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
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
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 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.
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 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.
An inherited condition due to a deficiency of either LIPOPROTEIN LIPASE or APOLIPOPROTEIN C-II (a lipase-activating protein). The lack of lipase activities results in inability to remove CHYLOMICRONS and TRIGLYCERIDES from the blood which has a creamy top layer after standing.
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 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.
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.
(Z)-9-Octadecenoic acid 1,2,3-propanetriyl ester.
A highly acidic mucopolysaccharide formed of equal parts of sulfated D-glucosamine and D-glucuronic acid with sulfaminic bridges. The molecular weight ranges from six to twenty thousand. Heparin occurs in and is obtained from liver, lung, mast cells, etc., of vertebrates. Its function is unknown, but it is used to prevent blood clotting in vivo and vitro, in the form of many different salts.
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.
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.
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.
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.
Specialized connective tissue composed of fat cells (ADIPOCYTES). It is the site of stored FATS, usually in the form of TRIGLYCERIDES. In mammals, there are two types of adipose tissue, the WHITE FAT and the BROWN FAT. Their relative distributions vary in different species with most adipose tissue being white.
The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils.
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 condition of elevated levels of TRIGLYCERIDES in the blood.
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.
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.
Cholesterol which is contained in or bound to high-density lipoproteins (HDL), including CHOLESTEROL ESTERS and free cholesterol.
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.
Compounds that increase the enzymatic activity of LIPOPROTEIN LIPASE. Lipoprotein lipase activators have a potential role in the treatment of OBESITY by increasing LIPID METABOLISM. Note that substances that increase the synthesis of lipoprotein lipase are not included here.
A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.
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.
Physiological processes in biosynthesis (anabolism) and degradation (catabolism) of LIPIDS.
Low-density subclass of the high-density lipoproteins, with particle sizes between 8 to 13 nm.
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.
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.
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.
An enzyme that catalyzes the hydrolysis of CHOLESTEROL ESTERS and some other sterol esters, to liberate cholesterol plus a fatty acid anion.
A family of structurally-related angiogenic proteins of approximately 70 kDa in size. They have high specificity for members of the TIE RECEPTOR FAMILY.
A LDL-receptor related protein involved in clearance of chylomicron remnants and of activated ALPHA-MACROGLOBULINS from plasma.
Cholesterol which is contained in or bound to low density lipoproteins (LDL), including CHOLESTEROL ESTERS and free cholesterol.
An enzyme that catalyzes the hydrolysis of glycerol monoesters of long-chain fatty acids EC
Conditions with excess LIPIDS in the blood.
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).
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.
The white liquid secreted by the mammary glands. It contains proteins, sugar, lipids, vitamins, and minerals.
FATTY ACIDS found in the plasma that are complexed with SERUM ALBUMIN for transport. These fatty acids are not in glycerol ester form.
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.
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.
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.
An enzyme of the isomerase class that catalyzes the eliminative cleavage of polysaccharides containing 1,4-linked D-glucuronate or L-iduronate residues and 1,4-alpha-linked 2-sulfoamino-2-deoxy-6-sulfo-D-glucose residues to give oligosaccharides with terminal 4-deoxy-alpha-D-gluc-4-enuronosyl groups at their non-reducing ends. (From Enzyme Nomenclature, 1992) EC
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)
The rate dynamics in chemical or physical systems.
Abstaining from all food.
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.
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.
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.
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 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 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.
Emulsions of fats or lipids used primarily in parenteral feeding.
The process of cleaving a chemical compound by the addition of a molecule of water.
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.
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
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.
Domesticated bovine animals of the genus Bos, usually kept on a farm or ranch and used for the production of meat or dairy products or for heavy labor.
The relatively long-lived phagocytic cell of mammalian tissues that are derived from blood MONOCYTES. Main types are PERITONEAL MACROPHAGES; ALVEOLAR MACROPHAGES; HISTIOCYTES; KUPFFER CELLS of the liver; and OSTEOCLASTS. They may further differentiate within chronic inflammatory lesions to EPITHELIOID CELLS or may fuse to form FOREIGN BODY GIANT CELLS or LANGHANS GIANT CELLS. (from The Dictionary of Cell Biology, Lackie and Dow, 3rd ed.)
Colipase I and II, consisting of 94-95 and 84-85 amino acid residues, respectively, have been isolated from porcine pancreas. Their role is to prevent the inhibitory effect of bile salts on the lipase-catalyzed intraduodenal hydrolysis of dietary long-chain triglycerides.
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)
A 51-amino acid pancreatic hormone that plays a major role in the regulation of glucose metabolism, directly by suppressing endogenous glucose production (GLYCOGENOLYSIS; GLUCONEOGENESIS) and indirectly by suppressing GLUCAGON secretion and LIPOLYSIS. Native insulin is a globular protein comprised of a zinc-coordinated hexamer. Each insulin monomer containing two chains, A (21 residues) and B (30 residues), linked by two disulfide bonds. Insulin is used as a drug to control insulin-dependent diabetes mellitus (DIABETES MELLITUS, TYPE 1).
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.
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.
Transport proteins that carry specific substances in the blood or across cell membranes.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
Cells in the body that store FATS, usually in the form of TRIGLYCERIDES. WHITE ADIPOCYTES are the predominant type and found mostly in the abdominal cavity and subcutaneous tissue. BROWN ADIPOCYTES are thermogenic cells that can be found in newborns of some species and hibernating mammals.
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.
LIPOLYSIS of stored LIPIDS in the ADIPOSE TISSUE to release FREE FATTY ACIDS. Mobilization of stored lipids is under the regulation of lipolytic signals (CATECHOLAMINES) or anti-lipolytic signals (INSULIN) via their actions on the hormone-sensitive LIPASE. This concept does not include lipid transport.
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.
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
Cholesterol present in food, especially in animal products.
The muscle tissue of the HEART. It is composed of striated, involuntary muscle cells (MYOCYTES, CARDIAC) connected to form the contractile pump to generate blood flow.
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 .
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.
The interstitial fluid that is in the LYMPHATIC SYSTEM.
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.
A group of carbon-oxygen lyases. These enzymes catalyze the breakage of a carbon-oxygen bond in polysaccharides leading to an unsaturated product and the elimination of an alcohol. EC 4.2.2.
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).
Substances that lower the levels of certain LIPIDS in the BLOOD. They are used to treat HYPERLIPIDEMIAS.
The time frame after a meal or FOOD INTAKE.
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.
An individual having different alleles at one or more loci regarding a specific character.
One of three major isoforms of apolipoprotein E. In humans, Apo E2 differs from APOLIPOPROTEIN E3 at one residue 158 where arginine is replaced by cysteine (R158--C). In contrast to Apo E3, Apo E2 displays extremely low binding affinity for LDL receptors (RECEPTORS, LDL) which mediate the internalization and catabolism of lipoprotein particles in liver cells. ApoE2 allelic homozygosity is associated with HYPERLIPOPROTEINEMIA TYPE III.
A thermogenic form of adipose tissue composed of BROWN ADIPOCYTES. It is found in newborns of many species including humans, and in hibernating mammals. Brown fat is richly vascularized, innervated, and densely packed with MITOCHONDRIA which can generate heat directly from the stored lipids.
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)
Relating to the size of solids.
The mass or quantity of heaviness of an individual. It is expressed by units of pounds or kilograms.
Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.
Elements of limited time intervals, contributing to particular results or situations.
Electrophoresis in which a polyacrylamide gel is used as the diffusion medium.
GLYCEROL esterified with FATTY ACIDS.
A group of fatty acids that contain 18 carbon atoms and a double bond at the omega 9 carbon.
A chromatographic technique that utilizes the ability of biological molecules to bind to certain ligands specifically and reversibly. It is used in protein biochemistry. (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)
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.
A membrane protein found in the rough endoplasm reticulum (ENDOPLASMIC RETICULUM, ROUGH) that binds to LDL-RECEPTOR RELATED PROTEINS. It may function to prevent ligand binding of receptors during protein processing events within endosomal compartments.
A nodular organ in the ABDOMEN that contains a mixture of ENDOCRINE GLANDS and EXOCRINE GLANDS. The small endocrine portion consists of the ISLETS OF LANGERHANS secreting a number of hormones into the blood stream. The large exocrine portion (EXOCRINE PANCREAS) is a compound acinar gland that secretes several digestive enzymes into the pancreatic ductal system that empties into the DUODENUM.
One of the Type II site-specific deoxyribonucleases (EC It recognizes and cleaves the sequence A/AGCTT at the slash. HindIII is from Haemophilus influenzae R(d). Numerous isoschizomers have been identified. EC 3.1.21.-.
A subfamily in the family MURIDAE, comprising the hamsters. Four of the more common genera are Cricetus, CRICETULUS; MESOCRICETUS; and PHODOPUS.
Lipid-laden macrophages originating from monocytes or from smooth muscle cells.
An individual in which both alleles at a given locus are identical.
A chemical reaction in which an electron is transferred from one molecule to another. The electron-donating molecule is the reducing agent or reductant; the electron-accepting molecule is the oxidizing agent or oxidant. Reducing and oxidizing agents function as conjugate reductant-oxidant pairs or redox pairs (Lehninger, Principles of Biochemistry, 1982, p471).
Established cell cultures that have the potential to propagate indefinitely.
A thickening and loss of elasticity of the walls of ARTERIES that occurs with formation of ATHEROSCLEROTIC PLAQUES within the ARTERIAL INTIMA.
Ubiquitous macromolecules associated with the cell surface and extracellular matrix of a wide range of cells of vertebrate and invertebrate tissues. They are essential cofactors in cell-matrix adhesion processes, in cell-cell recognition systems, and in receptor-growth factor interactions. (From Cancer Metastasis Rev 1996; 15(2): 177-86; Hepatology 1996; 24(3): 524-32)
The parts of a macromolecule that directly participate in its specific combination with another molecule.
Enzymes which catalyze the hydrolysis of carboxylic acid esters with the formation of an alcohol and a carboxylic acid anion.
Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.
Glucose in blood.
The protein components of a number of complexes, such as enzymes (APOENZYMES), ferritin (APOFERRITINS), or lipoproteins (APOLIPOPROTEINS).
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.
Glycoproteins with a molecular weight of approximately 620,000 to 680,000. Precipitation by electrophoresis is in the alpha region. They include alpha 1-macroglobulins and alpha 2-macroglobulins. These proteins exhibit trypsin-, chymotrypsin-, thrombin-, and plasmin-binding activity and function as hormonal transporters.
A family of scavenger receptors that are predominately localized to CAVEOLAE of the PLASMA MEMBRANE and bind HIGH DENSITY LIPOPROTEINS.
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).
Oils derived from plants or plant products.
A group of simple proteins that yield basic amino acids on hydrolysis and that occur combined with nucleic acid in the sperm of fish. Protamines contain very few kinds of amino acids. Protamine sulfate combines with heparin to form a stable inactive complex; it is used to neutralize the anticoagulant action of heparin in the treatment of heparin overdose. (From Merck Index, 11th ed; Martindale, The Extra Pharmacopoeia, 30th ed, p692)
A heteropolysaccharide that is similar in structure to HEPARIN. It accumulates in individuals with MUCOPOLYSACCHARIDOSIS.
CELL LINE derived from the ovary of the Chinese hamster, Cricetulus griseus (CRICETULUS). The species is a favorite for cytogenetic studies because of its small chromosome number. The cell line has provided model systems for the study of genetic alterations in cultured mammalian cells.
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.
Cell surface molecules on cells of the immune system that specifically bind surface molecules or messenger molecules and trigger changes in the behavior of cells. Although these receptors were first identified in the immune system, many have important functions elsewhere.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in enzyme synthesis.
The sum of the weight of all the atoms in a molecule.
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.
A ubiquitous sodium salt that is commonly used to season food.
The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.
A status with BODY WEIGHT that is grossly above the acceptable or desirable weight, usually due to accumulation of excess FATS in the body. The standards may vary with age, sex, genetic or cultural background. In the BODY MASS INDEX, a BMI greater than 30.0 kg/m2 is considered obese, and a BMI greater than 40.0 kg/m2 is considered morbidly obese (MORBID OBESITY).
Conjugated protein-carbohydrate compounds including mucins, mucoid, and amyloid glycoproteins.
The genetic constitution of the individual, comprising the ALLELES present at each GENETIC LOCUS.
A trihydroxy sugar alcohol that is an intermediate in carbohydrate and lipid metabolism. It is used as a solvent, emollient, pharmaceutical agent, and sweetening agent.
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.
The main trunk of the systemic arteries.
Treatment process involving the injection of fluid into an organ or tissue.
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 phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
Conversion of an inactive form of an enzyme to one possessing metabolic activity. It includes 1, activation by ions (activators); 2, activation by cofactors (coenzymes); and 3, conversion of an enzyme precursor (proenzyme or zymogen) to an active enzyme.
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.
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
Proteins prepared by recombinant DNA technology.
The relationship between the chemical structure of a compound and its biological or pharmacological activity. Compounds are often classed together because they have structural characteristics in common including shape, size, stereochemical arrangement, and distribution of functional groups.
A diet that contributes to the development and acceleration of ATHEROGENESIS.
A genus of zygomycetous fungi of the family Mucoraceae, order MUCORALES, a common saprophyte and facultative parasite of mature fruits and vegetables. It may cause cerebral mycoses in diabetes and cutaneous infection in severely burned patients.
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.
A large and highly glycosylated protein constituent of LIPOPROTEIN (A). It has very little affinity for lipids but forms disulfide-linkage to APOLIPOPROTEIN B-100. Apoprotein(a) has SERINE PROTEINASE activity and can be of varying sizes from 400- to 800-kDa. It is homologous to PLASMINOGEN and is known to modulate THROMBOSIS and FIBRINOLYSIS.
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.
Cyclic esters of hydroxy carboxylic acids, containing a 1-oxacycloalkan-2-one structure. Large cyclic lactones of over a dozen atoms are MACROLIDES.
Detection of RNA that has been electrophoretically separated and immobilized by blotting on nitrocellulose or other type of paper or nylon membrane followed by hybridization with labeled NUCLEIC ACID PROBES.
Inorganic oxides of sulfur.
Chromatography on non-ionic gels without regard to the mechanism of solute discrimination.
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.
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.
A family of proteins that share sequence similarity with the low density lipoprotein receptor (RECEPTORS, LDL).
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
Any substances taken in by the body that provide nourishment.
Errors in the metabolism of LIPIDS resulting from inborn genetic MUTATIONS that are heritable.
A mitosporic Saccharomycetales fungal genus, various species of which have been isolated from pulmonary lesions. Teleomorphs include Dipodascus and Galactomyces.
Lengthy and continuous deprivation of food. (Stedman, 25th ed)
Unstable isotopes of iodine that decay or disintegrate emitting radiation. I atoms with atomic weights 117-139, except I 127, are radioactive iodine isotopes.
The uptake of naked or purified DNA by CELLS, usually meaning the process as it occurs in eukaryotic cells. It is analogous to bacterial transformation (TRANSFORMATION, BACTERIAL) and both are routinely employed in GENE TRANSFER TECHNIQUES.
Enzymes that catalyze the reversible reduction of alpha-carboxyl group of 3-hydroxy-3-methylglutaryl-coenzyme A to yield MEVALONIC ACID.
A subtype of striated muscle, attached by TENDONS to the SKELETON. Skeletal muscles are innervated and their movement can be consciously controlled. They are also called voluntary muscles.
Electrophoresis in which agar or agarose gel is used as the diffusion medium.
Diminished effectiveness of INSULIN in lowering blood sugar levels: requiring the use of 200 units or more of insulin per day to prevent HYPERGLYCEMIA or KETOSIS.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.
A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.
The consumption of edible substances.
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.

Caloric restriction leads to regional specialisation of adipocyte function in the rat. (1/1971)

The study analysed the responses of three metabolic parameters in five distinct adipose tissue depots to caloric restriction (4 weeks) in the rat. The aims were to evaluate whether specific adipose tissue depots were recruited for triacylglycerol (TAG) storage and/or mobilisation, and to determine to what extent specific adipose tissue depots exhibited preferences for the source of fatty acid (FA) for TAG storage. Caloric restriction led to a general enhancement of the response of lipoprotein lipase (LPL), FA synthesis and glucose utilisation to a meal. Effects were particularly marked in the parametrial, perirenal and interscapular depots compared with mesenteric and subcutaneous depots. There was no evidence that individual depots selectively expressed a preference for the pathways concerned with the generation of FA for storage (the exogenous (LPL) and the endogenous (synthesis) pathway). However, the temporal sequence of activation of these pathways differed in a manner consistent with a switch from preponderant use of FA produced via de novo synthesis during the very early phase of feeding towards later use of FA derived from circulating TAG. The overall excursions in insulin levels observed in the calorie-restricted rats were comparable to those found in free-feeding rats, but the magnitude and the rapidity of the individual metabolic responses of the adipocyte were augmented. The data are consistent with a general enhancement of insulin sensitivity and responsiveness in adipose tissue of calorie-restricted rats, together with adaptive regional specialisation of adipocyte function. These adaptations would be predicted to facilitate the immediate conservation of dietary nutrients by promoting their storage as the FA or glycerol moieties of adipose tissue TAG and thereby to ensure the regulated release of FA and glycerol from adipose tissue in accordance with the requirement for glucose conservation and/or production.  (+info)

Binding of beta-VLDL to heparan sulfate proteoglycans requires lipoprotein lipase, whereas ApoE only modulates binding affinity. (2/1971)

The binding of beta-VLDL to heparan sulfate proteoglycans (HSPG) has been reported to be stimulated by both apoE and lipoprotein lipase (LPL). In the present study we investigated the effect of the isoform and the amount of apoE per particle, as well as the role of LPL on the binding of beta-VLDL to HSPG. Therefore, we isolated beta-VLDL from transgenic mice, expressing either APOE*2(Arg158-->Cys) or APOE*3-Leiden (E2-VLDL and E3Leiden-VLDL, respectively), as well as from apoE-deficient mice containing no apoE at all (Enull-VLDL). In the absence of LPL, the binding affinity and maximal binding capacity of all beta-VLDL samples for HSPG-coated microtiter plates was very low. Addition of LPL to this cell-free system resulted in a 12- to 55-fold increase in the binding affinity and a 7- to 15-fold increase in the maximal binding capacity (Bmax). In the presence of LPL, the association constant (Ka) tended to increase in the order Enull-VLDL+info)

Induced mutant mouse lines that express lipoprotein lipase in cardiac muscle, but not in skeletal muscle and adipose tissue, have normal plasma triglyceride and high-density lipoprotein-cholesterol levels. (3/1971)

The tissue-specific expression of lipoprotein lipase (LPL) in adipose tissue (AT), skeletal muscle (SM), and cardiac muscle (CM) is rate-limiting for the uptake of triglyceride (TG)-derived free fatty acids and decisive in the regulation of energy balance and lipoprotein metabolism. To investigate the tissue-specific metabolic effects of LPL, three independent transgenic mouse lines were established that expressed a human LPL (hLPL) minigene predominantly in CM. Through cross-breeding with heterozygous LPL knockout mice, animals were generated that produced hLPL mRNA and enzyme activity in CM but lacked the enzyme in SM and AT because of the absence of the endogenous mouse LPL gene (L0-hLPL). LPL activity in CM and postheparin plasma of L0-hLPL mice was reduced by 34% and 60%, respectively, compared with control mice. This reduced LPL expression was sufficient to rescue LPL knockout mice from neonatal death. L0-hLPL animals developed normally with regard to body weight and body-mass composition. Plasma TG levels in L0-hLPL animals were increased up to 10-fold during the suckling period but normalized after weaning and decreased in adult animals. L0-hLPL mice had normal plasma high-density lipoprotein (HDL)-cholesterol levels, indicating that LPL expression in CM alone was sufficient to allow for normal HDL production. The absence of LPL in SM and AT did not cause detectable morphological or histopathological changes in these tissues. However, the lipid composition in AT and SM exhibited a marked decrease in polyunsaturated fatty acids. From this genetic model of LPL deficiency in SM and AT, it can be concluded that CM-specific LPL expression is a major determinant in the regulation of plasma TG and HDL-cholesterol levels.  (+info)

Response of adipose tissue lipoprotein lipase to the cephalic phase of insulin secretion. (4/1971)

Modulation of lipoprotein lipase (LPL) allows a tissue-specific partitioning of triglyceride-derived fatty acids, and insulin is a major modulator of its activity. The present studies were aimed to assess in rats the contribution of insulin to the response of adipose tissue and muscle LPL to food intake. Epididymal and retroperitoneal adipose LPL rose 65% above fasting values as early as 1 h after the onset of a 30-min high-carbohydrate meal, with a second activity peak 1 h later that was maintained for an additional 2 h. Soleus muscle LPL was decreased by 25% between 0.5 and 4 h after meal intake. The essential contribution of insulin to the LPL response to food intake was determined by preventing the full insulin response to meal intake by administration of diazoxide (150 mg/kg body wt, in the meal). The usual postprandial changes in adipose and muscle LPL did not occur in the absence of an increase in insulinemia. However, the early (60 min) increase in adipose tissue LPL was not prevented by the drug, likely because of the maintenance of the early centrally mediated phase of insulin secretion. In a subsequent study, rats chronically implanted with a gastric cannula were used to demonstrate that the postprandial rise in adipose LPL is independent of nutrient absorption and can be elicited by the cephalic (preabsorptive) phase of insulin secretion. Obese Zucker rats were used because of their strong cephalic insulin response. After an 8-h fast, rats were fed a liquid diet ad libitum (orally, cannula closed), sham fed (orally, cannula opened), or fed directly into the stomach via the cannula during 4 h. Insulinemia increased 10-fold over fasting levels in ad libitum- and intragastric-fed rats and threefold in sham-fed rats. Changes in adipose tissue LPL were proportional to the elevation in plasma insulin levels, demonstrating that the cephalic-mediated rise in insulinemia, in the absence of nutrient absorption, stimulates adipose LPL. These results demonstrate the central role of insulin in the postprandial response of tissue LPL, and they show that cephalically mediated insulin secretion is able to stimulate adipose LPL.  (+info)

Sortilin/neurotensin receptor-3 binds and mediates degradation of lipoprotein lipase. (5/1971)

Lipoprotein lipase and the receptor-associated protein (RAP) bind to overlapping sites on the low density lipoprotein receptor-related protein/alpha2-macroglobulin receptor (LRP). We have investigated if lipoprotein lipase interacts with the RAP binding but structurally distinct receptor sortilin/neurotensin receptor-3. We show, by chemical cross-linking and surface plasmon resonance analysis, that soluble sortilin binds lipoprotein lipase with an affinity similar to that of LRP. The binding was inhibited by heparin and RAP and by the newly discovered sortilin ligand neurotensin. In 35S-labeled 3T3-L1 adipocytes treated with the cross-linker dithiobis(succinimidyl propionate), lipoprotein lipase-containing complexes were isolated by anti-sortilin antibodies. To elucidate function in cells, sortilin-negative Chinese hamster ovary cells were transfected with full-length sortilin and shown to express about 8% of the receptors on the cell surface. These cells degraded 125I-labeled lipoprotein lipase much faster than the wild-type cells. The degradation was inhibited by unlabeled lipoprotein lipase, indicating a saturable pathway, and by RAP and heparin. Moreover, inhibition by the weak base chloroquine suggested that degradation occurs in an acidic vesicle compartment. The results demonstrate that sortilin is a multifunctional receptor that binds lipoprotein lipase and, when expressed on the cell surface, mediates its endocytosis and degradation.  (+info)

Role of protein kinase C in the translational regulation of lipoprotein lipase in adipocytes. (6/1971)

The hypertriglyceridemia of diabetes is accompanied by decreased lipoprotein lipase (LPL) activity in adipocytes. Although the mechanism for decreased LPL is not known, elevated glucose is known to increase diacylglycerol, which activates protein kinase C (PKC). To determine whether PKC is involved in the regulation of LPL, we studied the effect of 12-O-tetradecanoyl phorbol 13-acetate (TPA) on adipocytes. LPL activity was inhibited when TPA was added to cultures of 3T3-F442A and rat primary adipocytes. The inhibitory effect of TPA on LPL activity was observed after 6 h of treatment, and was observed at a concentration of 6 nM. 100 nM TPA yielded maximal (80%) inhibition of LPL. No stimulation of LPL occurred after short term addition of TPA to cultures. To determine whether TPA treatment of adipocytes decreased LPL synthesis, cells were labeled with [35S]methionine and LPL protein was immunoprecipitated. LPL synthetic rate decreased after 6 h of TPA treatment. Western blot analysis of cell lysates indicated a decrease in LPL mass after TPA treatment. Despite this decrease in LPL synthesis, there was no change in LPL mRNA in the TPA-treated cells. Long term treatment of cells with TPA is known to down-regulate PKC. To assess the involvement of the different PKC isoforms, Western blotting was performed. TPA treatment of 3T3-F442A adipocytes decreased PKC alpha, beta, delta, and epsilon isoforms, whereas PKC lambda, theta, zeta, micro, iota, and gamma remained unchanged or decreased minimally. To directly assess the effect of PKC inhibition, PKC inhibitors (calphostin C and staurosporine) were added to cultures. The PKC inhibitors inhibited LPL activity rapidly (within 60 min). Thus, activation of PKC did not increase LPL, but inhibition of PKC resulted in decreased LPL synthesis by inhibition of translation, indicating a constitutive role of PKC in LPL gene expression.  (+info)

Association of lipoprotein lipase gene polymorphisms with coronary artery disease. (7/1971)

OBJECTIVES: The purpose of this study was to test whether the HindIII (+) and PvuII (-) or (+) restriction enzyme-defined alleles are associated with angiographic coronary artery disease (CAD). BACKGROUND: Lipoprotein lipase (LPL) plays a central role in lipid metabolism, hydrolyzing triglyceride in chylomicrons and very low density lipoproteins. Polymorphic variants of the LPL gene are common and might affect risk of CAD. METHODS: Blood was drawn from 725 patients undergoing coronary angiography. Leukocyte deoxyribonucleic acid segments containing the genomic sites were amplified by the polymerase chain reaction and digested, and polymorphisms were identified after electrophoresis in 1.5% agarose gel. RESULTS: In no-CAD control subjects (n = 168), HindIII (-) and (+) allelic frequencies were 28.6% and 71.4%, and (-) and (+) alleles were carried by 44.0% and 86.9% of subjects, respectively. Control PvuII (-) and (+) allelic frequencies were 41.7% and 58.3%, and (-) and (+) alleles were carried by 64.3% and 81.0%, respectively. In CAD patients (>60% stenosis; n = 483), HindIII (+) allelic carriage was increased (93.8% of patients, odds ratio [OR] = 2.28, confidence interval [CI] 1.27 to 4.00). Also, PvuII (-) allelic carriage tended to be more frequent in CAD patients (OR = 1.33, CI 0.92 to 1.93). Adjusted for six CAD risk factors and the other polymorphism, HindIII (+) carriage was associated with an OR = 2.86, CI 1.50 to 5.42, p = 0.0014, and PvulI (-) carriage, OR = 1.42, CI 0.95 to 2.12, p = 0.09. The two polymorphisms were in strong linkage disequilibrium, and a haplotype association was suggested. CONCLUSIONS: The common LPL polymorphic allele, HindIII (+), is moderately associated with CAD, and the PvuII (-) allele is modestly associated (trend). Genetic variants of LPL deserve further evaluation as risk factors for CAD.  (+info)

Lipoprotein lipase activity is decreased in a large cohort of patients with coronary artery disease and is associated with changes in lipids and lipoproteins. (8/1971)

Lipoprotein lipase (LPL) is crucial in the hydrolysis of triglycerides (TG) in TG-rich lipoproteins in the formation of HDL particles. As both these lipoproteins play an important role in the pathogenesis of atherosclerotic vascular disease, we sought to assess the relationship between post-heparin LPL (PH-LPL) activity and lipids and lipoproteins in a large, well-defined cohort of Dutch males with coronary artery disease (CAD). These subjects were drawn from the REGRESS study, totaled 730 in number and were evaluated against 75 healthy, normolipidemic male controls. Fasting mean PH-LPL activity in the CAD subjects was 108 46 mU/ml, compared to 138 44 mU/ml in controls (P < 0.0001). When these patients were divided into activity quartiles, those in the lowest versus the highest quartile had higher levels of TG (P < 0.001), VLDLc and VLDL-TG (P = 0.001). Conversely, levels of TC, LDL, and HDLc were lower in these patients (P = 0.001, P = 0.02, and P = 0.001, respectively). Also, in this cohort PH-LPL relationships with lipids and lipoproteins were not altered by apoE genotypes. The frequency of common mutations in the LPL gene associated with partial LPL deficiency (N291S and D9N carriers) in the lowest quartile for LPL activity was more than double the frequency in the highest quartile (12.0% vs. 5.0%; P = 0.006). By contrast, the frequency of the S447X LPL variant rose from 11.5% in the lowest to 18.3% (P = 0.006) in the highest quartile. This study, in a large cohort of CAD patients, has shown that PH-LPL activity is decreased (22%; P = 0.001) when compared to controls; that the D9N and N291S, and S447X LPL variants are genetic determinants, respectively, in CAD patients of low and high LPL PH-LPL activities; and that PH-LPL activity is strongly associated with changes in lipids and lipoproteins.  (+info)

Sixteen pigs from 2 distinct genetic lines (LGAH and VFIL) obtained after eight generations of divergent selection for high (H) and low (L) lean tissue growth rate with ad-libitum feeding (LGA) and voluntary feed intake (VFI), respectively, were used in this study. The objectives of this investigation were to establish appropriate working conditions for the postheparin plasma lipoprotein lipase (LPL) assay and to study relationships between fat deposition and plasma lipids, very low density lipoprotein (VLDL) lipids, VLDL-subfractions and postheparin plasma LPL activity in growing pigs. Four preliminary experiments were performed to determine the appropriate working conditions for the postheparin plasma LPL assays. Postheparin plasma preincubated with SDS (20-50 mM) at 26 C for 45 minutes inhibited hepatic lipase activity. A total of 2 l VLDL/assay produced maximum stimulation of LPL activity. Postheparin plasma protein and increasing incubation time contributed an optimum response. LGAH pigs ...
Fat feeding stimulated the release of gastric inhibitory polypeptide (GIP) without concomitant insulin secretion. Since antilipolytic effects of GIP have been demonstrated and the uptake of triglyceride fatty acid by adipose tissue postprandially is a process reciprocally regulated with lipolysis, a stimulatory role of GIP on adipose tissue lipoprotein lipase activity may be present. After cultured preadipocytes were incubated for 2 h with GIP, the release of lipoprotein lipase activity into the culture medium and the total cellular activity present in acetone-ether powders of cells were measured. GIP stimulated significant increases in the lipoprotein lipase activity released into the culture medium and in cells. A dose response relationship was strongest for the effect of GIP on the enzyme activity in extracts of acetone-ether powders of the cells. The increased lipoprotein lipase activity produced by GIP could provide a mechanism for clearance of chylomicron triglyceride after feeding in ...
Experiments were conducted to study the effects of high density lipoprotein (HDL) and apolipoproteins C, E, and A on lipoprotein lipase activity in rhesus monkeys. The lipoprotein lipase activity was inhibited up to 32 +/- 6 per cent by monkey HDL. This inhibition was considerably decreased (2 +/- 0.02%) by using apolipoprotein-poor HDL. Apolipoproteins C and E inhibited the hydrolysis of activated intralipid by monkey lipoprotein lipase to a maximum of 83 +/- 7 and 57 +/- 5 per cent respectively. Apolipoprotein A produced little inhibition of lipoprotein lipase activity. The results of these studies demonstrate that HDL and apolipoproteins compete with the substrate for the binding to lipoprotein lipase in rhesus monkeys.
Effects of a Six Month Training Program on Serum Lipids, Glucose, Insulin and Adipose Tissue Lipoprotein Lipase in Young Overweight Females, 10th International Conference Biochemistry of Exercise ...
article{5a0b5a06-4e09-4a23-a38a-02712684b3d8, abstract = {The location of lipoprotein lipase activity in rat adipose tissue was studied using intact epididymal fat pads, isolated adipocytes, and lipoprotein lipase activity secreted from adipocytes as enzyme sources. The enzyme activities of these preparations were characterized by gel filtration. The method used for isolation of adipocytes had been modified to minimize activation of lipoprotein lipase during the procedures. Extracts of intact adipose tissue separated into two major lipoprotein lipase activity peaks, designated a and b, the a fraction representing about 30 (fasted rats) to 50% (fed rats) of the total enzyme activity. An intermediate fraction (designated i) was frequently observed. Extracts of isolated adipocytes from fed rats contained about 35% and those from fasted rats about 65% of the lipoprotein lipase activity present in intact tissue. The b fraction constituted 80--97% of the adipocyte lipoprotein lipase ...
This study shows that LPL mass and activity in preheparin plasma and the increase of LPL after the administration of heparin are separate parameters. All four showed significant correlations with plasma lipoprotein lipid concentrations, but the relations were different for the four parameters. This is in line with available evidence from molecular biology, biochemistry, and cell biology that suggests that the LPL mass and activity in preheparin and postheparin plasma reflect different aspects of the function, turnover, and transport of LPL.2 The classical parameter is LPL activity in postheparin plasma, which is assumed to reflect the pool of functional LPL at endothelial surfaces.1 In the present study as well as others5 7 9 10 postheparin LPL activity showed a fairly strong positive relation to the HDL-C level and weak negative correlations with VLDL lipid concentrations. This accords with the idea that postheparin LPL activity would be expected to be related to the efficiency of lipolysis of ...
ApoC-II was the only apolipoprotein from human very low density lipoprotein that activated rat adipose tissue lipoprotein lipase. Activation was blocked by antiserum against apoC-II. Addition of increasing amounts of activator did not alter the apparent Km of lipoprotein lipase (0.32 mM triolein), but it did produce a progressive increase in the apparent Vmax from 0.8 to 2.2 µmoles free fatty acid/mg hour-1. Substrate concentrations above 1.27 mM triolein diminished activation by 0.25-5.0 µg/ml of apoC-II as much as 20%. Reversal of this apparent substrate inhibition was achieved by increasing the activator concentration to 50.0 µg/ml. Each of five nonactivating apolipoproteins-apoC-I, C-III-1, C-III-2, A-I, and A-II-inhibited lipoprotein lipase up to 85-100%. ApoC-II also produced less inhibition under appropriate conditions. Inhibition was dependent on apoprotein concentration, inversely related to substrate triglyceride concentration, and unobserved with nonlipoprotein proteins. The ...
1. Incubation of intact epididymal adipose tissue from fed rats at 37° in an albumin solution at pH7·4 in vitro results in rapid loss of clearing-factor lipase activity until a low activity, stable to prolonged incubation, is attained. The clearing-factor lipase activity of intact tissue from starved rats, which is initially much less than that of tissue from fed rats, is mainly stable to incubation at 37°. 2. Much of the clearing-factor lipase activity of intact epididymal adipose tissue from fed rats is inactivated by collagenase. The enzyme activity of intact tissue from starved rats is not inactivated by collagenase. 3. The clearing-factor lipase activity of fat cells isolated from the epididymal adipose tissue of fed rats is stable to prolonged incubation at 37°. It represents only a small proportion of the total activity of the intact tissue. In starved rats, the isolated fat cells contain a much higher proportion of the activity of the intact tissue. Their activity is also stable at ...
TY - CONF. T1 - Adenovirus-mediated rescue of lipoprotein lipase-deficient mice. Lipolysis of triglyceride-rich lipoproteins is essential for high density lipoprotein maturation in mice. AU - Strauss, Juliane Gertrude. PY - 2002. Y1 - 2002. M3 - Poster. ER - ...
The investigators hypothesize that Lipoprotein Lipase (LPL) expression on Chronic Lymphocytic Leukemia (CLL) cells will predict a more aggressive clinical course. The results from this proposal will validate the use of a novel antibody developed at Dartmouth-Hitchcock in CLL and will predict CLL patients that have a more aggressive form of the disease. The investigators work will also provide direct evidence that LPL is expressed on CLL cells and provides a critical source of fatty acids required by the CLL cells to grow and survive. Fatty acid metabolism may become a therapeutic target in CLL in the future ...
TY - JOUR. T1 - Differential effects of lipoprotein lipase on tumor necrosis factor-α and interferon-γ-mediated gene expression in human endothelial cells. AU - Kota, Rama S.. AU - Ramana, Chilakamarti V.. AU - Tenorio, Fatima A.. AU - Enelow, Richard I.. AU - Rutledge, John C. PY - 2005/9/2. Y1 - 2005/9/2. N2 - Lipoprotein lipase (LPL) is a key enzyme in the hydrolysis of triglyceride-rich lipoproteine. In vascular diseases, such as atherosclerosis, inflammation plays an important role in the pathogenesis of the disease. We examined the role of LPL in modulating tumor necrosis factor-α (TNF-α)- and interferon-γ (IFN-γ)-mediated inflammatory cytokine signal transduction pathways in human aortic endothelial cells (HAECs). LPL significantly suppressed TNF-α-induced gene expression, and this suppression was reversed by tetrahydrolipstatin and heparinase. In contrast, LPL synergistically enhanced IFN-γ-induced gene expression in HAECs. To elucidate the molecular mechanisms of LPL action, we ...
The molecular mechanism underlying the extinction of lipoprotein lipase (LPL) expression in rat liver during development was investigated. A mouse (BWTG3) and a rat (7777) hepatoma, both of which exhibit characteristics of fetal hepatocytes, were found to contain LPL mRNA, whereas the more differentiated human (Hep G2 and Hep 3B) or rat (Fa32) hepatoma cell lines did not. Somatic cell hybrids between LPL-producing hepatoma cells and non-LPL-producing cells, such as adult rat hepatocytes or fibroblasts, exhibited extinction of LPL gene expression. Assay of expression of nested deletions in the 5 regulatory sequences of the LPL gene in the Hep G2 cell line and in BWTG3 cells localized sequences involved in the suppression of LPL production to a region between -591 and -288 relative to the transcription initiation site. A site with sequence homology to a glucocorticoid responsive element (GRE) was shown not to play an important role in the extinction process. A novel transcription factor, termed RF-1-LPL,
Lipoprotein lipase is the principal enzyme that hydrolyzes circulating triglycerides and liberates free fatty acids that can be used as energy by cardiac muscle. Although lipoprotein lipase is expressed by and is found on the surface of cardiomyocytes, its transfer to the luminal surface of endothelial cells is thought to be required for lipoprotein lipase actions. To study whether nontransferable lipoprotein lipase has physiological actions, we placed an α-myosin heavy-chain promoter upstream of a human lipoprotein lipase minigene construct with a glycosylphosphatidylinositol anchoring sequence on the carboxyl terminal region. Hearts of transgenic mice expressed the altered lipoprotein lipase, and the protein localized to the surface of cardiomyocytes. Hearts, but not postheparin plasma, of these mice contained human lipoprotein lipase activity. More lipid accumulated in hearts expressing the transgene; the myocytes were enlarged and exhibited abnormal architecture. Hearts of transgenic mice ...
We have examined the regulation of lipoprotein lipase (LPL) activity in skeletal muscle during physical inactivity in comparison to low-intensity contractile activity of ambulatory controls. From studies acutely preventing ambulatory activity of one or both the hindlimbs in rats, it was shown that a …
TY - JOUR. T1 - A frequently occurring mutation in the lipoprotein lipase gene (Asn291Ser) results in altered postprandial chylomicron triglyceride and retinyl palmitate response in normolipidemic carriers. AU - Pimstone, Simon N.. AU - Clee, Susanne M.. AU - Gagné, S. Eric. AU - Miao, Li. AU - Zhang, Hanfang. AU - Stein, Evan A.. AU - Hayden, Michael R.. PY - 1996/8/1. Y1 - 1996/8/1. N2 - An Asn291Ser mutation in exon 6 of the lipoprotein lipase gene (LPL) frequently occurs in Caucasians (2-4%) and results in a partial catalytic defect. Although this mutation may be associated with low HDL cholesterol and elevated triglyceride levels, some carriers are normolipidemic and may have LPL activity in the normal range in the fasting state. To assess in vivo the influence of dietary stress on the function of this mutation, we have performed oral fat load studies on three unrelated normolipidemic Asn291Ser carriers and compared these results to five healthy controls and to a subject with a clear 50% ...
TY - JOUR. T1 - Lipoprotein lipase increases lipoprotein binding to the artery wall and increases endothelial layer permeability by formation of lipolysis products. AU - Rutledge, John C. AU - Woo, Mable M.. AU - Rezai, Allen A.. AU - Curtiss, Linda K.. AU - Goldberg, Ira J.. PY - 1997. Y1 - 1997. N2 - Mechanisms responsible for the accumulation of low-density lipoprotein (LDL) were investigated in a new model, the perfused hamster aorta. To do this, we developed a method to study LDL flux in real time in individually perfused arteries; each artery served as its own control. Using quantitative fluorescence microscopy, the rates of LDL accumulation and efflux were separately determined. Perfusion of arteries with buffer plus lipoprotein lipase (LpL) increased LDL accumulation 5-fold (0.1±0.03 mV/min [control] versus 0.5±0.05 mV/min [LpL]) by increasing LDL retention in the artery wall. This effect was blocked by heparin and monoclonal antibodies directed against the amino-terminal region of ...
Many of the metabolic effects of exercise are due to the most recent exercise session. With recent advances in nuclear magnetic resonance spectroscopy (NMRS), it is possible to gain insight about which lipoprotein particles are responsible for mediating exercise effects. Using a randomized cross-over design, very low density lipoprotein (VLDL) responses were evaluated in eight men on the morning after i) an inactive control trial (CON), ii) exercising vigorously on the prior evening for 100 min followed by fasting overnight to maintain an energy and carbohydrate deficit (EX-DEF), and iii) after the same exercise session followed by carbohydrate intake to restore muscle glycogen and carbohydrate balance (EX-BAL). The intermediate, low and high density lipoprotein particle concentrations did not differ between trials. Fasting triglyceride (TG) determined biochemically, and mean VLDL size were lower in EX-DEF but not in EX-BAL compared to CON, primarily due to a reduction in VLDL-TG in the 70-120 nm (large
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LPLD is a rare autosomal recessive disorder, characterized by the presence of marked chylomicronemia and hence hypertriglyceridemia. Clinically the most severe manifestation of chylomicronemia, is acute pancreatitis, which can be lethal. There is no effective therapy available to modulate the course of the illness and prevent complications for these patients. The current clinical management consists of severe reduction of dietary fat that is hard if not almost impossible to comply with. LPLD subjects continue to experience pancreatitis attacks, and are admitted to intensive care units on several occasions.. Alipogene tiparvovec corrects or restores lipoprotein lipase (LPL) function long term, and hence reverses some symptoms, halts the disease progression and prevents further complications. Alipogene tiparvovec gene therapy ensures that a catabolically beneficial variant of the human LPL gene, LPL[S447X] is expressed and active in the relevant tissues in humans. Delivery of the gene is realized ...
1. Intravenous injection of heparin into the trout resulted in the appearance in the plasma of a lipase with the properties of lipoprotein lipase. 2. The enzyme was purified to apparent electrophoretic homogeneity by means of heparin-Sepharose affinity chromatography. The enzyme was eluted with 1.5 M-NaCl and had a specific activity approx. 450-fold that of the post-heparin plasma. 3. The activity of the purified enzyme was inhibited by 1.0 M-NaCl and protamine sulphate and was stimulated between 3- and 8.8-fold by the addition of trout plasma. 4. The activity was strongly stimulated by trout very low density lipoproteins and to a lesser extent by high density lipoproteins. 5. The isolated enzyme fraction gave a single band on sodium dodecyl sulphate/polyacrylamide-gel electrophoresis and had an apparent subunit M4 of 63 000. 6. These results suggest that the uptake of lipid by the tissues in the trout can occur by a process similar to that in mammals. ...
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We examined the expression of lipoprotein lipase (LPL) gene and LPL activity following a two-thirds hepatectomy and during liver regeneration. In most of the tissues studied, LPL activity increased a few hours after partial hepatectomy, but soon returned to normal levels. The greatest increase was found in the adrenal glands, plasma and liver. This increase in LPL activity in the liver could be partially due to an increase in the influx of the enzyme from extrahepatic tissues. There is, however, also a re-expression of LPL mRNA in the liver after partial hepatectomy (during the first hours). It is well known that LPL is expressed in the liver of neonatal animals, but progressively decreases during post-natal development, to reach adult levels around the time of weaning. Our results show by the first time that the remaining liver re-expresses LPL gene during the regeneration process and that the hepatocytes de-differentiate and acquire some of the neonatal characteristics. The increase in LPL ...
To elucidate the intravascular TFPI distribution in the present study, it was necessary to differentiate the free form from the Lp-bound form of TFPI because of their different anticoagulant properties.12 13 The heparin infusion allowed us to measure the total intravascular TFPI levels, including the EC-TFPI concentration, which was 7.7 to 11.2 times greater than the preheparin free TFPI level, as previously reported.5 As determined by comparison of preheparin and postheparin plasmas, the distribution of intravascular TFPI in the CAD patients studied consisted of ,10% as the circulating preheparin free fraction (6% to 9%), 30% as the Lp-bound form (27% to 32%), and 60% as the EC-TFPI fraction (60% to 64%) regardless of the patients dyslipidemic profiles. The postheparin free TFPI was strongly correlated with preheparin free TFPI (r=0.6748), indicating a certain physiological equilibrium of free TFPI between the EC-TFPI pool and the preheparin circulating pool. In contrast, the preheparin LPL ...
The effects of treatment on plasma total triglyceride, total cholesterol, and plasma postheparin lipase activities have not been evaluated in non-insulin-dependent diabetic (NIDD) subjects without a coexisting familial lipid disorder. In 49 untreated NIDD subjects, there was a linear relationship between glycosylated hemoglobin (GHb) and triglyceride (r = 0.35, P , 0.02). This correlation was improved after adjusting for the effects of obesity by a partial correlation analysis. After therapy, there was a significant relationship between the change in GHb and the change in triglyceride.. To determine whether changes in lipid removal from plasma may contribute to the decrease in plasma lipid concentrations during treatment, the plasma postheparin lipoprotein lipase and hepatic lipase activities were evaluated in a subgroup (N = 8) of these NIDD subjects before and after 1 and 3 mo of therapy.. Plasma postheparin hepatic lipase activity in the NIDD subjects was not different from that observed in ...
Diacylglycerol (DAG) oil has been investigated in humans and animals as a potential therapy for hypertriglyceridemia and related disorders. DAG oil was evaluated in healthy cats and in a feline model of hypertriglyceridemia as a result of lipoprotein lipase (LPL) deficiency. In the first study, eight adult cats were offered a commercial dry diet enriched with either DAG or triglyceride (TAG) oil (48% metabolizable energy [ME] from fat) in a two-bowl palatability feeding trial. After 14 days, total food intakes were similar (DAG diet 470 ± 52 g, TAG diet 380 ± 88 g, P = 0.4). Both diets were well-accepted and no changes in health or fecal quality were observed. In the second study, eleven adult LPL-deficient male cats were fed a semipurified diet containing either DAG or TAG oil as the sole fat source (25% ME) in a crossover design for 8 days each after a 21-day acclimation period. Serum concentrations of TAG, cholesterol, and nonesterified fatty acids were measured on days 6, 7, 8 and days 14, ...
Peroxisome proliferator-activated receptor-alpha (PPAR alpha) activation attenuates cisplatin (CP)-mediated acute kidney injury by increasing fatty acid oxidation, but mechanisms leading to reduced renal triglyceride (TG) accumulation could also contribute. Here, we investigated the effects of PPAR alpha and CP on expression and enzyme activity of kidney lipoprotein lipase (LPL) as well as on expression of angiopoietin protein-like 4 (Angptl4), glycosylphosphatidylinositol-anchored-HDL-binding protein (GPIHBP1), and lipase maturation factor 1 (Lmf1), which are recognized as important proteins that modulate LPL activity. CP caused a 40% reduction in epididymal white adipose tissue (WAT) mass, with a reduction of LPL expression and activity. CP also reduced kidney LPL expression and activity. Angptl4 mRNA levels were increased by ninefold in liver and kidney tissue and by twofold in adipose tissue of CP-treated mice. Western blots of two-dimensional gel electrophoresis identified increased ...
TY - JOUR. T1 - Hippocampal lipoprotein lipase regulates energy balance in rodents. AU - Picard, Alexandre. AU - Rouch, Claude. AU - Kassis, Nadim. AU - Moullé, Valentine S.. AU - Croizier, Sophie. AU - Denis, Raphaël G.. AU - Castel, Julien. AU - Coant, Nicolas. AU - Davis, Kathryn. AU - Clegg, Deborah J.. AU - Benoit, Stephen C.. AU - Prévot, Vincent. AU - Bouret, Sébastien. AU - Luquet, Serge. AU - Le Stunff, Hervé. AU - Cruciani-Guglielmacci, Céline. AU - Magnan, Christophe. PY - 2014/1/1. Y1 - 2014/1/1. N2 - Brain lipid sensing is necessary to regulate energy balance. Lipoprotein lipase (LPL) may play a role in this process. We tested if hippocampal LPL regulated energy homeostasis in rodents by specifically attenuating LPL activity in the hippocampus of rats and mice, either by infusing a pharmacological inhibitor (tyloxapol), or using a genetic approach (adeno-associated virus expressing Cre-GFP injected into Lpllox/lox mice). Decreased LPL activity by either method led to increased ...
January 7th, 2010 - Lipoprotein lipase (LPL) is an enzyme that breaks apart fat (triglycerides) into their fatty acid components for transport and use inside cells. An increase in lipoprotein lipase activity means an increase in the flow of fatty acids into the cell. An increase in LPL activity in muscle cells means they will…
Tumour necrosis factor (TNF) has previously been shown to decrease lipoprotein lipase (LPL) activity and mRNA levels in 3T3-L1 cells and in adipose tissue from rats and guinea pigs when injected in vivo, but not to alter LPL activity in human adipocytes incubated in vitro. The effect of recombinant human TNF on LPL activity and mRNA levels in rat epididymal adipose tissue incubated in vitro was examined. LPL activity and mRNA levels fell in adipose tissue taken from fed rats and incubated in Krebs-Henseleit bicarbonate medium with glucose. The addition of insulin and dexamethasone prevented these falls. TNF (400 ng/ml) produced a fall of approx. 50% in LPL activity after 2 h of incubation and of approx. 30% in LPL mRNA levels after 3 h. TNF did not decrease LPL activity in isolated adipocytes. These results demonstrate that rat adipose tissue incubated in vitro is responsive to TNF whereas isolated adipocytes are not ...
FLow, P.-S.,Tay, J.S.H.,Arulkumaran, S.,Saha, N. (1998). Influence of PvuII (Intron 6) polymorphism of the lipoprotein lipase gene on cord plasma lipid and apolipoprotein levels in indian and chinese newborns of singapore. Pediatric Research 43 (2) : 240-244. [email protected] Repository ...
We studied the effects of a 3-day fast and 20 days of refeeding on lipoprotein lipase activity (LPL) in the interscapular brown adipose tissue (BAT) of sexually mature male rats. Rats were refed either ad libitum or restricted quantities (75 or 50% of normal ad libitum food intake). BAT-LPL, expressed on a per depot basis, decreased with fasting and returned to control values by day 3 of refeeding ad libitum. In contrast, refeeding restricted quantities for 5 to 20 days limited regain of body weight and increased BAT-LPL significantly above the values observed in rats refed ad libitum ...
Relative LPL expression of Group C compared to B. Fold difference of LPL expression in tissues studied, using BAC as the endogenous reference, tissues of rats f
So heres the deal, theres this great, little-known enzyme, called lipoprotein lipase, that we all have. The awesome thing about this enzyme is that it helps the body process and burn fat. Yes I know - lipoprotein lipase just became your best friend! But heres the catch, similar to many other enzymes, lipoprotein lipase is only generated when muscles are being used and active. Research done on lab rats shows that lipoprotein lipase was only produced in leg muscles when the rats were active, standing, or scurrying around. Therefore, if you want to get these enzymes to work, you need to get in motion and burn some energy. Besides, living a sedentary life is not good for your physical and mental health. Spending most of your time sitting around and being inactive can lead to a series of health problems like weight gain, diabetes, heart disease, high blood sugar, high blood pressure, and even cancer!. The key to get lipoprotein lipase to work is to spend as little time as possible inert. If you do ...
1] Navab M et al. HDL and cardiovascular disease: atherogenic and atheroprotective mechanisms. Nat Rev Cardiol. 2011 Apr;8(4):222-32. [2] Ahmed K et al. GPR109A, GPR109B and GPR81, a family of hydroxy-carboxylic acid receptors. Trends Pharmacol Sci. 2009 Nov;30(11):557-62. [3] Spate-Douglas T, Keyser RE. Exercise intensity: its effect on the high-density lipoprotein profile. Arch Phys Med Rehabil. 1999 Jun;80(6):691-5. [4] Bey L, Hamilton MT. Suppression of skeletal muscle lipoprotein lipase activity during physical inactivity: a molecular reason to maintain daily low-intensity activity. J Physiol. 2003 Sep 1;551(Pt 2):673-82. [5] Yanagibori R et al. The effects of 20 days bed rest on serum lipids and lipoprotein concentrations in healthy young subjects. J Gravit Physiol. 1997 Jan;4(1):S82-90. [6] Costa RR et al. Effects of resistance training on the lipid profile in ...
A 39-year-old man with lipoprotein lipase (LPL) deficiency (height 177.7 cm, body weight 67 kg, and body mass index 21.2 kg/m,sup,2,/sup,) showed severe hypertriglyceridemia (2, 032 mg/dl). LPL activity and concentration were markedly low in postheparin plasma. LPL gene analysis revealed a homozygous mutation, Asp204 → Glu in exon 5. Fasting plasma glucose (81 mg/dl) and insulin (2.7 (μU/ml) levels were normal. Plasma glucose pattern during oral glucose (75 g) tolerance test was normal, however 30 minutes after glucose-loading the insulin secretion unexpectedly increased to 89.4 μU/ml. These data suggested that chylomicronemia might be related to a hyper-response of insulin secretion to glucose without obesity.,br,(Internal Medicine 41: 300-303, 2002). ...
Plasmid,ELISA Kits,antibodies,strains Lpl ELISA Kit| Rat Lipoprotein lipase ELISA Kit [EF017174] - Rat Lpl ELISA Kit Catalog EF017174 Packing 48Tests/96Tests ELISA Method Sandwich ELISA Species Rat Sample Rat serum, plasma, tissue homogenates and other biological fluids and Recombinant Lpl Detect Range 0.78-50ng/ml sensitivity 0.469ng/ml ELISA Intend Use Rat Lpl ELISA Kit is a Sandwich ELISA KIT detecting the
S447X, a serine substitution by a stop codon on base 99 of exon 9 of the lipoprotein lipase (LPL) gene, has beneficial effects on blood lipids. Other LPL alleles are associated with lipid levels, but whether one of these variants predominates remains elusive. We performed a systematic survey to identify single-nucleotide polymorphisms (SNPs) in all 10 LPL exons and flanking regions by resequencing the gene in 95 subjects. Of 24 variants, 14 were common (≥3%). We assayed the common SNPs in 186 cases with atherogenic lipid profiles (low HDL, high LDL) and 185 nonatherogenic controls (high HDL, low LDL). Only S447X and exons 6 (base +73) and 10 (base −11) were individually associated with case-control status (P,0.05, adjusted for major nongenetic covariates with known lipid effects). There were no significant SNP×gender interactions. In adjusted multi-SNP and haplotypic analyses, S447X was interpretable as the sole predictor, with a 2-3-fold reduction in the odds of being atherogenic vs. ...
We have studied a cohort of FH heterozygotes to assess the effect of a common LPL mutation (N291S) on both lipoprotein phenotype and risk for atherosclerosis. Despite its previously reported association with dyslipoproteinemia, the association between this mutation and an increased incidence of atherosclerotic vascular disease remains controversial. To assess this possible association, we have studied a group of individuals already at high risk for CVD to determine whether this mutation altered the risk for developing atherosclerosis in this cohort.. Here, we demonstrate that the N291S LPL mutation, detected in 6.5% of 1045 FH heterozygotes studied, not only had a significant deleterious effect on lipoprotein phenotype but also significantly increased cardiovascular risk in subjects with this LPL mutation.. Individuals with heterozygous FH manifest with elevated TC and LDL cholesterol concentrations and have a significantly increased predisposition to premature CVD.10 It has been reported, ...
PubMed journal article: Variation at the lipoprotein lipase and apolipoprotein AI-CIII gene loci are associated with fasting lipid and lipoprotein traits in a population sample from Iceland: interaction between genotype, gender, and smoking status. Download Prime PubMed App to iPhone, iPad, or Android
Rabbits given a single subcutaneous injection of an alkaline extract of hog, bovine, or human anterior pituitary glands developed marked hyperlipemia within 12 to 24 hours. The injections in some instances were followed by sickening and death of the animal, though no anatomical changes responsible for these consequences could be determined. No such sequelae were observed in animals given much larger injections of comparable extracts made from other tissues. An inhibitor to lipoprotein lipase appeared regularly in the serum of the injected animals in association with the hyperlipemia. The injection of heparin into such animals failed to result in the elaboration of clearing factor, and serum from these animals inhibited in vitro the hydrolysis of lipid emulsions by active lipoprotein lipase obtained from normal rabbits or human beings. The inhibitor was produced only in vitro by the pituitary extracts. It did not antagonize the anticoagulant action of heparin, and is probably a lipoprotein ...
Lipoprotein Lipase/LPL Antibody Pair. Matched antibody pairs validated for ELISA or IP-Western Blot. Backed by our 100% Guarantee.
In mammals, several well-defined metabolic changes occur during infection, many of which are attributable to products of the reticuloendothelial system1-3. Among these changes, a hypertrigly-ceridaemic state is frequently evident4-9, resulting from defective triglyceride clearance, caused by systemic suppression of the enzyme lipoprotein lipase (LPL)9. We have found previously that macrophages secrete the hormone cachectin, which specifically suppresses LPL activity in cultured adipocytes (3T3-L1 cells)10-17. When originally purified from RAW 264.7 (mouse macrophage) cells, cachectin was shown to have a pI of 4.7, a subunit size of relative molecular mass (Mr) 17,000 and to form non-covalent multimers17. A receptor for cachectin was identified on non-tumorigenic cultured cells and on normal mouse liver membranes17. A new high-yield purification technique has enabled us to determine further details of the structure of mouse cachectin. We now report that a high degree of homology exists between the N
Insulin and lipoprotein lipase work together in your body to use extra calories from carbohydrates in your diet to make and store fats. Insulin is a pancreatic hormone that is commonly known to regulate your blood sugar level, but it also regulates the production of fats from carbohydrates.
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The purpose of this study was to evaluate the consequences of the acarbose-induced attenuation of postprandial glycemia and insulinemia on plasma lipid concentrations and on tissue lipoprotein lipase (LPL) activity. Rats were fed a high-sucrose diet AD LIBITUM for two weeks. On the day of the... mehr ...
Familial chylomicronemia syndrome (FCS) is a serious disease that prevents the body from breaking down fats.. Eating even a little fat can make someone with FCS ill, and the condition causes chronic symptoms and can lead to potentially fatal pancreatitis. FCS is a genetic disorder passed down from parents. Because it is rare, many healthcare providers have never heard of FCS or may not know how to diagnose it.. Lipoprotein lipase is a digestive enzyme that helps the body break down structures called chylomicrons. People who have FCS have a problem with lipoprotein lipase: it is either missing or broken. Chylomicrons carry triglycerides (a type of fat) to where they are needed in the body for energy. A buildup of these particles causes an increase in triglycerides levels.. Patients with FCS have extremely high levels of triglycerides. Normal triglyceride levels fall below 150 mg/dL. For people with FCS, triglyceride levels can exceed 1,000 mg/dL, even after medication and/or a low-fat diet are ...
Lipoprotein lipase (LPL) hydrolyzes triglycerides in plasma lipoproteins causing release of fatty acids for metabolic purposes in muscles and adipose tissue. LPL in macrophages in the artery wall may, however, promote foam cell formation and atherosclerosis. Angiopoietin-like protein (ANGPTL) 4 inactivates LPL and ANGPTL4 expression is controlled by peroxisome proliferator-activated receptors (PPAR). The mechanisms for inactivation of LPL by ANGPTL4 was studied in THP-1 macrophages where active LPL is associated with cell surfaces in a heparin-releasable form, while LPL in the culture medium is mostly inactive. The PPAR delta agonist GW501516 had no effect on LPL mRNA, but increased ANGPTL4 mRNA and caused a marked reduction of the heparin-releasable LPL activity concomitantly with accumulation of inactive, monomeric LPL in the medium. Intracellular ANGPTL4 was monomeric, while dimers and tetramers of ANGPTL4 were present in the heparin-releasable fraction and medium. GW501516 caused an increase ...
TY - JOUR. T1 - Adipose tissue fatty acid composition in humans with lipoprotein lipase deficiency. AU - Ullrich, Nathan F.E.. AU - Purnell, Jonathan Q.. AU - Brunzell, John D.. PY - 2001/5. Y1 - 2001/5. N2 - Background: Lipid stores in human adipose tissue are maintained primarily by incorporating lipid from circulating chylomicrons and very low density lipoproteins. Adipose tissue lipoprotein lipase (LPL) hydrolyzes triglyceride from these lipoprotein particles to facilitate their entry into adipocytes for storage. Subjects deficient in LPL still have normal adiposity, and this may result from increased adipocyte lipogenesis or from uptake of circulating lipid through alternate mechanisms. The objective of this study was to determine whether fatty acid composition of adipose tissue from LPL-deficient subjects reflects maintenance of lipid stores through increased lipogenesis or through alternate mechanisms of lipoprotein uptake. Methods: Adipose tissue samples from LPL-deficient subjects who ...
TY - JOUR. T1 - Action of Lipoprotein Lipase on Phospholipid Monolayers. Activation by Apolipoprotein C-II. AU - Vainio, Petri. AU - Virtanen, Jorma A.. AU - Kinnunen, Paavo K.J.. AU - Voyta, John C.. AU - Smith, Louis C.. AU - Gotto, Antonio. AU - Sparrow, James T.. AU - Pattus, Franc. AU - Verger, Robert. PY - 1983/1/1. Y1 - 1983/1/1. N2 - Action of lipoprotein lipase and its activation by apolipoprotein C-II (apoC-II) were studied with monomolecular films of 1,2-didodecanoyl-sn-glycero-3-phosphoglycerol as a substrate. The enzyme velocity and the specific activity of the interface-bound enzyme show a bell-shaped curve as a function of lipid packing, both in the presence and absence of apoC-II. Above critical surface pressure of 20 dyn cm-1, lipoprotein lipase alone is no longer able to hydrolyze a monolayer of 1,2-didodecanoyl-sn-glycero-3-phosphoglycerol. However, lipoprotein lipase readily penetrates into the phospholipid interface up to surface pressures exceeding 40 dyn cm-1, without any ...
LPL encodes for the enzyme lipoprotein lipase. It plays a role in breaking down fat in the form of triglycerides. When lipoprotein lipase breaks down triglycerides, the fat molecules are used by the body as energy or stored in fatty tissue for later use (R). Mutations in this can cause familial lipoprotein lipase deficiency, which will lead to an increase in fat and cause inflammation (R). familial lipoprotein lipase deficiency More than 220 mutations in the LPL gene have been found to cause familial lipoprotein lipase deficiency. This condition disrupts the normal breakdown of triglycerides in the body, resulting in an increase of these fats. The most common mutation in people of European ancestry replaces the protein building block (amino acid) glycine with the amino acid glutamic acid at position 188 in the enzyme (written as Gly188Glu or G188E). Mutations that cause familial lipoprotein lipase deficiency reduce or eliminate lipoprotein lipase activity, which prevents the enzyme from ...
Familial lipoprotein lipase deficiency is usually caused by a defective gene that is passed down through families.. Persons with this condition lack an enzyme called lipoprotein lipase. Without this enzyme, the body cannot break down fat from digested food. Fat particles called chylomicrons build up in the blood.. Risk factors include a family history of lipoprotein lipase deficiency.. The disorder affects about 1 out of 1,000,000 people. The condition is usually first seen during infancy or childhood.. ...
Lipoprotein lipase deficiency (also known as familial chylomicronemia syndrome, chylomicronemia, chylomicronemia syndrome and hyperlipoproteinemia type Ia) is a rare autosomal recessive lipid disorder caused by a mutation in the gene which codes lipoprotein lipase. As a result, afflicted individuals lack the ability to produce lipoprotein lipase enzymes necessary for effective breakdown of triglycerides. Laboratory changes: massive accumulation of chylomicrons in the plasma and corresponding severe hypertriglyceridemia. Typically, the plasma in a fasting blood sample appears creamy (plasma lactescence). Clinical symptoms: The disease often presents in infancy with colicky pain, failure to thrive, and other symptoms and signs of the chylomicronemia syndrome. In women the use of estrogens or first pregnancy are also well known trigger factors for initial manifestation of LPLD. At all ages, the most common clinical manifestation is recurrent abdominal pain and acute pancreatitis. The pain ...
Cardiovascular disease is stabilizing in high-income countries and has continued to rise in low-to-middle-income countries. Association of lipid profile with lipoprotein lipase gene was studied in case and control subject. The family history, hypertension, diabetes mellitus, smoking and alcohol consumption were the most risk factors for early-onset of coronary heart disease (CHD). Sudanese patients had significantly (P , 0.05) lower TC and LDL-C levels compared to controls. Allele frequency of LPL D9N, N291S and S447X carrier genotype was 4.2%, 30.7% and 7.1%, respectively. We conclude that lipoprotein lipase polymorphism was not associated with the incidence of CHD in Sudan. ª 2015 Published by Elsevier Ltd. on behalf of Ministry of Health, Saudi ...
The triglyceride lipase gene subfamily plays a central role in lipid and lipoprotein metabolism. There are three members of this subfamily: lipoprotein lipase, hepatic lipase, and endothelial lipase. Although these lipases are implicated in the pathophysiology of hyperlipidemia and atherosclerosis, their structures have not been fully solved. In the current study, we established homology models of these three lipases, and carried out analysis of their activity sites. In addition, we investigated the kinetic characteristics for the catalytic residues using a molecular dynamics simulation strategy. To elucidate the molecular interactions and determine potential key residues involved in the binding to lipase inhibitors, we analyzed the binding pockets and binding poses of known inhibitors of the three lipases. We identified the spatial consensus catalytic triad Ser-Asp-His, a characteristic motif in all three lipases. Furthermore, we found that the spatial characteristics of the binding pockets ...
Objective: Lipoprotein lipase (LPL) is a key regulator of circulating triglyceride rich lipoprotein hydrolysis. In brain LPL regulates appetite and energy expenditure. Angiopoietin-like 4 (Angptl4) is a secreted protein that inhibits LPL activity and, thereby, triglyceride metabolism, but the impact of Angptl4 on central lipid metabolism is unknown. Methods: We induced type 1 diabetes by streptozotocin (STZ) in whole-body Angptl4 knockout mice (Angptl4-/-) and their wildtype littermates to study the role of Angptl4 in central lipid metabolism. Results: In type 1 (streptozotocin, STZ) and type 2 (ob/ob) diabetic mice, there is a ~2-fold increase of Angptl4 in the hypothalamus and skeletal muscle. Intracerebroventricular insulin injection into STZ mice at levels which have no effect on plasma glucose restores Angptl4 expression in hypothalamus. Isolation of cells from the brain reveals that Angptl4 is produced in glia, whereas LPL is present in both glia and neurons. Consistent with the in vivo ...
Definition of Familial lipoprotein lipase inhibitor with photos and pictures, translations, sample usage, and additional links for more information.
Animal Research, formerly Annales de Zootechnie, publishes original articles, reviews, notes and symposium proceedings concerning research on farm animals
Two important regulators for circulating lipid metabolisms are lipoprotein lipase (LPL) and hepatic triglyceride lipase (HTGL). In relation to this, glycosylphosphatidylinositol anchored high-density lipoprotein binding protein 1 (GPIHBP1) has been shown to have a vital role in LPL lipolytic processing. However, the relationships between skeletal muscle mass and lipid metabolism, including LPL, GPIHBP1, and HTGL, remain to be elucidated. Demonstration of these relationships may lead to clarification of the metabolic dysfunctions caused by sarcopenia. In this study, these relationships were investigated in young Japanese men who had no age-related factors; participants included wrestling athletes with abundant skeletal muscle. A total of 111 young Japanese men who were not taking medications were enrolled; 70 wrestling athletes and 41 control students were included. The participants body compositions, serum concentrations of lipoprotein, LPL, GPIHBP1 and HTGL and thyroid function test results were
Lipoprotein lipase (LPL) (EC is a member of the lipase gene family, which includes pancreatic lipase, hepatic lipase, and endothelial lipase. It is a water-soluble enzyme that hydrolyzes triglycerides in lipoproteins, such as those found in chylomicrons and very low-density lipoproteins (VLDL), into two free fatty acids and one monoacylglycerol molecule. It is also involved in promoting the cellular uptake of chylomicron remnants, cholesterol-rich lipoproteins, and free fatty acids. LPL requires ApoC-II as a cofactor. LPL is attached to the luminal surface of endothelial cells in capillaries by the protein glycosylphosphatidylinositol HDL-binding protein 1 (GPIHBP1) and by heparan sulfated proteoglycans. It is most widely distributed in adipose, heart, and skeletal muscle tissue, as well as in lactating mammary glands. In brief, LPL is secreted from parenchymal cells as a glycosylated homodimer, after which it is translocated through the extracellular matrix and across endothelial ...
Familial LPL deficiency should be considered in anybody with the chylomicronemia syndrome (massive plasma elevations of the large lipoprotein particles that originate from dietary fat, with a concomitant increase in TG concentrations), especially in the absence of secondary causes of hypertriglyceridemia.. This disorder usually presents in childhood following repeated episodes of abdominal pain (including colicky infants), sometimes radiating to the back, attacks of pancreatitis and eruptive cutaneous xanthomas in about 50% of patients (when TG levels exceed 22.5 mmol/L or 2000 mg/dL). These non-tender yellow papular lesions are located in areas of injury or pressure (e.g. the buttocks, knees, elbows and back). They result from foam cell deposition within the skin and are more common in adult patients than children.. Hepatomegaly is common, and, if the plasma TG levels are very high, splenomegaly may also be seen. Organomegaly occurs as a result of TG uptake by macrophages, which become foam ...
LPL is a key regulator of fatty acid release from triglyceride-rich lipoproteins in muscle, heart, and fat (22). Increased adipocyte LPL activity leads to increased cellular uptake of fatty acids and adipocyte triglyceride accumulation. In white fat, LPL is regulated posttranscriptionally by nutritional status: fasting reduces and refeeding increases enzyme activity (23). Intriguingly, we found that a 14-d conventionalization increased LPL activity 122% in epididymal fat pads (Fig. 4C ). Moreover, the effect was not confined to fat: enzymatic assays of heart revealed a 99% increase with conventionalization (Fig. 4C ). Increased insulin levels produce reductions in muscle LPL activity (24). Therefore, our findings indicated that the microbiota induces the observed general increase in LPL through another mechanism.. Fiaf, also known as angiopoietin-like protein 4, is produced by brown and white fat, liver, and intestine (13, 25, 26). This secreted protein is an inhibitor of LPL in vitro [IC50 = ...
In this population-based sample of Australian adults, sitting time and TV viewing time were deleteriously associated with several biomarkers of cardio-metabolic risk, independent of leisure-time physical activity (and also independent of waist circumference for sitting time). This is the first study to report the associations of sitting time (in both leisure and nonleisure contexts) with risk biomarkers. It is also the first study to concurrently report associations for sitting time and for TV viewing time with metabolic biomarkers in the same cohort of women and men.. The mechanisms through which prolonged sitting might contribute to an adverse cardio-metabolic profile are yet to be determined. Physiologically, it has been suggested that the loss of local contractile stimulation induced through sitting leads to both the suppression of skeletal muscle lipoprotein lipase (LPL) activity (which is necessary for triglyceride uptake and HDL cholesterol production) and reduced glucose uptake through ...
This project is supported by the Canadian Institutes of Health Research (award #111062), Alberta Innovates - Health Solutions, and by The Metabolomics Innovation Centre (TMIC), a nationally-funded research and core facility that supports a wide range of cutting-edge metabolomic studies. TMIC is funded by Genome Alberta, Genome British Columbia, and Genome Canada, a not-for-profit organization that is leading Canadas national genomics strategy with funding from the federal government. Maintenance, support, and commercial licensing is provided by OMx Personal Health Analytics, Inc. Designed by Educe Design & Innovation Inc. ...
Daily News Thousands of Mutations Accumulate in the Human Brain Over a Lifetime Single-cell genome analyses reveal the amount of mutations a human brain cell will collect from its fetal beginnings until death.. ...
The discovery reveals the role of a growth factor and endothelial cells in thymus repair, and could have implications for chemotherapy and radiation patients recovery following treatment.. 0 Comments. ...
ECM1 Lipoprotein glomerulopathy; 611771; APOE Lipoprotein lipase deficiency; 238600; LPL Lissencephaly 3; 611603; TUBA1A ... TP63 Lipase deficiency, combined; 246650; LMF1 Lipodystrophy, congenital generalized, type 1; 608594; AGPAT2 Lipodystrophy, ...
... (NO-1886) is a cholesterol lowering drug from the statin family, which acts as a lipoprotein lipase activator. The ... Yin W, Tsutsumi K (2003). "Lipoprotein lipase activator NO-1886". Cardiovascular Drug Reviews. 21 (2): 133-42. doi:10.1111/j. ...
APOC3 inhibits lipoprotein lipase and hepatic lipase; it is thought to inhibit hepatic uptake of triglyceride-rich particles. ... "Metabolism of very-low-density lipoprotein and low-density lipoprotein containing apolipoprotein C-III and not other small ... Apo-CIII is secreted by the liver as well as the small intestine, and is found on triglyceride-rich lipoproteins such as ... "A human APOC3 missense variant and monoclonal antibody accelerate apoC-III clearance and lower triglyceride-rich lipoprotein ...
... and increased activity of lipoprotein lipase in blood. The synthesis of triglycerides is reduced in the liver as EPA and DHA ... and to enhance clearance of triglycerides from circulating very low-density lipoprotein (VLDL) particles; the way it does that ...
The triglycerides in chylomicrons are hydrolyzed by lipoprotein lipase (LPL) along the luminal surface of capillaries, mainly ... "GPIHBP1 stabilizes lipoprotein lipase and prevents its inhibition by angiopoietin-like 3 and angiopoietin-like 4". The Journal ... That Cannot Bind Lipoprotein Lipase". Arteriosclerosis, Thrombosis, and Vascular Biology. 29 (6): 956-962. doi:10.1161/ATVBAHA. ... "The Acidic Domain of GPIHBP1 is Important for the Binding of Lipoprotein Lipase and Chylomicrons". Journal of Biological ...
... and increased activity of lipoprotein lipase in blood. Omega-3 carboxylic acids are derived from fish oil and are a purified ... and to enhance clearance of triglycerides from circulating very low-density lipoprotein (VLDL) particles; the way it does that ... carboxylic acids in statin-treated patients with high levels of triglycerides and low levels of high-density lipoprotein ...
... and increased activity of lipoprotein lipase in blood. Ethyl eicosapentaenoic acid (E-EPA) is an ethyl ester of ... and to enhance clearance of triglycerides from circulating very low-density lipoprotein (VLDL) particles; the way it does that ... DHA alone appears to raise low-density lipoprotein (the variant which drives atherosclerosis; sometimes very inaccurately ...
... where their triglyceride components are hydrolyzed by the activity of the lipoprotein lipase, allowing the released free fatty ... APOC2 is the coenzyme for lipoprotein lipase (LPL) activity. Once triglyceride stores are distributed, the chylomicron returns ... also known as ultra low-density lipoproteins (ULDL), are lipoprotein particles that consist of triglycerides (85-92%), ... ULDLs, if in the region of 1,000 nm or more, are the only lipoprotein particles that can be seen using a light microscope, at ...
Lipoprotein lipase (LPL) is a type of digestive enzyme that helps regulate the uptake of triacylglycerols from chylomicrons and ... Lipoprotein lipase is downregulated by high levels of insulin, and upregulated by high levels of glucagon and adrenaline. ... Lipase assays are done using a lipid agar with a spirit blue dye. If the bacteria has lipase, a clear streak will form in the ... Kiens B, Lithell H, Mikines KJ, Richter EA (October 1989). "Effects of insulin and exercise on muscle lipoprotein lipase ...
It shares with ANGPTL4 and ANGPTL8 the ability to inhibit the enzyme Lipoprotein lipase (LPL), and its hepatic overexpression ... with its interacting partner lipoprotein lipase". Computational Biology and Chemistry. 61: 210-20. doi:10.1016/j.compbiolchem. ... antibody lowers mouse serum triglycerides involving increased postprandial activity of the cardiac lipoprotein lipase". ... mice lacking ANGPTL8 exhibit markedly decreased uptake of Very low-density lipoprotein-derived fatty acids into white adipose ...
Other processes involving sortilin include endocytosis, negative regulation of lipoprotein lipase activity, myotube ... "Sortilin/neurotensin receptor-3 binds and mediates degradation of lipoprotein lipase". The Journal of Biological Chemistry. 274 ... "Sortilin/neurotensin receptor-3 binds and mediates degradation of lipoprotein lipase". The Journal of Biological Chemistry. 274 ... Strong A, Rader DJ (June 2012). "Sortilin as a regulator of lipoprotein metabolism". Current Atherosclerosis Reports. 14 (3): ...
"Placental lipoprotein lipase (LPL) gene expression in a placentotrophic lizard, Pseudemoia entrecasteauxii". Journal of ...
Griffith, O. W., Ujvari, B., Belov, K., & Thompson, M. B. (2013). Placental lipoprotein lipase (LPL) gene expression in a ... Griffith, OW; Ujvari, B; Belov, K; Thompson, MB (2013). "Placental lipoprotein lipase (LPL) gene expression in a ...
Griffith, OW; Ujvari, B; Belov, K; Thompson, MB (2013). "Placental lipoprotein lipase (LPL) gene expression in a ... most likely occurs through the yolk sac placenta and is facilitated in part by the production of the protein lipoprotein lipase ...
Glybera treats one such disease, caused by a defect in lipoprotein lipase. DNA must be administered, reach the damaged cells, ... In 2012 Glybera, a treatment for a rare inherited disorder, lipoprotein lipase deficiency became the first treatment to be ... The treatment used Alipogene tiparvovec (Glybera) to compensate for lipoprotein lipase deficiency, which can cause severe ...
... on the dimerization of lipoprotein lipase". Biochimica et Biophysica Acta. 1344 (2): 132-8. doi:10.1016/s0005-2760(96)00146-4. ...
"Angiopoietin-like protein 4 converts lipoprotein lipase to inactive monomers and modulates lipase activity in adipose tissue". ... Lafferty MJ, Bradford KC, Erie DA, Neher SB (October 2013). "Angiopoietin-like protein 4 inhibition of lipoprotein lipase: ... causing elevation of serum TG levels via inhibition of the enzyme lipoprotein lipase (LPL). Biochemical studies indicate that ...
"Intramuscular Administration of AAV1-Lipoprotein LipaseS447X Lowers Triglycerides in Lipoprotein Lipase-Deficient Patients". ... The adeno-associated virus serotype 1 (AAV1) viral vector delivers an intact copy of the human lipoprotein lipase (LPL) gene to ... Alipogene tiparvovec, sold under the brand name Glybera, is a gene therapy treatment designed to reverse lipoprotein lipase ... Scott, Lesley J. (2015). "Alipogene Tiparvovec: A Review of Its Use in Adults with Familial Lipoprotein Lipase Deficiency". ...
He has done significant research in the biology and pathophysiology of lipoprotein lipase. Eckel was on the Scientific Advisory ...
... increases the activity of extrahepatic lipoprotein lipase (LL), thereby increasing lipoprotein triglyceride ... This increase in the synthesis of lipoprotein lipase thereby increases the clearance of triglycerides. Chylomicrons are ... levels Modest reduction of low density lipoprotein (LDL) levels Moderate increase in high density lipoprotein (HDL) levels GI ... several theories exist regarding the very low density lipoprotein (VLDL) effect; it can inhibit lipolysis and decrease ...
Thus one extra sialyl residue on apolipoprotein C3 impairs its action on lipoprotein lipase. This can affect expression of the ... Stocks, J; Holdsworth, G; Galton, DJ (1982). "An abnormal triglyceride-rich lipoprotein containing excess sialylated ... Stocks, J; Holdsworth, G; Galton, DJ (1979). "Hypertriglyceridaemia associated with an abnormal triglyceride-rich lipoprotein ...
Inactivity of lipoprotein lipase (LPL) plays the predominant role in the development of familial hypertriglyceridemia. LPL ... Individuals with the disorder are mostly heterozygous in an inactivating mutation of the gene encoding for lipoprotein lipase ( ... 2019). "Characterization of lipoprotein profiles in patients with hypertriglyceridemic Fredrickson-Levy and Lees dyslipidemia ... is a genetic disorder characterized by the liver overproducing very-low-density lipoproteins (VLDL). As a result, an afflicted ...
The role of lipoproteins, lipases and thyroid hormones in coronary lesion growth". Atherosclerosis. 68 (1-2): 51-8. doi:10.1016 ...
Zhang, Cuilin (2003). Variants in the Lipoprotein Lipase Gene and Paraoxonase Gene and Risk of Preeclampsia (Ph.D. thesis). ... Zhang's dissertation was titled Variants in the Lipoprotein Lipase Gene and Paraoxonase Gene and Risk of Preeclampsia. Her ...
Implications for a novel response elicited through the proximal octamer site of the lipoprotein lipase promoter". J. Biol. Chem ...
... binds lipoprotein lipase in vitro". J. Biol. Chem. 268 (19): 14176-81. PMID 7686151. Kounnas MZ, Loukinova EB, Stefansson S, ... Low density lipoprotein-related protein 2 also known as LRP2 or megalin is a protein which in humans is encoded by the LRP2 ... LRP2/megalin is a member of a family of receptors with structural similarities to the low density lipoprotein receptor (LDLR). ... "Entrez Gene: LRP2 low density lipoprotein-related protein 2". Korenberg JR, Argraves KM, Chen XN, Tran H, Strickland DK, ...
regulation of lipoprotein lipase activity. • intracellular protein transport. • protein import. • protein localization to cell ... positive regulation of lipoprotein lipase activity. • triglyceride homeostasis. • positive regulation of chylomicron remnant ... an endothelial cell transporter for lipoprotein lipase". The Journal of Lipid Research. 52 (11): 1869-1884. doi:10.1194/jlr. ... "GPIHBP1 stabilizes lipoprotein lipase and prevents its inhibition by angiopoietin-like 3 and angiopoietin-like 4". The Journal ...
TNF-alpha and TNF-gamma may also lead to inhibition of lipoprotein lipase or stimulate triglyceride synthesis. Activated ...
Mori M, Yamaguchi K, Abe K (May 1989). "Purification of a lipoprotein lipase-inhibiting protein produced by a melanoma cell ...
"Relationship of organ lipoprotein lipase activity and ketonuria to hypertriglyceridemia in starved and streptozocin-induced ...
脂蛋白脂酶缺乏症/Ia型(英语:Lipoprotein lipase deficiency) ...
Lipoprotein lipase deficiency. *Familial apoprotein CII deficiency. ReferencesEdit. *^ Goldberg, AC; Hopkins, PN; Toth, PP; ... markedly raised level of low-density lipoprotein (LDL), normal level of high-density lipoprotein (HDL), and normal level of ... Apolipoprotein B, in its ApoB100 form, is the main apolipoprotein, or protein part of the lipoprotein particle. Its gene is ... Several studies found that a high level of lipoprotein(a) was an additional risk factor for ischemic heart disease.[19][20] The ...
Gastric lipase secreted by the chief cells in the fundic glands in the gastric mucosa of the stomach, is an acidic lipase, in ... The liver synthesises the bulk of lipoproteins. The liver is located in the upper right quadrant of the abdomen and below the ... Lipase starts to work on breaking down fats. Lipase is further produced in the pancreas where it is released to continue this ... The presence of salivary lipase is of prime importance in young babies whose pancreatic lipase has yet to be developed.[14] ...
The role of lipoproteins, lipases and thyroid hormones in coronary lesion growth". Atherosclerosis. 68 (1-2): 51-8. doi:10.1016 ...
Lipemia retinalis is a white appearance of the retina, and can occur by lipid deposition in lipoprotein lipase deficiency. ...
high-density lipoprotein particle remodeling. • negative regulation of lipase activity. • regulation of intestinal cholesterol ... spherical high-density lipoprotein particle. • extracellular region. • early endosome. • high-density lipoprotein particle. • ... high-density lipoprotein particle binding. • heat shock protein binding. • receptor binding. Cellular component. • cytosol. • ... lipoprotein metabolic process. • post-translational modification. • cellular protein metabolic process. • transport. • positive ...
The best characterized are the RTX toxins and the lipases. Type I secretion is also involved in export of non-proteinaceous ... Porosomes are permanent cup-shaped lipoprotein structure at the cell plasma membrane, where secretory vesicles transiently dock ...
... hydrolysis of triglycerides by lipoprotein lipase and the enzymatic hydrolysis of diglycerides by diacylglycerol lipase; or as ...
Lipoprotein lipase. *Apolipoproteins. *Growth factors. *Chemokines. The enzymes and proteins listed above serve to reinforce ... Initial dysfunction of the glycocalyx can be caused by hyperglycemia or oxidized low-density lipoproteins (LDLs), which then ...
"Familial lipoprotein lipase deficiency - Genetics Home Reference". Arquivado dende o orixinal o 18 de novembro de 2004. ... Lipases humanasEditar. As principais lipases do aparato dixestivo humano son a lipase pancreática humana (HPL) e a proteína 2 ... Os humanos temos tamén outros encimas relacionados, como a lipase hepática (HL), lipase endotelial, e lipoproteína lipase. Non ... A lipase é un tipo de encima que cataliza hidrólise de lípidos.[1] As lipases son unha subclase de esterases. ...
lipase activity. • triglyceride lipase activity. • hormone-sensitive lipase activity. • protein binding. • hydrolase activity. ... "Entrez Gene: LIPE lipase, hormone-sensitive".. *^ Kraemer FB, Shen WJ (October 2002). "Hormone-sensitive lipase: control of ... Hormone-sensitive lipase (EC, HSL), also previously known as cholesteryl ester hydrolase (CEH),[5] sometimes referred ... LIPE, AOMS4, FPLD6, HSL, LHS, lipase E, hormone sensitive type. External IDs. OMIM: 151750 MGI: 96790 HomoloGene: 3912 ...
Free fatty acids are liberated from lipoproteins by lipoprotein lipase (LPL) and enter the adipocyte, where they are ...
In lipoproteins. Main article: Lipoprotein. Cholesterol is minimally soluble in water; it cannot dissolve and travel in the ... The largest lipoproteins, which primarily transport fats from the intestinal mucosa to the liver, are called chylomicrons. They ... Hyperlipidemia is the presence of elevated or abnormal levels of lipids and/or lipoproteins in the blood, and is a major risk ... After a meal, some of the fatty acids taken up by the liver is converted into very low density lipoproteins (VLDL) and again ...
In testing for gallbladder disease, specifically, liver panel tests and pancreatic enzymes such as lipase will be within normal ... reduced high density lipoprotein (HDL) cholesterol and the metabolic syndrome.[13] ...
Lipase. *Lipid. *Lipid anchored protein. *Lipoamide. *Lipoprotein. *Low density lipoprotein,LDL. *Luteinizing hormone (LH) ...
Although a clear consensus has not been reached, a large number of scientists adhere to a substrate-transport model to account for the catalytic properties of glucose 6-phosphatase. In this model, glucose 6-phosphatase has a low degree of selectivity. The transfer of the glucose 6-phosphate is carried out by a transporter protein (T1) and the endoplasmic reticulum (ER) contains structures allowing the exit of the phosphate group (T2) and glucose (T3).[6] Glucose 6-phosphatase consists of 357 amino acids, and is anchored to the endoplasmic reticulum (ER) by nine transmembrane helices. Its N-terminal and active site are found on the lumen side of the ER and its C-terminus projects into the cytoplasm. Due to its tight association to the ER, the exact structure of glucose 6-phosphatase remains unknown. However, sequence alignment has shown that glucose 6-phosphatase is structurally similar to the active site of the vanadium-containing chloroperoxidase found in Curvularia inaequalis.[7] Based on pH ...
... an AAV vector-based gene therapy product for the treatment of lipoprotein lipase deficiency in adults.[24] It was the first ...
"Characterization of regional and gender differences in glucocorticoid receptors and lipoprotein lipase activity in human ... Whole-grain, ready-to-eat, oat cereal diets reduce low-density lipoprotein cholesterol and waist circumference in overweight or ... reduces low-density lipoprotein cholesterol in adults with overweight and obesity more than a dietary program including low- ...
Tokiwa Y, Suzuki T (November 1977). "Hydrolysis of polyesters by lipases". Nature. 270 (5632): 76-8. doi:10.1038/270076a0. PMID ... PETase exhibits shared qualities with both lipases and cutinases in that it possesses an α/β-hydrolase fold; although, the ... According to ESTHER, it falls into the Polyesterase-lipase-cutinase family. There are approximately 69 PETase-like enzymes ... lipases, esterases, and cutinases.[5] Discoveries of polyester degrading enzymes date at least as far back as 1975 (α- ...
Vance JE, Vance DE (2002). Biochemistry of Lipids, Lipoproteins and Membranes. Amsterdam: Elsevier. ISBN 978-0-444-51139-3. .. ... with breakdown controlled mainly by the activation of hormone-sensitive enzyme lipase.[67] The complete oxidation of fatty ... In Vance JE, Vance EE (eds.). Biochemistry of Lipids, Lipoproteins and Membranes (4th ed.). Amsterdam: Elsevier. pp. 373-407. ... The fatty acids may be subsequently converted to triglycerides that are packaged in lipoproteins and secreted from the liver. ...
This enzyme belongs to the family of hydrolases, specifically those acting on phosphoric monoester bonds. The systematic name of this enzyme class is O-phosphoserine phosphohydrolase. This enzyme participates in glycine, serine and threonine metabolism. ...
Lipoprotein lipase on the endothelial surfaces of the capillaries, especially in adipose tissue, but to a lesser extent also in ... is carried out by lipases. These lipases are activated by high epinephrine and glucagon levels in the blood (or norepinephrine ... This is catalyzed either by phospholipase A2 acting directly on a membrane phospholipid, or by a lipase acting on DAG (diacyl- ... They are broken down into mono- and di-glycerides plus free fatty acids (but no free glycerol) by pancreatic lipase, which ...
... elevated low-density lipoprotein cholesterol, decreased high-density lipoprotein cholesterol and elevated serum transaminases.[ ... Lysosomal acid lipase deficiency (LAL deficiency or LAL-D), also known as Wolman disease, is an autosomal recessive inborn ... which is responsible for the gene coding of the lysosomal lipase protein (also called lysosomal acid lipase or LAL), which ... Lysosomal acid lipase deficiency is a genetic disease that is autosomal recessive. It is an inborn error of metabolism that ...
Third, an enzyme in breast milk called lipoprotein lipase produces increased concentration of nonesterified free fatty acids ... Poland, R L; Schultz GE; Gayatri G (1980). "High milk lipase activity associated with breastmilk jaundice". Pediatr Res. 14 (12 ...
"Endothelial cell-derived lipase mediates uptake and binding of high-density lipoprotein (HDL) particles and the selective ... low-density lipoprotein particle binding. • 1-phosphatidylinositol binding. • protein binding. • high-density lipoprotein ... high-density lipoprotein particle receptor activity. • phosphatidylserine binding. • apolipoprotein A-I binding. • ... low-density lipoprotein particle clearance. • blood vessel endothelial cell migration. • positive regulation of cholesterol ...
High Density Lipoprotein. Level of "good cholesterol" in the blood (ratio of HDL:LDL is usually more significant than actual ... Lipase *Pancreatic lipase. ‹ The template below (Myeloid blood tests) is being considered for merging. See templates for ... Low Density Lipoprotein. Level of "bad cholesterol" in the blood (ratio of HDL:LDL is usually more significant than actual ...
... cell surface binding of lipoprotein lipase and other proteins, angiogenesis, viral invasion, and tumor metastasis.[12]. CSGAGs ...
"Frameshift mutation in exon 3 of the lipoprotein lipase gene causes a premature stop codon and lipoprotein lipase deficiency". ...
Familial lipoprotein lipase deficiency is an inherited condition that disrupts the normal breakdown of fats in the body, ... Mutations that cause familial lipoprotein lipase deficiency lead to a reduction or elimination of lipoprotein lipase activity, ... Familial lipoprotein lipase deficiency. ... Mutations in the LPL gene cause familial lipoprotein lipase deficiency. The LPL gene provides instructions for producing an ...
Lipoprotein lipase: from gene to atherosclerosis.. Li Y1, He PP2, Zhang DW3, Zheng XL4, Cayabyab FS5, Yin WD6, Tang CK7. ... Lipoprotein lipase (LPL) is a key enzyme in lipid metabolism and responsible for catalyzing lipolysis of triglycerides in ... lipoproteins. LPL is produced mainly in adipose tissue, skeletal and heart muscle, as well as in macrophage and other tissues. ...
NIH/UW entry on Familial Lipoprotein Lipase Deficiency Gene therapy for lipoprotein lipase deficiency Lipoprotein+lipase at the ... Lipoprotein lipase (LPL) (EC is a member of the lipase gene family, which includes pancreatic lipase, hepatic lipase ... "Entrez Gene: LPL lipoprotein lipase". Wang H, Eckel RH (2009). "Lipoprotein lipase: from gene to obesity". Am J Physiol ... Zechner R (1997). "The tissue-specific expression of lipoprotein lipase: implications for energy and lipoprotein metabolism". ...
Lipoprotein lipase deficiency is a genetic disorder in which a person has a defective gene for lipoprotein lipase, which leads ... More than 220 mutations in the LPL gene have been found to cause familial lipoprotein lipase deficiency so far. Treatment of ... "Familial lipoprotein lipase deficiency: MedlinePlus Medical Encyclopedia". Retrieved 17 April 2019. Burnett, ... "Familial Lipoprotein Lipase Deficiency". In Adam, MP; Ardinger, HH; Pagon, RA; et al. (eds.). GeneReviews. Seattle: University ...
Glybera Registry, Lipoprotein Lipase Deficient (LPLD) Patients. *Lipoprotein Lipase Deficiency. *Familial Hyperlipoproteinemia ... Lipoprotein Lipase Enzyme Activity Assay Validation and Clinical Assessment. *Lipoprotein Lipase Deficiency ... Episodes in Lipoprotein Lipase Deficient (LPLD) Subjects Previously Enrolled on AMT Clinical Studies. *Lipoprotein Lipase ... an Adeno-Associated Viral Vector Expressing Human Lipoprotein Lipase [S447X]. *Familial Lipoprotein Lipase Deficiency ...
Lipoprotein lipase (LPL) is responsible for the intravascular processing of triglyceride-rich lipoproteins. The LPL within ... The intravascular processing of triglyceride-rich lipoproteins by the lipoprotein lipase (LPL)-GPIHBP1 complex is crucial for ... Structure of the lipoprotein lipase-GPIHBP1 complex that mediates plasma triglyceride hydrolysis. Gabriel Birrane, Anne P. ... Structure of the lipoprotein lipase-GPIHBP1 complex that mediates plasma triglyceride hydrolysis ...
Molecular cloning and sequence of a cDNA coding for bovine lipoprotein lipase. M Senda, K Oka, W V Brown, P K Qasba, and Y ... Lipoprotein lipase (LPL; triacylglycero-protein acylhydrolase, EC was purified from bovine milk. Synthetic ... Molecular cloning and sequence of a cDNA coding for bovine lipoprotein lipase ... Molecular cloning and sequence of a cDNA coding for bovine lipoprotein lipase ...
Lipoprotein lipase transporter GPIHBP1 and triglyceride-rich lipoprotein metabolism.. Liu C1, Li L2, Guo D3, Lv Y3, Zheng X4, ... Increased plasma triglyceride serves as an independent risk factor for cardiovascular disease (CVD). Lipoprotein lipase (LPL), ... Glycosylphosphatidylinositol-anchored high-density lipoprotein-binding protein 1 (GPIHBP1), a newly identified factor, appears ... of evidence indicate that GPIHBP1 exerts distinct functions and plays diverse roles in human triglyceride-rich lipoprotein (TRL ...
Lipoprotein Lipase Expression in Chronic Lymphocytic Leukemia. This study is ongoing, but not recruiting participants. ... The investigators hypothesize that Lipoprotein Lipase (LPL) expression on Chronic Lymphocytic Leukemia (CLL) cells will predict ...
tags: lipoprotein lipase deficiency x microbiology x The Scientist. » lipoprotein lipase deficiency and microbiology ...
Triglyceride-induced diabetes associated with familial lipoprotein lipase deficiency.. G Mingrone, F L Henriksen, A V Greco, L ... Triglyceride-induced diabetes associated with familial lipoprotein lipase deficiency.. G Mingrone, F L Henriksen, A V Greco, L ... Triglyceride-induced diabetes associated with familial lipoprotein lipase deficiency. Message Subject (Your Name) has forwarded ... and postheparin plasma lipoprotein lipase (LPL) activity. In addition, GC-clamped polymerase chain reaction-amplified DNA from ...
Mouse monoclonal Lipoprotein lipase antibody [LPL.A4]. Validated in WB, ELISA, IHC, Flow Cyt, ICC/IF and tested in Mouse, Cow, ... Lane 1 : Human Lipoprotein lipase.. Lane 2 : Bovine Lipoprotein lipase. Lysates/proteins at 10 µg per lane.. Predicted band ... Anti-Lipoprotein lipase antibody [LPL.A4]. See all Lipoprotein lipase primary antibodies. ... Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) abreview for Anti-Lipoprotein lipase antibody [LPL.A4]. ...
Lipoprotein lipase transport in plasma: role of muscle and adipose tissues in regulation of plasma lipoprotein lipase ... Lipoprotein lipase bound to apolipoprotein B lipoproteins accelerates clearance of postprandial lipoproteins in humans. ... Associations between lipoprotein lipase gene polymorphisms and plasma correlations of lipids, lipoproteins and lipase ... Lipoprotein lipase and its role in regulation of plasma lipoproteins and cardiac risk. Curr Atheroscler Rep. 2004; 6: 335-342. ...
Lipoprotein Lipase, lipoprotein lipase gene, low fat diet, male, medium chain triacylglycerol, multivitamin, promoter region, ... Sa Nampoothiri, Radhakrishnan, Nb, Schwentek, Ac, and Hoffmann, M. Ma, "Lipoprotein lipase deficiency in an infant", Indian ... The child was found to be heterozygous for two novel mutations in the lipoprotein lipase gene. ... triacylglycerol, very low density lipoprotein Abstract:. Patients with isolated hypertriglyceridemia usually present with ...
... , Triglycerides, Ultra Rare Diseases Akcea Therapeutics Inc. and Ionis Pharmaceuticals Inc. announced ...
リポ蛋白リパーゼの活性発現機構に関する研究 [in Japanese] A Study of Catalytic Function and Structure of Lipoprotein Lipase. [in Japanese] * * 田代 淳 ... We studied the catalytic process of lipoprotein lipase (LPL) and the structure which affects the catalytic activity of LPL. LPL ... しかしtriolein添加によるtributyrin水解活性上昇反応はみらWe studied the catalytic process of lipoprotein lipase (LPL) and the structure which ... The trypsin-treated LPL retained the ability to
This rare autosomal recessive disorder (frequency 1 per million) is characterized by the absence of lipoprotein lipase (LPL) ... and hepatic lipase deficiency). LPL promoter mutations are not rare and may contribute to the lipoprotein phenotype of FCH, at ... Lipoproteins, Lipids Similarly Linked With MI, Ischemic Stroke. *Familial Hypercholesterolemia Ups Risk of Cardiovascular ... and lowered high-density lipoprotein cholesterol (HDL-C; often ,0.5 mmol/L) in plasma. VLDL levels may remain fairly normal. ...
Lipoprotein Lipase/LPL Mouse anti-Human, Alexa Fluor 405, Clone: OTI3A10, Novus Biologicals 0.1 mL; Alexa Fluor 405 ... Lipoprotein Lipase/LPL Monoclonal antibody specifically detects Lipoprotein Lipase/LPL in Human samples. It is validated for ... Lipoprotein Lipase/LPL Mouse anti-Human, Alexa Fluor 405, Clone: OTI3A10, Novus Biologicals ... Recombinant protein fragment corresponding to amino acids 28-475 of human Lipoprotein Lipase/LPL (NP_000228) produced in ...
This rare autosomal recessive disorder (frequency 1 per million) is characterized by the absence of lipoprotein lipase (LPL) ... and hepatic lipase deficiency). LPL promoter mutations are not rare and may contribute to the lipoprotein phenotype of FCH, at ... and lowered high-density lipoprotein cholesterol (HDL-C; often ,0.5 mmol/L) in plasma. VLDL levels may remain fairly normal. ... massive plasma elevations of the large lipoprotein particles that originate from dietary fat, with a concomitant increase in TG ...
Although lipoprotein lipase is expressed by and is found on the surface of cardiomyocytes, its transfer to the luminal surface ... Lipoprotein lipase is the principal enzyme that hydrolyzes circulating triglycerides and liberates free fatty acids that can be ... Lipoprotein lipase (LpL) on the surface of cardiomyocytes increases lipid uptake and produces a cardiomyopathy. ... Lipoprotein lipase (LpL) on the surface of cardiomyocytes increases lipid uptake and produces a cardiomyopathy. ...
Lipoprotein Lipase/LPL Antibody Pair. Matched antibody pairs validated for ELISA or IP-Western Blot. Backed by our 100% ... Additional Lipoprotein Lipase/LPL Products. Lipoprotein Lipase/LPL H00004023-PW1 * Lipoprotein Lipase/LPL Antibodies ... Home » Lipoprotein Lipase/LPL » Lipoprotein Lipase/LPL Antibody Pairs » Lipoprotein Lipase/LPL Antibody Pair ... Blogs on Lipoprotein Lipase/LPL. There are no specific blogs for Lipoprotein Lipase/LPL, but you can read our latest blog posts ...
Lipoprotein lipase plays a central role in lipid metabolism and the gene that encodes this enzyme (LPL) is a candidate ... DNA sequence diversity in a 9.7-kb region of the human lipoprotein lipase gene Nat Genet. 1998 Jul;19(3):233-40. doi: 10.1038/ ... Lipoprotein lipase plays a central role in lipid metabolism and the gene that encodes this enzyme (LPL) is a candidate ...
Insulin and lipoprotein lipase work together in your body to use extra calories from carbohydrates in your diet to make and ... Lipoprotein Lipase & Insulin. Written by Michael R. Peluso, Ph.D.; Updated December 27, 2018 Lipoprotein Lipase & Insulin ... Lipoprotein Lipase. Lipoprotein lipase is an enzyme that is important for the transfer of triglycerides from your blood ... R., Michael. "Lipoprotein Lipase & Insulin" last modified ...
Lipoprotein lipase deficiency, familial a rare familial condition characterised by massive chylomicronaemia and decreased ... It is due to deficiency of lipoprotein lipase, an alkaline triglyceride hydrolase which catalyses an important step in the ... Retrieved from "" ...
Joint Linkage and Association Analysis of Hepatic Lipase Promoter Polymorphism and Lipoprotein Size Phenotypes. Laura Almasy, ... Joint Linkage and Association Analysis of Hepatic Lipase Promoter Polymorphism and Lipoprotein Size Phenotypes ... Joint Linkage and Association Analysis of Hepatic Lipase Promoter Polymorphism and Lipoprotein Size Phenotypes ... Joint Linkage and Association Analysis of Hepatic Lipase Promoter Polymorphism and Lipoprotein Size Phenotypes ...
... hydrolyses circulating triacylglycerol-rich lipoproteins. Thereby, LPL acts as a metabolic gate-keeper for fatty acids ... Lipoprotein lipase activity Lipoprotein lipase (LPL) activity was assessed after homogenization of the tissues in a buffer ... Catalytically inactive lipoprotein lipase expression in muscle of transgenic mice increases very low density lipoprotein uptake ... BACKGROUND: The lipoprotein lipase (LPL) hydrolyses circulating triacylglycerol-rich lipoproteins. Thereby, LPL acts as a ...
The lipoprotein lipase and free fatty acid values in the milk from mothers of infants without jaundice were found to increas … ... Lipoprotein lipase activity and free fatty acid concentrations were measured in samples of milk collected from mothers of ... Breast milk jaundice; the role of lipoprotein lipase and the free fatty acids Eur J Pediatr. 1980 Jun;134(1):35-8. doi: 10.1007 ... The lipoprotein lipase and free fatty acid values in the milk from mothers of infants without jaundice were found to increase ...
Candida rugosa can produce lipoprotein lipase by fermentation in the medium on a rotary shaker, the optimal medium compositions ... HomeAdvanced Materials ResearchMaterials for Environmental Protection and Energy...Study on Lipoprotein Lipase Production by ... X. X. Zhao and Y. G. He, "Study on Lipoprotein Lipase Production by Candida rugosa", Advanced Materials Research, Vols. 343-344 ... Candida rugosa can produce lipoprotein lipase by fermentation in the medium on a rotary shaker, the optimal medium compositions ...
Li Xie, You-Mei Li, Lipoprotein Lipase (LPL) Polymorphism and the Risk of Coronary Artery Disease: A Meta-Analysis, ... Cholesterol ester transfer protein, apolipoprotein E and lipoprotein lipase genotypes in patients with coronary artery disease ... and lipoprotein lipase (LPL). The relationship between CETP MspI, apo E and LPL PvuII gene polymorphisms and serum lipids were ... Lipoprotein lipase gene variants: Association with acute myocardial infarction and lipid profiles, Egyptian Journal of Medical ...
  • Familial lipoprotein lipase deficiency is an inherited condition that disrupts the normal breakdown of fats in the body, resulting in an increase of certain kinds of fats. (
  • People with familial lipoprotein lipase deficiency typically develop signs and symptoms before age 10, with one-quarter showing symptoms by age 1. (
  • Approximately half of individuals with familial lipoprotein lipase deficiency develop small yellow deposits of fat under the skin called eruptive xanthomas. (
  • The blood of people with familial lipoprotein lipase deficiency can have a milky appearance due to its high fat content. (
  • In people with familial lipoprotein lipase deficiency, increased fat levels can also cause neurological features, such as depression , memory loss, and mild intellectual decline (dementia). (
  • Mutations in the LPL gene cause familial lipoprotein lipase deficiency. (
  • Mutations that cause familial lipoprotein lipase deficiency lead to a reduction or elimination of lipoprotein lipase activity, which prevents the enzyme from effectively breaking down triglycerides. (
  • As a result, triglycerides attached to lipoproteins build up in the blood and tissues, leading to the signs and symptoms of familial lipoprotein lipase deficiency. (
  • Severe mutations that cause LPL deficiency result in type I hyperlipoproteinemia, while less extreme mutations in LPL are linked to many disorders of lipoprotein metabolism. (
  • Lipoprotein lipase deficiency is a genetic disorder in which a person has a defective gene for lipoprotein lipase, which leads to very high triglycerides, which in turn causes stomach pain and deposits of fat under the skin, and which can lead to problems with the pancreas and liver, which in turn can lead to diabetes. (
  • ApoC2, ApoA5, LMF-1, GPIHBP-1 and GPD1) should also be considered The diagnosis of familial lipoprotein lipase deficiency is finally confirmed by detection of either homozygous or compound heterozygous pathogenic gene variants in LPL with either low or absent lipoprotein lipase enzyme activity. (
  • More than 220 mutations in the LPL gene have been found to cause familial lipoprotein lipase deficiency so far. (
  • Also searched for Hyperlipoproteinemia Type I , Lipoprotein lipase deficiency , and Familial Chylomicronemias . (
  • Triglyceride-induced diabetes associated with familial lipoprotein lipase deficiency. (
  • Familial LPL deficiency should be considered in anybody with the chylomicronemia syndrome (massive plasma elevations of the large lipoprotein particles that originate from dietary fat, with a concomitant increase in TG concentrations), especially in the absence of secondary causes of hypertriglyceridemia. (
  • More severe hypertriglyceridemia can occur in compound heterozygotes, when other known genetic defects are present in addition to the heterozygous LPL state (e.g., the apoE2 allele, familial combined hyperlipidemia (FCH) and hepatic lipase deficiency). (
  • It is due to deficiency of lipoprotein lipase , an alkaline triglyceride hydrolase which catalyses an important step in the extrahepatic removal of triglyceride -rich lipoproteins from the blood . (
  • Familial lipoprotein lipase deficiency and other causes of the chylomicronemia syndrome. (
  • Phenotypic expression of heterozygous lipoprotein lipase deficiency in the extended pedigree of a proband homozygous for a missense mutation. (
  • Indeed, the rare autosomal recessive deficiency of apo C2 can lead to a decrease in lipoprotein lipase deficiency as profound as that in familial lipoprotein lipase deficiency (34, 35). (
  • Glybera is a gene therapy for patients with the genetic disorder lipoprotein lipase deficiency (LPLD). (
  • This trial is designed to expand the currently available data on the safety and efficacy of alipogene tiparvovec treatment in lipoprotein lipase deficiency (LPLD) and to further the understanding of possible mechanisms of action of the therapy. (
  • The goal of this study was to characterize the effect of microcoated fenofibrate (160 mg/day for 6 months) on plasma lipoprotein composition and kinetics in 2 patients with complete hepatic lipase (HL) deficiency. (
  • 53 Familial lipoprotein lipase deficiency is a rare genetic disorder is which a person lacks the enzyme lipoprotein lipase, a protein needed to break down fat molecules. (
  • Familial Lipoprotein Lipase Deficiency, also known as familial lpl deficiency , is related to hyperlipoproteinemia, type v and pancreatitis . (
  • An important gene associated with Familial Lipoprotein Lipase Deficiency is LPL (Lipoprotein Lipase), and among its related pathways/superpathways are Metabolism and Metabolism of water-soluble vitamins and cofactors . (
  • 12 A familial hyperlipemia characterized by a deficiency of the enzyme lipoprotein lipase and the subsequent build up of chylomicrons and increased plasma concentration of triglycerides. (
  • DAG oil was evaluated in healthy cats and in a feline model of hypertriglyceridemia as a result of lipoprotein lipase (LPL) deficiency. (
  • Familial lipoprotein lipase deficiency is caused by a defective gene that is passed down through families. (
  • Risk factors include a family history of lipoprotein lipase deficiency. (
  • Pancreatitis that is related to lipoprotein lipase deficiency responds to treatments for that disorder. (
  • Call your provider for screening if someone in your family has lipoprotein lipase deficiency. (
  • similar in symptoms to familial lipoprotein lipase deficiency. (
  • Molecular basis of lipoprotein lipase deficiency in two Austrian families with type I hyperlipoproteinemia. (
  • To determine the molecular basis for type I hyperlipoproteinemia in two Austrian families, the lipoprotein lipase (LPL) gene of two patients exhibiting LPL deficiency was analyzed by Southern blotting and by direct genomic sequencing of DNA amplified by polymerase chain reaction (PCR). (
  • Lipoprotein metabolism in hepatic lipase deficiency: studies on the turnover of apolipoprotein B and on the effect of hepatic lipase on high density lipoprotein. (
  • Hepatic lipase deficiency produces significant distortion in the plasma lipoprotein profile. (
  • The present study examines apolipoprotein B turnover in a patient with hepatic lipase deficiency. (
  • Objective - To assess effects of deficiency of lipoprotein lipase (LPL) on body condition scores and lean and fat body masses of adult cats. (
  • She was diagnosed with partial lipoprotein lipase (LPL) deficiency but without an associated LPL gene mutation in the presence of the apolipoprotein E3/2 genotype. (
  • Babirak, S.P et al: The detection and characterization of the heterozygote state for lipoprotein lipase deficiency. (
  • What is the definition of Familial Lipoprotein Lipase Deficiency? (
  • What are the causes for Familial Lipoprotein Lipase Deficiency? (
  • How prevalent is Familial Lipoprotein Lipase Deficiency? (
  • Is Familial Lipoprotein Lipase Deficiency an inherited disorder? (
  • This enzyme helps break down fats called triglycerides, which are carried by molecules called lipoproteins . (
  • It is a water-soluble enzyme that hydrolyzes triglycerides in lipoproteins, such as those found in chylomicrons and very low-density lipoproteins (VLDL), into two free fatty acids and one monoacylglycerol molecule. (
  • Lipoprotein lipase (LPL) is a key enzyme in lipid metabolism and responsible for catalyzing lipolysis of triglycerides in lipoproteins. (
  • The intravascular processing of triglyceride-rich lipoproteins by the lipoprotein lipase (LPL)-GPIHBP1 complex is crucial for clearing triglycerides from the bloodstream and for the delivery of lipid nutrients to vital tissues. (
  • The primary function of this lipase is the hydrolysis of triglycerides of circulating chylomicrons and very low density lipoproteins (VLDL). (
  • Lipoprotein lipase (LPL) hydrolyzes triglycerides in the circulation and promotes the hepatic uptake of remnant lipoproteins. (
  • 1 The main function of this enzyme is the hydrolysis of plasma triglycerides (TGs) that are packaged in apolipoprotein (apo) B containing lipoproteins. (
  • Lipoprotein lipase is the principal enzyme that hydrolyzes circulating triglycerides and liberates free fatty acids that can be used as energy by cardiac muscle. (
  • Lipoprotein lipase then provides essential assistance for the transfer of triglycerides from the lipoproteins in your blood to your fatty tissues, heart and muscles. (
  • Lipoprotein lipase is an enzyme that is important for the transfer of triglycerides from your blood lipoproteins into your tissues. (
  • Lipoprotein lipase breaks down the triglycerides in the lipoproteins to smaller fatty acids and monoglycerides that are transported into your tissues and either burned for fuel or re-assembled into triglycerides for storage. (
  • Lipases, such as lipoprotein lipase and endothelial lipase, are enzymes that breakdown circulating triglycerides (tg). (
  • We studied the activity and expression of lipoprotein lipase (LPL), which catalyzes the hydrolysis of plasma triglycerides, in different ocular regions. (
  • LPL hydrolyzes triglycerides in plasma lipoproteins. (
  • The effects of polymorphisms in the lipoprotein lipase (LPL) gene (HindIII and S447X) and in the apolipoprotein (apo) AI-CIII gene cluster (G75A and C1100T) on levels of fasting plasma triglycerides, apoCIII, high density lipoprotein cholesterol (HDL-C), and apoAI were examined in 315 healthy men and women from Iceland. (
  • Lipoprotein lipase (LPL), an enzyme which hydrolyzes triglycerides and participates in the catabolism of remnant lipoproteins, plays a crucial role in energy and lipid metabolism. (
  • In mammals, GPIHBP1 is absolutely essential for transporting lipoprotein lipase (LPL) to the lumen of capillaries, where it hydrolyzes the triglycerides in triglyceride-rich lipoproteins. (
  • Hepatic lipase (HL) and endothelial lipase (EL) are extracellular lipases that both hydrolyze triglycerides and phospholipids and display potentially overlapping or complementary roles in lipoprotein metabolism. (
  • 1 , - , 6 These 3 heparin-binding lipases are anchored to the endothelial surface and mediate the hydrolysis of triglycerides (TGs) and phospholipids (PLs) within circulating lipoproteins. (
  • Catalyzes the hydrolysis of triglycerides from circulating chylomicrons and very low density lipoproteins (VLDL), and thereby plays an important role in lipid clearance from the blood stream, lipid utilization and storage (PubMed:8675619, PubMed:11342582, PubMed:27578112). (
  • lipo·pro·tein li·pase (lip″o-proґtēn liґpās) [EC] an enzyme of the hydrolase class that catalyzes the hydrolytic cleavage of fatty acyl groups from triglycerides (or di- or monoglycerides) in chylomicrons, very-low-density lipoproteins, and low-density lipoproteins. (
  • lipoprotein lipase - an enzyme that catalyses the hydrolysis of triglycerides in chylomicrons and very low density lipoproteins to free fatty acids, which are absorbed from the capillaries into local tissues. (
  • Lipase is transported through the pancreatic duct into the first part of the small intestine ( ) where it helps break down dietary triglycerides ( a form of fat) into fatty acids. (
  • Use Lipoprotein Lipase in diagnostic tests for the determination of triglycerides together with Glycerol Kinase, Catalog No. 10 539 937 103 or 11 499 530 103 and Glycerol-3-phosphate Dehydrogenase, Catalog No. 11 654 730 103 or 11 582 003 103. (
  • Lipoprotein lipase (LPL) (EC is a member of the lipase gene family, which includes pancreatic lipase, hepatic lipase, and endothelial lipase. (
  • LPL gene encodes lipoprotein lipase, which is expressed in the heart, muscle, and adipose tissue. (
  • Lipoprotein lipase: from gene to atherosclerosis. (
  • The LPL gene locus is highly polymorphic and many single nucleotide polymorphisms (SNP) in both coding and noncoding regions have been used to study associations with lipids, lipoproteins, and risk for atherosclerosis. (
  • The child was found to be heterozygous for two novel mutations in the lipoprotein lipase gene. (
  • Lipoprotein lipase plays a central role in lipid metabolism and the gene that encodes this enzyme (LPL) is a candidate susceptibility gene for cardiovascular disease. (
  • The hepatic lipase gene (LIPC) has repeatedly been implicated as a potential regulator of HDL cholesterol concentration and HDL and LDL particle size. (
  • The aim of this study was to compare patients with coronary artery disease (CAD) to healthy objects, in order to explore a possible association between CAD and the variants in the gene encoding cholesterol ester transfer protein (CETP), apolipoprotein E (Apo E) and lipoprotein lipase (LPL). (
  • Association between lipoprotein lipase (LPL) gene and blood lipids: A common variant for a common trait? (
  • Background -Recently, a mutation in the lipoprotein lipase (LPL) gene (N291S) has been reported in 2% to 5% of individuals in western populations and is associated with increased triglyceride (TG) and reduced HDL cholesterol (HDLC) concentrations. (
  • 4. Eight of the subjects were found to possess genetic variants at the lipoprotein lipase gene locus. (
  • Comparative gene identification‑58 (CGI‑58) and lipoprotein lipase (LPL) are involved in the first step of triglyceride hydrolysis and serve an important role in lipid transport in the placenta. (
  • Mutations of the human LPL-gene have been shown to cause partial or complete malfunction of the enzyme, resulting in accumulation of lipoproteins in the blood. (
  • Based on these findings we were evaluating a possible role of the lipoprotein lipase gene in the development of pancreatitis and hyperlipidemia in the Miniature Schnauzer. (
  • We conclude that pancreatitis associated with hyperlipidemia in the Miniature Schnauzer is not linked to mutations of the lipoprotein lipase gene or its splicing regions. (
  • The Effects of Dietary Fatty Acids On Lipoprotein Lipase Activity and Gene Expression. (
  • The aim of the study was to evaluate the influence of single nucleotide polymorphism (SNP) in lipoprotein lipase gene (LPL) on the basic sheep milk parameters and the fatty acid profile in milk and yoghurt drinks made from it. (
  • Peterson, al: Structural and functional consequences of missense mutations in Exon 5 of the lipoprotein lipase gene. (
  • article{5a0b5a06-4e09-4a23-a38a-02712684b3d8, abstract = {The location of lipoprotein lipase activity in rat adipose tissue was studied using intact epididymal fat pads, isolated adipocytes, and lipoprotein lipase activity secreted from adipocytes as enzyme sources. (
  • Abstract Lipoprotein lipase (LPL), the enzyme responsible for hydrolyzing triglyceride (TG) in plasma lipoproteins, is a key regulator of plasma TG levels. (
  • Lipoprotein lipase transporter GPIHBP1 and triglyceride-rich lipoprotein metabolism. (
  • Lipoprotein lipase (LPL), which hydrolyzes circulating triglyceride, plays a crucial role in normal lipid metabolism and energy balance. (
  • Numerous lines of evidence indicate that GPIHBP1 exerts distinct functions and plays diverse roles in human triglyceride-rich lipoprotein (TRL) metabolism. (
  • Lipoprotein lipase (LPL) plays a central role in human lipid homeostasis and energy metabolism. (
  • LPL plays a pivotal role in lipids and the metabolism of lipoprotein. (
  • Ocular tissues are highly dependent on lipid turnover and metabolism, which requires an uptake mechanism for fatty acids from lipoproteins. (
  • FH is a common autosomal dominant disorder of lipoprotein metabolism, affecting ≈1 in 500 people in the western world. (
  • To this end, we explored the effect of CsA therapy on hepatic 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase (the rate-limiting enzyme in cholesterol synthesis), LDL, and high-density lipoprotein (HDL) receptors (the critical factors in metabolism of the cholesterol-rich LDL and HDL particles), and of cholesterol 7α-hydroxylase, (the rate-limiting step in cholesterol catabolism to bile acids). (
  • OBJECTIVE To evaluate the impact of chronic inflammation on lipoprotein lipase (LPL) levels and tri-glyceride metabolism in patients wit rheumatoid arthritis (RA). (
  • These studies reveal an additive effect of HL and EL on HDL metabolism but not macrophage reverse cholesterol transport in mice and an unexpected redundant role of HL and EL in apolipoprotein B lipoprotein metabolism. (
  • Both HL and EL influence the metabolism of high-density lipoproteins (HDLs). (
  • HL also modulates the metabolism of apolipoprotein (apo)B-containing lipoproteins (LpBs). (
  • The metabolism of large and small very low density lipoproteins was determined in four control subjects and compared to the pattern seen in the patient. (
  • Since mice lacking neuronal lipoprotein lipase (LPL) develop perturbations in neuronal lipid-sensing and systemic energy balance, we reasoned that LPL might be a component of pre-autonomic neurons involved in the regulation of hepatic metabolism. (
  • BackgroundLysosomal acid lipase is an essential lipid- metabolizing enzyme that breaks down endocytosed lipid particles and regulates lipid metabolism. (
  • Lipoprotein lipase (LPL) plays a critical role in the metabolism of lipoproteins because this enzyme hydrolyzes the triacylglycerides in chylomicrons and very low density lipoproteins. (
  • It is also involved in promoting the cellular uptake of chylomicron remnants, cholesterol-rich lipoproteins, and free fatty acids. (
  • it has a higher affinity for large triacylglyceride-rich lipoproteins than cholesterol-rich lipoproteins. (
  • These mutations occur at high frequencies in the general population (up to 5%) and are associated with elevated TGs, decreased high-density lipoprotein (HDL) cholesterol levels, and concomitantly with a higher incidence of cardiovascular disease (CVD), 6-13 compared with noncarriers. (
  • In the CAD group, those with the Msp M1 allele had higher levels of total cholesterol (TC) (p = 0026) and low-density lipoprotein cholesterol (LDL-C) than those with the Msp M2 allele. (
  • In the control group, CETP, the Msp M2 allele was associated with a higher level of high-density lipoprotein cholesterol (HDL-C) (p = 0.012) than the Msp M1 allele. (
  • I had Fasting test Cholesterol 158/triglyceride 45/ HDL 77 / LDL calculated 72 \cholesterol high density lipoprotein 2.1 /cholesterol nonHDL81 Normal? (
  • The kinetics of plasma apoA-I and apoA-II as well as the capacity of total plasma and of high-density lipoprotein particles to efflux cellular cholesterol from normal human skin fibroblasts was not altered by fenofibrate. (
  • Thus, hepatic expressions of cholesterol 7α-hydroxylase (the rate-limiting step in cholesterol conversion to bile acids), LDL receptor, and high-density lipoprotein (HDL) receptor proteins, as well as 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase activity were determined in rats treated with CsA (18 mg/kg/day) or placebo for 3 weeks. (
  • This was associated with a marked down-regulation of cholesterol 7α-hydroxylase in the liver and a severe reduction of lipoprotein lipase abundance in skeletal muscle and adipose tissue. (
  • In conclusion, CsA administration for 3 weeks resulted in a significant reduction of hepatic cholesterol 7α-hydroxylase and marked down-regulation of skeletal muscle and adipose tissue lipoprotein lipase abundance in rats. (
  • The former abnormality can contribute to hypercholesterolemia by limiting cholesterol catabolism, whereas the latter may contribute to hypertriglyceridemia and VLDL accumulation by limiting triglyceride-rich lipoprotein clearance in CsA-treated animals. (
  • The plasma levels of total cholesterol, high-density lipoprotein (HDL) cholesterol, non-HDL cholesterol, and phospholipids in the HL/EL-dko mice were markedly higher than those in the single-knockout mice. (
  • HDL from all 3 lipase knockout models had an increased cholesterol efflux capacity but reduced clearance of HDL cholesteryl esters versus control mice. (
  • lipoprotein - n. one of a group of compounds, found in blood plasma and lymph, each consisting of a protein (see apolipoprotein) combined with a lipid (which may be cholesterol, a triglyceride, or a phospholipid). (
  • Lipase is absolutely key to proper fat digestion, which affects so many bodily functions as well as health st Heart Rate Zone For Fat Burn - Weight Loss Clinic Opelousas La Best Heart Rate Zone For Fat Burn Hdl High Density Lipoprotein Cholesterol Weight Loss Management In Flint Mi. (
  • A review of low- density lipoprotein cholesterol its impact on cardiovascular disease morbidity , treatment strategies mortality. (
  • The study has broad- ranging implications relative to increased free radical damage , although carried out on pigs loss of mitochondria productionThis is a st Heart Rate Zone For Fat Burn - Weight Loss Clinic Opelousas La Best Heart Rate Zone For Fat Burn Hdl High Density Lipoprotein Cholesterol Weight Loss Management In. (
  • Body fat decreases in total low- density lipoprotein cholesterol were greater in women whose adipose tissue LPL activity decreased with weight loss. (
  • This process influences the production of high-density lipoprotein (HDL), which takes up tissue cholesterol for transport to the liver for excretion. (
  • To help clarify this issue, we investigated 144 outwardly healthy male Mediterranean migrants (from Italy and Greece), age between 40 and 70 years and resident in Australia, for associations between two common LPL restriction site polymorphisms and the following lipid and lipoprotein phenotypes: total plasma cholesterol, low-density lipoprotein (LDL), high-density lipoprotein (HDL), and triacylglycerides. (
  • 76 Hyperlipidemia is abnormally elevated levels of any or all lipids or lipoproteins in the blood. (
  • As the underlying mechanism of the enhancing effect has not been investigated previously, we here show that in the presence of soybean 15LO (SLO) or human 15LO (rhLO), the addition of lipoprotein lipase, porcine pancreatic, or human type IIa secretory phospholipase A2 (sPLA2) greatly enhanced the accumulation of hydro(pero)xides of all major classes of LDL's lipids. (
  • With SLO, formation of oxidized esterified lipids occurred nonenzymically, independent of the presence of lipase and despite the oxygenase remaining active until the end of the incubation. (
  • LDL depleted of alpha-tocopherol was resistant to oxidation by 15LO alone, whereas lipase overcame this resistance, demonstrating that lipases enhance 15LO-induced enzymic and nonenzymic peroxidation of LDL lipids. (
  • is an enzyme that hydrolyzes lipids in lipoproteins, like those found in chylomicrons and very low density lipoproteins (VLDL), into three free fatty acids and one glycerol molecule. (
  • green (phospholipids)] A lipoprotein is a biochemical assembly that contains both proteins and lipids. (
  • We investigated the effect of HMBA on hyperlipidaemia induced by ethanol, exploring food intake, body weight, and hepatic and plasma lipids and lipoproteins. (
  • Hepatic lipase (HL) and endothelial lipase (EL) are members of an extracellular lipase family that includes lipoprotein lipase (LPL). (
  • This study was performed to compare the effects of three different lipid-lowering therapies (statins, ezetimibe, and colestimide) on lipoprotein lipase and endothelial lipase masses in pre-heparin plasma (pre-heparin LPL and EL mass, respectively) from patients with familial hypercholesterolemia (FH). (
  • Lipoprotein lipase can bind with your blood lipoproteins, including VLDL from your liver and chylomicrons from your small intestine, after a meal. (
  • Specifically, lipases degrade tg rich lipoproteins including chylomicrons, very low density lipoprotein (vldl) and remnant particles produced by breakdown of chylomicron and vldl particles. (
  • In addition, we determined the effects of CsA therapy on skeletal muscle and adipose tissue abundance of lipoprotein lipase and the novel VLDL receptor, which are the principal clearance pathways of triglyceride-rich lipoproteins, namely, chylomicrons and VLDL. (
  • It catalyses the hydrolysis of the triacylglycerol component of chylomicrons and very low-density lipoproteins (VLDL), providing non-esterified fatty acids for tissue utilization. (
  • The primary sources of these extracellular fatty acids are those that are 1) associated with circulating albumin or 2) hydrolyzed from triacylglycerol-rich lipoprotein particles such as chylomicrons or very low density lipoproteins (VLDL). (
  • Lipoprotein lipase activity was studied in rat parametrial adipose tissue perfused with chylomicrons and in gelatin blocks containing postheparin plasma and chylomicrons. (
  • It hydrolyzes triacylglycerols in chylomicrons, lipoproteins and diacylglycerols. (
  • In this instance besides LPL also other loss-of-function mutations in genes that regulate catabolism of triglyceride-rich lipoproteins (like e.g. (
  • LPL promoter mutations are not rare and may contribute to the lipoprotein phenotype of FCH, at least in the subset of patients who show reduced postheparin plasma LPL activity. (
  • T polymorphism can not explain the observed linkage of lipoprotein size phenotypes to the LIPC region and, therefore, that there are one or more additional functional mutations in or near LIPC influencing HDL, and potentially LDL, size variation. (
  • ApoC-II was the only apolipoprotein from human very low density lipoprotein that activated rat adipose tissue lipoprotein lipase. (
  • The fats made in your liver from extra carbohydrates in your diet are packaged into blood transporters called very low-density lipoproteins, or VLDL, which are shipped into your blood. (
  • Long-term administration of cyclosporine (CsA) has been shown to cause hypercholesteremia, hypertriglyceridemia, and elevations of plasma low-density and very low-density lipoprotein (LDL and VLDL) levels in humans. (
  • In addition, skeletal muscle and adipose tissue expressions of lipoprotein lipase and VLDL receptor were measured. (
  • Objective Circulating hepatitis C virus (HCV) virions are associated with triglyceride-rich lipoproteins, including very low-density lipoprotein (VLDL) and low-density lipoprotein (LDL), designated as lipo-viro-particles (LVPs). (
  • Previous studies showed that lipoprotein lipase (LPL), a key enzyme for hydrolysing the triglyceride in VLDL to finally become LDL, may suppress HCV infection. (
  • In vitro, EL is capable of hydrolyzing very-low-density lipoprotein (VLDL) TG and PL. 8 Moderate transgenic overexpression of EL does not affect LpB levels, 18 but adenoviral-mediated overexpression of EL in mice reduces LpB levels. (
  • Particles with reduced electrophoretic mobility appear in very low density lipoprotein (VLDL). (
  • Absence of the enzyme did not affect the rate at which large very low density lipoproteins were converted to smaller particles within this density interval (i.e., of VLDL). (
  • However, subsequent transfer of small very low density lipoproteins to intermediate density particles was retarded by 50%, explaining the abnormal accumulation of VLDL in the patient's plasma. (
  • Background: In recent years, the lipoprotein lipase (LPL) polymorphism has been extensively investigated as a potential risk factor for coronary artery disease (CAD). (
  • tg rich lipoprotein particles. (
  • Transformation of high density lipoprotein 2 particles by hepatic lipase and phospholipid transfer protein. (
  • A major portion of available fatty acids for adipocyte uptake is derived from lipoprotein lipase (LPL)-mediated hydrolysis of circulating lipoprotein particles. (
  • Mediates margination of triglyceride-rich lipoprotein particles in capillaries (PubMed:24726386). (
  • Associates with lipoprotein particles in blood plasma (PubMed:11342582, PubMed:11893776). (
  • Despite this, intermediate density particles accumulated to a level 2.4-times normal because their subsequent conversion to low density lipoprotein has been almost totally inhibited. (
  • On the basis of these observations, hepatic lipase appears to be essential for the conversion of small very low density and intermediate density particles to low density lipoproteins. (
  • Lipoproteins are complex particles composed of multiple proteins which transport all fat molecules around the body within the water outside cells. (
  • 1. Alloxan-diabetic rats showed raised plasma triglyceride levels and low adipose tissue lipoprotein lipase activity compared with controls. (
  • Obese subjects have elevated adipose tissue lipoprotein lipase activity per fat cell when compared with lean control subjects. (
  • After secretion, LPL is carried across endothelial cells and presented into the capillary lumen by the protein glycosylphosphatidylinositol-anchored high-density lipoprotein-binding protein 1. (
  • Glycosylphosphatidylinositol-anchored high-density lipoprotein-binding protein 1 (GPIHBP1), a newly identified factor, appears essential for transporting LPL to the luminal side of the blood vessel and offering a platform for TG hydrolysis. (
  • Recombinant protein fragment corresponding to amino acids 28-475 of human Lipoprotein Lipase/LPL (NP_000228) produced in HEK293T. (
  • Hearts of transgenic mice expressed the altered lipoprotein lipase, and the protein localized to the surface of cardiomyocytes. (
  • Here, we investigated the effects of PPAR alpha and CP on expression and enzyme activity of kidney lipoprotein lipase (LPL) as well as on expression of angiopoietin protein-like 4 (Angptl4), glycosylphosphatidylinositol-anchored-HDL-binding protein (GPIHBP1), and lipase maturation factor 1 (Lmf1), which are recognized as important proteins that modulate LPL activity. (
  • Lipoprotein lipase is a multifunctional protein, playing a major role in the hydrolysis of TG-rich lipoproteins. (
  • 2. We have therefore, studied 18 patients with diabetes mellitus, obesity and severe hypertriglyceridaemia for defects of a key protein involved in the clearance of plasma triacylglycerols, lipoprotein lipase. (
  • The acidic domain of the endothelial membrane protein GPIHBP1 stabilizes lipoprotein lipase activity by preventing unfolding of its catalytic domain. (
  • GPIHBP1 is a glycolipid-anchored membrane protein of capillary endothelial cells that binds lipoprotein lipase (LPL) within the interstitial space and shuttles it to the capillary lumen. (
  • Lipase is a protein (enzyme) released by the pancreas into the small intestine. (
  • 17 In a more recent study, Fisher et al showed that LPL D9N causes enhanced low-density lipoprotein (LDL) binding and monocyte adhesion compared with LPL WT and was thus suggested to enhance foam cell formation in the vascular wall. (
  • The trypsin-treated LPL retained the ability to bind to very density lipoproteins. (
  • LPL-S132N showed no activity against triolein or tributyrin, whereas the mutant LPL bound to very low density lipoproteins as effectively as wild type LPL. (
  • and high density lipoproteins (HDL). (
  • high density lipoproteins which migrate in the alpha position in paper chromatography. (
  • It is possible that these apoproteins function partly to modulate the hydrolysis of very low density lipoprotein triglyceride by lipoprotein lipase. (
  • The oxidation of low-density lipoprotein (LDL) is thought to contribute to atherogenesis. (
  • 4. The activity was strongly stimulated by trout very low density lipoproteins and to a lesser extent by high density lipoproteins. (
  • Most notably, the HL/EL-dko mice exhibited an unexpected substantial increase in small low-density lipoproteins. (
  • Kinetic studies with [ 3 H]cholesteryl ether-labeled very-low-density lipoproteins demonstrated that the HL/EL-dko mice accumulated counts in the smallest low-density lipoprotein-sized fractions, as assessed by size exclusion chromatography, suggesting that it arises from lipolysis of very-low-density lipoproteins. (
  • in contrast, HL-knockout (ko) mice fed a high-fat diet exhibit a modest increase in plasma LpB levels, 17 which is exacerbated in the absence of apoE 27 or the low-density lipoprotein (LDL) receptor. (
  • Low density lipoprotein (LDL) isolated from th LHPO group exhibited high TBA values about 6 times the control LDL. (
  • As a result of which the balance between the fat deposition and clearing is disturbed in the arterial walls giving rise to more and more deposition of a type of fat called as Low Density Lipoprotein giving rise to atherosclerosis resulting in CAD and Stroke. (
  • Intermediate density lipoprotein (IDL) increases markedly in the circulation and plasma low density lipoprotein (LDL) levels fall. (
  • At the same time there is a mass redistribution within the high density lipoprotein (HDL) spectrum leading to dominance in the less dense HDL2 subfraction. (
  • Consequently, the plasma concentration of low density lipoprotein was only 10% of normal. (
  • High- density lipoproteins ( HDL) are one of the five major groups of lipoproteins. (
  • In all of the family members (parents, two affected sisters, ages 18 and 15 years, and an 11-year-old unaffected sister), we measured oral glucose tolerance, insulin sensitivity (by the euglycemic-hyperinsulinemic clamp technique), substrate oxidation (indirect calorimetry), endogenous glucose production (by the [6,6-2H2]glucose technique), and postheparin plasma lipoprotein lipase (LPL) activity. (
  • Insulin and lipoprotein lipase work together in your body to use extra calories from carbohydrates in your diet to make and store fats. (
  • Insulin stimulates lipoprotein lipase production, especially in your fatty tissues. (
  • (
  • Lipoprotein Lipase & Insulin" last modified December 27, 2018. (
  • Amylase, lipase and insulin blood test? (
  • Skeletal muscle-specific deletion of lipoprotein lipase enhances insulin signaling in skeletal muscle but causes insulin resistance in liver and other tissues," Diabetes , vol. 58, no. 1, pp. 116-124, 2009. (
  • Normal triglyceride levels despite insulin resistance in African Americans: role of lipoprotein lipase. (
  • Lipoprotein lipase in mouse peritoneal macrophages: the effects of insulin and dexamethasone. (
  • The effects of insulin and dexamethasone on the secretion of lipoprotein lipase (LPL) by mouse peritoneal macrophages were examined in vitro. (
  • Compared to sedentary controls, exercise decreased plasma insulin, epididymal and retroperitoneal depot weight and cell size, and retroperitoneal lipoprotein lipase (LPL) activity. (
  • Selective measurement of two lipase activities in post heparin plasma from normal subjects and patients with hyperlipoproteinemia. (
  • Yes research has suggested that fluorinated water may be responsible for the decreased activity of both pancreatic lipase protease. (
  • GPIHBP1 complex is responsible for margination of triglyceride-rich lipoproteins along capillaries and their lipolytic processing. (
  • Little is known about the fate of the lipolytic products produced by the action of lipoprotein lipase (LPL) on circulating triglyceride-rich lipoproteins in humans. (
  • These results indicate that there is escape, or spillover, of the lipolytic products of LPL action on triglyceride-rich lipoproteins in humans. (
  • Adipose triglyceride lipase and the lipolytic catabolism of cellular fat. (
  • Lipoprotein Lipase has both lipolytic and sterol ester hydrolytic activities. (
  • These findings indicate that increased values of lipoprotein lipase and free fatty acids in the milk are not responsible for the development of breast-milk jaundice. (
  • Lipoprotein lipase (LPL) serves as a central factor in hydrolysis of triacylglycerol and uptake of free fatty acids from the plasma. (
  • Lipoprotein Lipase/LPL Monoclonal antibody specifically detects Lipoprotein Lipase/LPL in Human samples. (
  • There are currently no images for Lipoprotein Lipase/LPL Antibody Pair (H00004023-PW1). (
  • This investigation considers the regulation of LPL by lipoproteins and LVPs, and their roles in the LPL-mediated anti-HCV function. (
  • Regulation of Lipolysis and Lipoprotein Lipase after Weight Loss in. (
  • The Lipoprotein Lipase ( LPL ) Activity Assay Kit is a simple, fluorometric assay that quantitatively measures LPL activity in plasma, serum, and lysates in a 96-well microtiter plate format. (
  • 5. We conclude that genetic variants at the lipoprotein lipase locus occur commonly in subjects with this syndrome (four out of 18 subjects with probably functional mutants) and may affect the individual's response to obesity and diabetes mellitus for the development of lipaemia. (
  • R. J. Brown and D. J. Rader, "Lipases as modulators of atherosclerosis in murine models," Current Drug Targets , vol. 8, no. 12, pp. 1307-1319, 2007. (
  • Lipoprotein lipase for treating Atherosclerosis. (
  • Atherosclerosis is a disease process due to increased fat level in blood called as lipoproteins resulting deposition of these fat in the wall of the blood vessels causing narrowing/obstruction of the lumen of the blood vessels, as a result of which blood flow is compromised to the various organs of the body. (
  • It is concluded that plasma glycerides are hydrolyzed by lipoprotein lipase in capillary endothelial cells and in the subendothelial space of adipose tissue and that glycerides across the endothelial cells within a membrane-bounded system. (
  • Addition of apoC-III reduced the initial rate of hydrolysis by LPL, but the inhibition became less prominent with time when the lipoproteins were triglyceride poor. (
  • The inhibition of lipoprotein lipase increased as the concentration of the extracts increased. (
  • Zheng, al : Lipoprotein lipase bound to apoB lipoproteins accelerates clearance of postprandial lipoproteins in humans. (
  • Genest J, Libby P. Lipoprotein disorders and cardiovascular disease. (
  • Skeletal muscle lipoprotein lipase activity in CON, EX-DEF and EX-BAL. (
  • LPL functions as a homodimer, and has the dual functions of triglyceride hydrolase and ligand/bridging factor for receptor-mediated lipoprotein uptake. (
  • Thus, lipoprotein lipase expressed on the surface of cardiomyocytes can increase lipid uptake and produce cardiomyopathy. (
  • Lipoprotein lipase (LPL), the primary enzyme responsible for tissue uptake of triglyceride fatty acids, may strongly influence both maternal milk fat secretion and pup blubber deposition. (
  • Peterson, al: Human lipoprotein lipase: relationship of activity, heparin affinity, and conformation as studied with monoclonal antibodies. (
  • The extent and duration of this postprandial response is regulated by lipoprotein lipase (LPL). (
  • Locates to the plasma membrane of microvilli of hepatocytes with triacyl-glycerol-rich lipoproteins (TRL). (
  • Hearts, but not postheparin plasma, of these mice contained human lipoprotein lipase activity. (
  • 1. Intravenous injection of heparin into the trout resulted in the appearance in the plasma of a lipase with the properties of lipoprotein lipase. (
  • In vitro studies were performed by adding purified hepatic lipase to the patient's plasma. (
  • Extracts of intact adipose tissue separated into two major lipoprotein lipase activity peaks, designated "a" and "b", the "a" fraction representing about 30 (fasted rats) to 50% (fed rats) of the total enzyme activity. (
  • Purified human and bovine recombinant Lipoprotein lipase. (