...

https://en.wikipedia.org/wiki/Apolipoprotein_H

The gene, APOE, is mapped to chromosome 19 in a cluster with apolipoprotein C1 (APOC1) and the apolipoprotein C2 (APOC2). The ... "Genetic studies of human apolipoproteins. X. The effect of the apolipoprotein E polymorphism on quantitative levels of ... Apolipoprotein E (APOE) is a protein involved in the metabolism of fats in the body of mammals. A subtype is implicated in ... Apolipoprotein E enhances proteolytic break-down of this peptide, both within and between cells. The isoform APOE-ε4 is not as ...

https://en.wikipedia.org/wiki/Apolipoprotein_E

... (ApoB) is a protein that in humans is encoded by the APOB gene. Apolipoprotein B is the primary apolipoprotein ... Su Q, Tsai J, Xu E, Qiu W, Bereczki E, Santha M, Adeli K (2009). "Apolipoprotein B100 acts as a molecular link between lipid- ... MedlinePlus Encyclopedia: Apolipoprotein B100 Cromwell WC, Otvos JD, Keyes MJ, Pencina MJ, Sullivan L, Vasan RS, Wilson PW, ... Overproduction of apolipoprotein B can result in lipid-induced endoplasmic reticulum stress and insulin resistance in the liver ...

https://en.wikipedia.org/wiki/Apolipoprotein_B

... (ApoA-I) is a protein that in humans is encoded by the APOA1 gene. As the major component of HDL particles, ... The encoded apolipoprotein A-I, is a 28.1 kDa protein composed of 243 amino acids; 21 peptides have been observed through mass ... Apolipoprotein AI has also been isolated as a prostacyclin (PGI2) stabilizing factor, and thus may have an anticlotting effect ... Apolipoprotein AI is the major protein component of high density lipoprotein (HDL) particles in plasma. Chylomicrons secreted ...

https://en.wikipedia.org/wiki/Apolipoprotein_AI

... (Apo L) is found in high-density lipoprotein complexes that plays a central role in cholesterol transport. The ... reproducible up-regulation of several members of the apolipoprotein L family located in a high-susceptibility locus for ...

https://en.wikipedia.org/wiki/Apolipoprotein_L

In the field of molecular biology, apolipoprotein C is a family of four low molecular weight apolipoproteins, designated as C-I ... In the fasting state, the C apolipoproteins are mainly associated with HDL. During absorption of dietary fat, the C ... v t e (Articles with short description, Short description matches Wikidata, Apolipoproteins, All stub articles, Protein stubs) ... Mahley RW, Innerarity TL, Rall SC, Weisgraber KH (December 1984). "Plasma lipoproteins: apolipoprotein structure and function ...

https://en.wikipedia.org/wiki/Apolipoprotein_C

... is the first chondroitine sulphate chain containing apolipoprotein. Apolipoproteins are proteins that binds to ... APOO is a member of the apolipoprotein family. The human, apolipoprotein O is a 198 amino acids protein that contains a 23 ... Apolipoprotein O also known as protein FAM121B is a protein that in humans is encoded by the APOO gene. ... 2009). "Gene-centric association signals for lipids and apolipoproteins identified via the HumanCVD BeadChip". Am. J. Hum. ...

https://en.wikipedia.org/wiki/Apolipoprotein_O

... (Apo-CII, or Apoc-II), or apolipoprotein C2 is a protein that in humans is encoded by the APOC2 gene. The ... 1989). "A nonsense mutation in the apolipoprotein C-IIPadova gene in a patient with apolipoprotein C-II deficiency". J. Clin. ... Connelly PW, Maguire GF, Little JA (1988). "Apolipoprotein CIISt. Michael. Familial apolipoprotein CII deficiency associated ... "Entrez Gene: APOC2 apolipoprotein C-II". Jackson RL, Baker HN, Gilliam EB, Gotto AM (1977). "Primary structure of very low ...

https://en.wikipedia.org/wiki/Apolipoprotein_C-II

... , also known as apolipoprotein C4, is a protein that in humans is encoded by the APOC4 gene. APOC4 is a ... "Entrez Gene: apolipoprotein C-IV". Allan CM, Walker D, Segrest JP, Taylor JM (July 1995). "Identification and characterization ... 2008). "Expression of apolipoprotein C-IV is regulated by Ku antigen/peroxisome proliferator-activated receptor gamma complex ... 2002). "Regulated expression of the apolipoprotein E/C-I/C-IV/C-II gene cluster in murine and human macrophages. A critical ...

https://en.wikipedia.org/wiki/Apolipoprotein_C-IV

... is an autosomal dominant disorder resulting from a missense mutation which reduces the affinity of ...

https://en.wikipedia.org/wiki/Apolipoprotein_B_deficiency

In autoimmune disease, anti-apolipoprotein H (AAHA) antibodies, also called anti-β2 glycoprotein I antibodies, comprise a ...

https://en.wikipedia.org/wiki/Anti-apolipoprotein_antibodies

... also known as apo-CIII, and apolipoprotein C3, is a protein that in humans is encoded by the APOC3 gene. ... Karathanasis SK (Oct 1985). "Apolipoprotein multigene family: tandem organization of human apolipoprotein AI, CIII, and AIV ... Apolipoprotein+C-III at the US National Library of Medicine Medical Subject Headings (MeSH) Human APOC3 genome location and ... Zannis VI, Cole FS, Jackson CL, Kurnit DM, Karathanasis SK (Jul 1985). "Distribution of apolipoprotein A-I, C-II, C-III, and E ...

https://en.wikipedia.org/wiki/Apolipoprotein_C-III

Myklebost O, Rogne S (August 1986). "The gene for human apolipoprotein CI is located 4.3 kilobases away from the apolipoprotein ... "Two copies of the human apolipoprotein C-I gene are linked closely to the apolipoprotein E gene". The Journal of Biological ... Apolipoprotein C-I is a protein component of lipoproteins that in humans is encoded by the APOC1 gene. The protein encoded by ... "Entrez Gene: APOC1 apolipoprotein C-I". Puppione DL, Ryan CM, Bassilian S, Souda P, Xiao X, Ryder OA, Whitelegge JP (March 2010 ...

https://en.wikipedia.org/wiki/Apolipoprotein_C-I

... is a protein that in humans is encoded by the APOA2 gene. APOA2 encodes apolipoprotein A-II, (ApoA-II) ... "Entrez Gene: APOA2 apolipoprotein A-II". Pussinen PJ, Jauhiainen M, Metso J, Pyle LE, Marcel YL, Fidge NH, Ehnholm C (Jan 1998 ... Brewer HB, Lux SE, Ronan R, John KM (May 1972). "Amino acid sequence of human apoLp-Gln-II (apoA-II), an apolipoprotein ... The protein is found in plasma as a monomer, homodimer, or heterodimer with apolipoprotein D. Defects in this gene may result ...

https://en.wikipedia.org/wiki/Apolipoprotein_A-II

The apolipoprotein B (apoB) 5′ UTR cis regulatory element is an RNA element located in the 5′ UTR of the human apoB mRNA. This ... Page for Apolipoprotein B (apoB) 5′ UTR cis-regulatory element at Rfam v t e (Articles with short description, Short ... Pontrelli L, Sidiropoulos KG, Adeli K (June 2004). "Translational control of apolipoprotein B mRNA: regulation via cis elements ...

https://en.wikipedia.org/wiki/Apolipoprotein_B_(apoB)_5′_UTR_cis-regulatory_element

1996). Apolipoprotein E and Alzheimer's Disease. Research and Perspectives in Alzheimer's Disease. Berlin, Heidelberg: Springer ... "Maestre CV" (PDF). Maestre, Gladys Elena (1996). Apolipoproteins and Alzheimer's disease (Thesis). OCLC 36257436. Staff, M. D. ... "The apolipoprotein ?4 allele in patients with Alzheimer's disease". Annals of Neurology. 34 (5): 752-754. doi:10.1002/ana. ... "Apolipoprotein E and alzheimer's disease: Ethnic variation in genotypic risks". Annals of Neurology. 37 (2): 254-259. doi: ...

https://en.wikipedia.org/wiki/Gladys_Maestre

... apolipoprotein D; beta-lactoglobulin; complement component C8 gamma chain; crustacyanin; epididymal-retinoic acid binding ...

https://en.wikipedia.org/wiki/Lipocalin

Apolipoprotein A-1 Milano (also ETC-216, now MDCO-216) is a naturally occurring mutated variant of the apolipoprotein A1 ... Weisgraber KH, Rall SC, Bersot TP, Mahley RW, Franceschini G, Sirtori CR (25 February 1983). "Apolipoprotein A-IMilano. ...

https://en.wikipedia.org/wiki/ApoA-1_Milano

Kim DH, Iijima H, Goto K, Sakai J, Ishii H, Kim HJ, Suzuki H, Kondo H, Saeki S, Yamamoto T (Jun 1996). "Human apolipoprotein E ... Apolipoprotein E (ApoE) plays an important role in phospholipid and cholesterol homeostasis. After binding ApoER2, ApoE is ... Riddell DR, Sun XM, Stannard AK, Soutar AK, Owen JS (2001). "Localization of apolipoprotein E receptor 2 to caveolae in the ... Herz J (June 2009). "Apolipoprotein E receptors in the nervous system". Curr. Opin. Lipidol. 20 (3): 190-6. doi:10.1097/MOL. ...

https://en.wikipedia.org/wiki/Low-density_lipoprotein_receptor-related_protein_8

Apolipoprotein M is a protein that in humans is encoded by the APOM gene. The protein encoded by this gene is an apolipoprotein ... "Entrez Gene: APOM apolipoprotein M". Albertella MR, Jones H, Thomson W, et al. (1997). "Localization of eight additional genes ... Overview of all the structural information available in the PDB for UniProt: O95445 (Human Apolipoprotein M) at the PDBe-KB. v ... 2004). "Regulation of apolipoprotein M gene expression by MODY3 gene hepatocyte nuclear factor-1alpha: haploinsufficiency is ...

https://en.wikipedia.org/wiki/APOM

Xu, Ning; Dahlbäck, Björn (1999). "A Novel Human Apolipoprotein (ApoM)". Journal of Biological Chemistry. 274 (44): 31286-31290 ... "Endothelium-protective sphingosine-1-phosphate provided by HDL-associated apolipoprotein M". Proceedings of the National ...

https://en.wikipedia.org/wiki/Björn_Dahlbäck

"Genetic studies of human apolipoproteins. XVIII. apolipoprotein polymorphisms in Australian Aborigines", Human Biology, 63 (2 ...

https://en.wikipedia.org/wiki/Susan_Serjeantson

"Entrez Gene: APOL3 apolipoprotein L, 3". Gaudet RG, Zhu S, Halder A, Kim BH, Bradfield CJ, Huang S, et al. (2021). "A human ... Apolipoprotein L3 is a protein that in humans is encoded by the APOL3 gene. Expressed in the gut, it has antibiotic properties ... This gene is a member of the apolipoprotein L gene family. The encoded protein is found in the cytoplasm, where it may affect ... Duchateau PN, Pullinger CR, Cho MH, Eng C, Kane JP (April 2001). "Apolipoprotein L gene family: tissue-specific expression, ...

https://en.wikipedia.org/wiki/APOL3

Gain of toxic Apolipoprotein E4 effects in Human iPSC-Derived Neurons Is Ameliorated by a Small-Molecule Structure Corrector. ... Alzheimer's disease and apolipoprotein E (apoE). Uncovered the molecular pathways that link apoE and Alzheimer's disease, and ...

https://en.wikipedia.org/wiki/Gladstone_Institutes

Apolipoprotein L2 is a protein that in humans is encoded by the APOL2 gene. This gene is a member of the apolipoprotein L gene ... "Entrez Gene: APOL2 apolipoprotein L, 2". "The Human Protein atlas Gene: APOL2 apolipoprotein L, 2". Liao W, Goh FY, Betts RJ, ... "The Human Protein atlas Gene: APOL2 apolipoprotein L, 2". Rao SK, Pavicevic Z, Du Z, Kim JG, Fan M, Jiao Y, Rosebush M, Samant ... "Nextprot Gene: APOL2 apolipoprotein L, 2". Luo, Audrey; Jung, Jeesun; Longley, Martha; Rosoff, Daniel B.; Charlet, Katrin; ...

https://en.wikipedia.org/wiki/APOL2

Apolipoprotein L6 is a protein that in humans is encoded by the APOL6 gene. This gene is a member of the apolipoprotein L gene ... "Entrez Gene: APOL6 apolipoprotein L, 6". Human APOL6 genome location and APOL6 gene details page in the UCSC Genome Browser. ... Liu Z, Lu H, Jiang Z, Pastuszyn A, Hu CA (Jan 2005). "Apolipoprotein l6, a novel proapoptotic Bcl-2 homology 3-only protein, ... Page NM, Butlin DJ, Lomthaisong K, Lowry PJ (May 2001). "The human apolipoprotein L gene cluster: identification, ...

https://en.wikipedia.org/wiki/APOL6

The HDL donates apolipoprotein C-II (APOC2) and apolipoprotein E (APOE) to the nascent chylomicron and, thus, converts it to a ... The main apolipoprotein component is ApoB48. While circulating in blood, chylomicrons exchange components with high-density ... Apolipoproteins are significant in the synthesis and metabolism of chylomicrons. Newly formed chylomicrons are secreted through ... The triglycerides are then combined with phospholipids, cholesteryl esters, and apolipoprotein B48 (ApoB48) to form a nascent ...

https://en.wikipedia.org/wiki/Chylomicron

LBXAPB - Apolipoprotein (B) (mg/dL). Variable Name: LBXAPB. SAS Label: Apolipoprotein (B) (mg/dL). English Text: Apolipoprotein ... LBDAPBSI - Apolipoprotein (B) (g/L). Variable Name: LBDAPBSI. SAS Label: Apolipoprotein (B) (g/L). English Text: Apolipoprotein ... Apolipoprotein B (ApoB_G) Data File: ApoB_G.xpt First Published: January 2014. Last Revised: NA ... Apolipoprotein B is the main protein component of LDL and accounts for approximately 95% of the total protein content of LDL. ...

https://wwwn.cdc.gov/Nchs/Nhanes/2011-2012/APOB_G.htm

Apolipoprotein B100 (apoB100) is a protein that plays a role in moving cholesterol around your body. It is a form of low ... Apolipoprotein B100 (apoB100) is a protein that plays a role in moving cholesterol around your body. It is a form of low ... Apolipoprotein measurements may provide more detail about your risk for heart disease, but the added value of this test beyond ... Regulation and clearance of apolipoprotein B-containing lipoproteins. In: Ballantyne CM, ed. Clinical Lipidology: A Companion ...

https://medlineplus.gov/ency/article/003502.htm

Apolipoprotein E (apoE), the major apolipoprotein of the CNS and an important regulator of cholesterol and … ... Apolipoprotein E (apoE), the major apolipoprotein of the CNS and an important regulator of cholesterol and lipid transport, ... Genetic association of apolipoprotein E with age-related macular degeneration Am J Hum Genet. 1998 Jul;63(1):200-6. doi: ...

https://pubmed.ncbi.nlm.nih.gov/9634502/

Mouse Monoclonal Apolipoprotein B antibody [F2C13]. Validated in ICC/IF, IP, ELISA, RIA. Tested in Human. ... There are currently no reviews for Apolipoprotein B antibody [F2C13] (GTX15663). Be the first to share your experience with ... This gene product is the main apolipoprotein of chylomicrons and low density lipoproteins. It occurs in plasma as two main ... ICC/IF analysis of HepG2 cells using GTX15663 Apolipoprotein B antibody [F2C13]. Panel e is a no primary antibody control. ...

https://www.genetex.com/Product/Detail/Apolipoprotein-B-antibody-F2C13/GTX15663

The ε4 allele of apolipoprotein E is a risk factor for Alzheimers disease. The effect of apolipoprotein E polymorphism on ... 5-8 The apolipoprotein E gene, located on chromosome 19, has three major alleles: ε2, ε3, and ε4. Apolipoprotein E is present ... 1995) Apolipoprotein E type 4 allele and cerebral glucose metabolism in relatives at risk for familial Alzheimer disease. JAMA ... 1994) Apolipoprotein E in animal models of CNS injury and in Alzheimers disease. TINS 17:525-530. ...

https://jnnp.bmj.com/content/64/6/742

Among them, apolipoprotein C-II (apoC-II) was found to have the highest abundance among the CKD patients with hypertension. As ... As such, we hypothesized that apoC-II and apolipoprotein C-III (ApoC-III) levels were related to BP abnormalities and CVD in ... Among them, apolipoprotein C-II (ApoC-II) was found to have the highest abundance among the CKD patients with hypertension. ... such, we hypothesized that apoC-II and apolipoprotein C-III (apoC-III) levels were related to BP abnormalities and CVD in ...

https://www.frontiersin.org/articles/10.3389/fped.2021.706323/full

Effects of omega-3 fatty acid supplements on serum lipids, apolipoproteins and malondialdehyde in type 2 diabetes patients ... The aim of this study was to determine the effects of purified omega-3 fatty acids on serum lipoproteins, apolipoprotein B-100 ... Apo B-100), apolipoprotein A-I (Apo A-I), malondialdehyde (MDA) (as index for lipid peroxidation), and glycaemic control in ... apolipoproteins and malondialdehyde in type 2 diabetes patients ... apolipoproteins and malondialdehyde in type 2 diabetes patients ...

http://www.emro.who.int/emhj-volume-14-2008/volume-14-issue-2/article8.html

... and apoE as well as the ratios of apolipoproteins with apoA1 with the risk of T2D. All apolipoproteins, ratios, and HDL-C ... Serum levels of apolipoproteins and incident type 2 diabetes: A prospective cohort study. Publication. Publication. Diabetes ... OBJECTIVE We aimed to investigate the role of serumlevels of various apolipoproteins on the risk for type 2 diabetes (T2D). ... Second, Cox proportional hazard models were used to examine whether apolipoproteins predict the risk for T2D among individuals ...

https://repub.eur.nl/pub/108658

Genotypes were determined using DNA markers for the low-density lipoprotein receptor, apolipoprotein B, apolipoprotein CIII and ... Genetic Variation Associated with Differences in the Response of Plasma Apolipoprotein B Levels to Dietary Fibre Robert A. ... Fasting blood lipid, lipoprotein and apolipoprotein concentrations were measured at the start and end of the 2 week metabolic ... 1. We hypothesized that differences within genes whose protein products are involved in apolipoprotein B metabolism could ...

https://portlandpress.com/clinsci/article-abstract/85/3/269/75884/Genetic-Variation-Associated-with-Differences-in?redirectedFrom=fulltext

APOLIPOPROTEIN E-DEFICIENT MICE. The generation of the apolipoprotein E-deficient mouse has been one of the most important ... These apolipoprotein A-IV-enriched particles were very effective in inactivating the peroxides present in the low-density ... apoE: apolipoprotein E. HDL: high-density lipoprotein. LDL: low-density lipoprotein. VLDL: very low-density lipoprotein ... Accelerated atherosclerosis in apolipoprotein E-deficient mice fed Western diets containing palm oil compared with extra virgin ...

https://www.revespcardiol.org/en-knowledge-biological-actions-extra-virgin-articulo-13135142

Tissue and/or cellular expressions of interleukin-1 alpha (IL-1α), apolipoprotein E (ApoE), amyloid β (Aβ) precursor protein ( ... Aboud, O., Mrak, R.E., Boop, F. et al. Apolipoprotein epsilon 3 alleles are associated with indicators of neuronal resilience. ... Apolipoprotein epsilon 3 alleles are associated with indicators of neuronal resilience. *Orwa Aboud1,3, ... Liu L, Aboud O, Jones RA, Mrak RE, Griffin ST, Barger SW: Apolipoprotein E expression is elevated by interleukin 1 and other ...

https://bmcmedicine.biomedcentral.com/articles/10.1186/1741-7015-10-35

This is a miscellaneous resource located at http://www.genome.jp/dbget-bin/www_bget?hsa:335

https://edrn.nci.nih.gov/data-and-resources/miscellaneous-resources/kegg-entry-for-human-apolipoprotein-a-i-apoa1/

Beta 2-glycoprotein-1 (apolipoprotein H) excretion in chronic renal tubular disorders: comparison with other protein markers of ... Beta 2-glycoprotein-1 (apolipoprotein H) excretion in chronic renal tubular disorders: comparison with other protein markers of ... Beta 2-glycoprotein-1 (apolipoprotein H) excretion in chronic renal tubular disorders: comparison with other protein markers of ...

https://jcp.bmj.com/content/44/10/812.citation-tools

The EU Joint Programme - Neurodegenerative Disease Research (JPND) is the largest global research initiative aimed at tackling the challenge of neurodegenerative diseases, in particular, Alzheimers.. Join Us ...

https://neurodegenerationresearch.eu/survey/cell-autonomous-mechanisms-of-apolipoprotein-e-isoform-dependent-neurodegeneration/

Deletion of the propeptide of apolipoprotein A-I impairs exit of nascent apolipoprotein A-I from the endoplasmic reticulum. ... Structural proteins of the alpha-lipoproteins (HIGH DENSITY LIPOPROTEINS), including APOLIPOPROTEIN A-I and APOLIPOPROTEIN A-II ... Apolipoprotein A5 gene variants and the risk of coronary heart disease: a case-control study and meta-analysis. Mol Med Rep. ... "Apolipoproteins A" is a descriptor in the National Library of Medicines controlled vocabulary thesaurus, MeSH (Medical Subject ...

https://profiles.uchicago.edu/profiles/display/11442

The Apolipoprotein A-II (APOA2) gene is associated with the synthesis of Apolipoprotein 2, the second most common protein found ...

https://www.xcode.life/tag/apolipoprotein-ii/

The role of apolipoprotein N-acyl transferase, Lnt, in the lipidation of factor H binding protein of Neisseria meningitidis ... In a mutant with markedly reduced binding, the transposon was located in the lnt gene which encodes apolipoprotein N-acyl ... The role of apolipoprotein N-acyl transferase, Lnt, in the lipidation of factor H binding protein of Neisseria meningitidis ... The role of apolipoprotein N-acyl transferase, Lnt, in the lipidation of factor H binding protein of Neisseria meningitidis ...

https://eprints.nottingham.ac.uk/48687/

The initial apolipoproteins are apolipoprotein (apo) A, which are soluble and can transfer to HDL; and apo B48, a structural ... VLDLs and apolipoproteins. VLDLs are produced by a process analogous to the exogenous pathway. Triglycerides may derive from de ... As IDL is metabolized by hepatic lipase to LDL, the remaining surface apolipoproteins are lost. [6, 4, 7] ... Corbo RM, Scacchi R. Apolipoprotein E (APOE) allele distribution in the world. Is APOE*4 a thrifty allele?. Ann Hum Genet. ...

https://emedicine.medscape.com/article/126568-overview

Apolipoprotein E (apoE) is highly expressed in the brain and plays a pivotal role in cholesterol metabolism. ApoE can also ... Altered apolipoprotein e glycosylation is associated with Aβ(42) accumulation in an animal model of Niemann-Pick Type C disease ... Chua, C.-C., Lim, M.-L., Wong, B.-S. (2010-03). Altered apolipoprotein e glycosylation is associated with Aβ(42) accumulation ...

https://scholarbank.nus.edu.sg/handle/10635/109163

Apolipoprotein E genotype status affects habitual human blood mononuclear cell gene expression and its response to fish oil ... SCOPE: People who carry the apolipoprotein E4 (APOE4) SNP have an increased risk of cardiovascular disease (CVD). Fish-oil ... ORCID: https://orcid.org/0000-0002-5930-9905 and Afman, Lydia (2016) Apolipoprotein E genotype status affects habitual human ...

https://ueaeprints.uea.ac.uk/id/eprint/58184/

Yang CY, Gu ZW, Blanco-Vaca F, Gaskell SJ, Yang M, Massey JB, Gotto AM Jr, Pownall HJ: Structure of human apolipoprotein D: ... Balbin M, Freije JM, Fueyo A, Sanchez LM, Lopez-Otin C: Apolipoprotein D is the major protein component in cyst fluid from ... Peitsch MC, Boguski MS: Is apolipoprotein D a mammalian bilin-binding protein? New Biol. 1990 Feb;2(2):197-206. 2083249 ... Holzfeind P, Merschak P, Dieplinger H, Redl B: The human lacrimal gland synthesizes apolipoprotein D mRNA in addition to tear ...

http://www.t3db.ca/biodb/polypeptides/P05090

Interaction of apolipoprotein E gene polymorphisms on miscarriage risk in black and white American women.. ... Apolipoprotein E4, Abortion, Spontaneous, Apolipoprotein E2, Pregnancy, Black People, White People ... Interaction of apolipoprotein E gene polymorphisms on miscarriage risk in black and white American women. Fertil Steril 2016 ... Home Publications Interaction of apolipoprotein E gene polymorphisms on miscarriage risk in black and white American women. ...

https://biolincc.nhlbi.nih.gov/publications/56722dcbc72c460aa3b4f48c1ca3b9a4

Identification of apolipoprotein A-I as a plasma ligand for macrophage scavenger receptor A ... Identification of apolipoprotein A-I as a plasma ligand for macrophage scavenger receptor A ...

https://www.phc.ox.ac.uk/publications/17816

Heart HealthApolipoprotein Evaluation. Home » Shop » Lab Test Categories (USA) » Alphabetical,Lab Test Categories (USA) » ...

https://truehealthlabs.com/product/apolipoprotein-evaluation/

Apolipoprotein E. The gene regulating the apolipoprotein E is considered a significant risk factor in the presence of AD in ... Another important factor could be the apolipoprotein E (APOE) epsilon four allele, which is also associated with a higher risk ...

https://emedicine.medscape.com/article/1136117-overview

Apolipoprotein A-1. $15.93. [ApoA1] Apo A-1 has been suggested as a better discrimination of Coronary Artery Disease [CAD] than ... Alpha-Apolipoprotein. Apo A-1 has been suggested as a better discrimination of [coronary artery disease] CAD than HDL. Apo A-1 ...

https://ownyourlabs.com/product/apolipoprotein-a-1/

Apolipoprotein A2 isoforms associated with exocrine pancreatic insufficiency in early chro Apolipoprotein A2 isoforms ... Apolipoprotein A2 (apoA2) isoforms have been reported to undergo the aberrant processing in pancreatic cancer and pancreatic ... apolipoprotein A2; early chronic pancreatitis; endosonography; exocrine pancreatic dysfunction; exocrine pancreatic ...

https://pesquisa.bvsalud.org/bolivia/resource/es/mdl-37501507

This test measures the amount of a protein in your blood related to LDL and HDL cholesterol. It can help predict your risk for heart disease.

https://healthinfo.uclahealth.org/Wellness/BloodPressure/167,apolipoprotein_a

Recombinant Human Apolipoprotein C-II Protein. Synthesized inE.coli ;Yeast. Protein Tag: His-SUMO. Purity: Greater than 90% as ... Recombinant Human Apolipoprotein C-II Protein. $ 448.00 - $ 2,148.00. Please Select Product Options Below To View The Catalog ... Be the first to review "Recombinant Human Apolipoprotein C-II Protein" Cancel reply. Your email address will not be published. ... Protein Construction: A DNA sequence encoding the Homo sapiens (Human) Apolipoprotein C-II, was expressed in the hosts and tags ...

https://enquirebio.com/proteins/QP5665-Apolipoprotein-C-II

We studied the association of HDL cholesterol (HDL-C), apoA1, apoCIII, apoD, and apoE as well as the ratios of apolipoproteins with apoA1 with the risk of T2D. (eur.nl)
Apolipoprotein E (APOE) is found in VLDL and binds to potential receptors involved in HCV entry into cells, the LDL receptor, and the scavenger receptor protein SR-B1. (ncl.ac.uk)
BACKGROUND AND AIMS: The human Apolipoprotein E (APOE) gene is polymorphic. (nih.gov)
Apolipoprotein E (ApoE) genotype is the strongest genetic risk factor for late-onset Alzheimer's disease, with the ε4 allele increasing risk in a dose-dependent fashion. (nih.gov)

Regulation and clearance of apolipoprotein B-containing lipoproteins. (medlineplus.gov)
We examined the plasma lipids, lipoproteins, and selected apolipoproteins in approximately 9,000 men and women from six different regions of Turkey with markedly different diets, ranging from an Aegean coast diet high in olive oil (plasma cholesteryl ester fatty acids enriched in monounsaturated fatty acids) to an inland Anatolian diet high in meat and dairy products (plasma cholesteryl esters enriched in saturated fatty acids). (nih.gov)
This gene product is the main apolipoprotein of chylomicrons and low density lipoproteins. (genetex.com)
Month-to-month variability of lipids, lipoproteins, and apolipoproteins and the impact of acute infection in adolescents. (uchicago.edu)
ApoCIII is a plasma apolipoprotein playing a major role in the metabolism of triglyceride -rich lipoproteins , namely chylomicrons and very-low-density lipoproteins as well as in the pathological processes involved in atherosclerosis . (bvsalud.org)
BACKGROUND: ApoAI (apolipoproteins AI) and apoAII (apolipoprotein AII) are structural and functional proteins of high-density lipoproteins (HDL) which undergo post-translational modifications at specific residues, creating distinct proteoforms. (umn.edu)

The ultimate goal is to gain an in depth understanding of the mechanisms by which the Apolipoprotein E e4 allele confers increased AD risk for the purpose of advancing the overall search for efficacious AD treatments and Apolipoprotein E e4-directed therapeutics in particular. (nih.gov)
The ε4 allele of apolipoprotein E is a risk factor for Alzheimer's disease. (bmj.com)
CONCLUSION Apolipoprotein E polymorphism is involved in the pathogenesis and heterogeneity of Alzheimer's disease as the most severe cerebral hypoperfusion was found in the ε4 allele subgroups. (bmj.com)
1-4 The ε4 allele of apolipoprotein E is a risk factor for Alzheimer's disease and accelerates the onset of dementia. (bmj.com)

Genotypes were determined using DNA markers for the low-density lipoprotein receptor, apolipoprotein B, apolipoprotein CIII and hepatic lipase gene loci. (portlandpress.com)
Hypertriglyceridemia and the apolipoprotein CIII gene locus: lack of association with the variant insulin response element in Italian school children. (uchicago.edu)
Recent Apolipoprotein CIII trials. (bvsalud.org)
PURPOSE OF REVIEW This review will briefly revise the evidence concerning the pharmacological inhibition of Apolipoprotein CIII (ApoCIII) in patients with hypertriglyceridemia . (bvsalud.org)

This patent covers cellular models expressing variants of the human gene Apolipoprotein E. This invention not only allows for the evaluation of cellular phenotypes but also enables the creation of models for genetic and chemical screening. (nih.gov)
5-8 The apolipoprotein E gene, located on chromosome 19, has three major alleles: ε2, ε3, and ε4. (bmj.com)
Although there have been some recent cell and animal experiments indicating that expression of the gene encoding apolipoprotein B mRNA editing enzyme catalytic subunit 3B ( APOBEC3B ) is closely related to cancer, it still lacks pan-cancer analysis. (biomedcentral.com)
The apolipoprotein B mRNA editing enzyme catalytic subunit 3B ( APOBEC3B ) protein, also known as A3B or ARP4, is a member of the cytidine deaminase gene family [ 6 ]. (biomedcentral.com)
Apolipoprotein A5 gene variants and the risk of coronary heart disease: a case-control study and meta-analysis. (uchicago.edu)
In a mutant with markedly reduced binding, the transposon was located in the lnt gene which encodes apolipoprotein N-acyl transferase, Lnt, responsible for the addition of the third fatty acid to apolipoproteins prior to their sorting to the outer membrane. (nottingham.ac.uk)

In an immunochemical reaction, Apolipoprotein B in the human serum sample form immune complexes with specific antibodies. (cdc.gov)
Serum apolipoprotein E is associated with long-term risk of Alzheimer's disease: The Rotterdam Study. (ox.ac.uk)

Apolipoprotein E is present in senile plaques, neurofibrillary tangles, and cerebrovascular amyloid, the major neuropathological changes seen in Alzheimer's disease. (bmj.com)
Different binding properties of the apolipoprotein isoforms to β-amyloid and tau protein also suggests that it is involved in the pathogenesis of Alzheimer's disease. (bmj.com)

Holzfeind P, Merschak P, Dieplinger H, Redl B: The human lacrimal gland synthesizes apolipoprotein D mRNA in addition to tear prealbumin mRNA, both species encoding members of the lipocalin superfamily. (t3db.ca)

There was no significant variation in the reduction of plasma total cholesterol, low-density lipoprotein cholesterol or apolipoprotein B concentrations for alleles of other genes tested. (portlandpress.com)

These results pro-vide "proof-of-concept" that precise chemical characterization of human apolipoproteins will yield improved insights into the complex pathways through which proteins signify and mediate health and disease. (umn.edu)

This FOA encouarges multidisciplinary and interdisciplinary research to elucidate how Apolipoprotein E, lipoprotein receptors and CNS lipid homeostasis influence brain aging and the transition to neurodegeneration in Alzheimers disease (AD). (nih.gov)

Apolipoprotein E (Apo-E) is a major cholesterol carrier that supports lipid transport and injury repair in the brain. (nih.gov)
Apolipoprotein B100 (apoB100) is a protein that plays a role in moving cholesterol around your body. (medlineplus.gov)

There is now much evidence implicating apolipoprotein E (apo E) in the pathogenesis of CAD and AD. (europa.eu)

The effect of apolipoprotein E polymorphism on cerebral perfusion was studied. (bmj.com)

What are the relationships between apolipoprotein (apo) A-I and apoB concentrations, the apoB/apoA-I ratio and the prevalences of dyslipidemia and metabolic syndrome (MS) in south-west Chinese women with polycystic ovary syndrome (PCOS). (unboundmedicine.com)
Publication: Apolipoprotein E4 association with metabolic syndrome depends on body fatness. (nih.gov)

3. Reductions in plasma concentrations of apolipoprotein B were significantly different depending on genotype determined with a low-density lipoprotein receptor DNA marker ( P = 0.03). (portlandpress.com)

1. We hypothesized that differences within genes whose protein products are involved in apolipoprotein B metabolism could influence the response of plasma apolipoprotein B-containing lipoprotein concentrations to increases in dietary fibre. (portlandpress.com)

The analyst should use the special sampling weights in this file to analyze Apolipoprotein B (ApoB). (cdc.gov)

Endotoxin contamination of apolipoprotein A-I: effect on macrophage proliferation--a cautionary tale. (nih.gov)

Elements in the C terminus of apolipoprotein [a] responsible for the binding to the tenth type III module of human fibronectin. (uchicago.edu)
Lysine-phosphatidylcholine adducts in kringle V impart unique immunological and potential pro-inflammatory properties to human apolipoprotein(a). (uchicago.edu)
Cloning and expression of human apolipoprotein D cDNA. (t3db.ca)
Yang CY, Gu ZW, Blanco-Vaca F, Gaskell SJ, Yang M, Massey JB, Gotto AM Jr, Pownall HJ: Structure of human apolipoprotein D: locations of the intermolecular and intramolecular disulfide links. (t3db.ca)
Balbin M, Freije JM, Fueyo A, Sanchez LM, Lopez-Otin C: Apolipoprotein D is the major protein component in cyst fluid from women with human breast gross cystic disease. (t3db.ca)

4. Thus, genetic variability is associated with inter-individual differences in the fibre-related reduction in plasma apolipoprotein B and apolipoprotein B-containing lipoprotein concentrations. (portlandpress.com)

The intensity of the scattered light is proportional to the concentration of Apolipoprotein B in the sample. (cdc.gov)
Second, Cox proportional hazard models were used to examine whether apolipoproteins predict the risk for T2D among individuals free of diabetes at baseline. (eur.nl)

Below are the most recent publications written about "Apolipoproteins A" by people in Profiles. (uchicago.edu)

Apolipoprotein B is the main protein component of LDL and accounts for approximately 95% of the total protein content of LDL. (cdc.gov)

Fasting blood lipid, lipoprotein and apolipoprotein concentrations were measured at the start and end of the 2 week metabolic period. (portlandpress.com)

OBJECTIVE We aimed to investigate the role of serumlevels of various apolipoproteins on the risk for type 2 diabetes (T2D). (eur.nl)

ICC/IF analysis of HepG2 cells using GTX15663 Apolipoprotein B antibody [F2C13]. (genetex.com)

As such, we hypothesized that apoC-II and apolipoprotein C-III (apoC-III) levels were related to BP abnormalities and CVD in children suffering from mild-to-moderate CKD. (frontiersin.org)
All apolipoproteins, ratios, and HDL-C levels were naturally logtransformed to reach normal distribution. (eur.nl)

This graph shows the total number of publications written about "Apolipoproteins A" by people in this website by year, and whether "Apolipoproteins A" was a major or minor topic of these publications. (uchicago.edu)

Nous avons réalisé un essai en double aveugle contre placebo sur 50 patients atteints de diabète de type 2 randomisés pour recevoir 2 g/jour d'acides gras oméga 3 purifiés ou un placebo pendant 10 semaines. (who.int)

Among them, apolipoprotein C-II (apoC-II) was found to have the highest abundance among the CKD patients with hypertension. (frontiersin.org)
These apolipoproteins are low in atherosclerotic patients. (uchicago.edu)

Apolipoprotein E has been nominated as a potential target for AD. (nih.gov)

While specific post-translational modifications have been reported to alter apolipoprotein function, the full spectrum of apoAI and apoAII proteoforms and their associations with cardiometabolic phenotype remains unknown. (umn.edu)

Apolipoprotein measurements may provide more detail about your risk for heart disease, but the added value of this test beyond a lipid panel is unknown. (medlineplus.gov)

Beta 2-glycoprotein-1 (apolipoprotein H) excretion in chronic renal tubular disorders: comparison with other protein markers of tubular malfunction. (bmj.com)

Anatomy3

Organisms4

Diseases19

Chemicals and Drugs71

Analytical, Diagnostic and Therapeutic Techniques and Equipment22

Phenomena and Processes14

Disciplines and Occupations1

Technology, Industry, Agriculture3

Information Science2

Health Care1

The isolation and partial characterization of the serum lipoproteins and apolipoproteins of the rainbow trout. (1/2216)

Transgenic rabbits as models for atherosclerosis research. (2/2216)

The heparin/heparan sulfate-binding site on apo-serum amyloid A. Implications for the therapeutic intervention of amyloidosis. (3/2216)

Potent inhibition of CD4/TCR-mediated T cell apoptosis by a CD4-binding glycoprotein secreted from breast tumor and seminal vesicle cells. (4/2216)

Effects of alcohol and cholesterol feeding on lipoprotein metabolism and cholesterol absorption in rabbits. (5/2216)

Lipid transfer inhibitor protein defines the participation of lipoproteins in lipid transfer reactions: CETP has no preference for cholesteryl esters in HDL versus LDL. (6/2216)

Levels of soluble cell adhesion molecules in patients with angiographically defined coronary atherosclerosis. (7/2216)

CREB-binding protein is a transcriptional coactivator for hepatocyte nuclear factor-4 and enhances apolipoprotein gene expression. (8/2216)

Apolipoproteins

Apolipoproteins A

Apolipoproteins C

Apolipoproteins B

Apolipoprotein A-I

Apolipoprotein A-II

Apolipoproteins E

Apolipoprotein C-II

Apolipoprotein C-III

Lipoproteins, HDL

Apolipoproteins D

Lipoproteins

Apolipoprotein C-I

Cholesterol

Lipoproteins, VLDL

Triglycerides

Lipids

Apolipoprotein B-100

Apolipoprotein B-48

Cholesterol, HDL

Lipoproteins, HDL3

Tangier Disease

Phosphatidylcholine-Sterol O-Acyltransferase

Lipoproteins, LDL

Nephelometry and Turbidimetry

ATP Binding Cassette Transporter 1

Cholesterol Esters

Isoelectric Focusing

Receptors, Lipoprotein

Lipid Metabolism

Chylomicrons

Cholesterol, LDL

Phospholipids

Ultracentrifugation

Hypolipoproteinemias

Lipoproteins, HDL2

Lipoprotein(a)

Lymph

Electrophoresis, Polyacrylamide Gel

Apoproteins

Hyperlipidemias

Liver

Immunodiffusion

Lipoprotein Lipase

Triolein

Hyperlipoproteinemia Type IV

Phosphatidylcholines

Kinetics

ATP-Binding Cassette Transporters

Hyperlipoproteinemias

Apolipoprotein E3

Chemistry, Clinical

Cholesterol, VLDL

Hypertriglyceridemia

Cholesterol Ester Transfer Proteins

Lipoproteins, IDL

Reference Values

Scavenger Receptors, Class B

Freeze Drying

Ethinyl Estradiol

Particle Size

Immunoassay

Serum Amyloid A Protein

Dietary Fats

Microscopy, Electron

Immunoelectrophoresis

Hyperlipoproteinemia Type V

Abetalipoproteinemia

Dimyristoylphosphatidylcholine

Receptors, Scavenger

Amino Acid Sequence

Oleic Acid

Chromatography, Gel

Molecular Weight

Arteriosclerosis

Biological Transport

Lipolysis

Sterol O-Acyltransferase

Rats, Inbred Strains

Callitrichinae