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Lipoprotein LipaseLipaseLipoproteinsLipoproteins, LDLLipoproteins, VLDLLipoproteins, HDLHyperlipoproteinemia Type ITriglyceridesApolipoprotein C-IILipoprotein(a)ChylomicronsTrioleinHeparinApolipoproteins CApolipoproteinsReceptors, LipoproteinLipolysisAdipose TissueCholesterolLipidsHypertriglyceridemiaApolipoproteins BReceptors, LDLCholesterol, HDLLipoproteins, IDLLipoprotein Lipase ActivatorsLiverApolipoproteins ELipid MetabolismLipoproteins, HDL2Lipoproteins, HDL3Cholesterol EstersHyperlipoproteinemiasSterol EsteraseAngiopoietinsLow Density Lipoprotein Receptor-Related Protein-1Cholesterol, LDLMonoacylglycerol LipasesHyperlipidemiasApolipoprotein C-IIIApolipoproteins AMilkFatty Acids, NonesterifiedCholesterol, VLDLDietary FatsApolipoprotein B-100Heparin LyaseFatty AcidsKineticsFastingArteriosclerosisHyperlipoproteinemia Type IVMolecular Sequence DataEmulsionsHyperlipidemia, Familial CombinedApolipoprotein A-IIFat Emulsions, IntravenousHydrolysisCells, CulturedRNA, MessengerApolipoprotein B-48CattleCholesterol Ester Transfer ProteinsMacrophagesColipasesUltracentrifugationInsulinHypercholesterolemiaPhospholipidsCarrier ProteinsBase SequenceAdipocytesAmino Acid SequenceLipid MobilizationHyperlipoproteinemia Type IIIPhosphatidylcholine-Sterol O-AcyltransferaseCholesterol, DietaryMyocardiumHyperlipoproteinemia Type VRats, Inbred StrainsLymphEsterificationPolysaccharide-LyasesHyperlipoproteinemia Type IIHypolipidemic AgentsPostprandial PeriodProtein BindingHeterozygoteApolipoprotein E2Adipose Tissue, BrownOleic AcidParticle SizeBody WeightMutationTime FactorsElectrophoresis, Polyacrylamide GelGlyceridesOleic AcidsChromatography, AffinityBiological TransportLDL-Receptor Related Protein-Associated ProteinPancreasDeoxyribonuclease HindIIICricetinaeFoam CellsHomozygoteOxidation-ReductionCell LineAtherosclerosisHeparan Sulfate ProteoglycansBinding SitesCarboxylic Ester HydrolasesMice, KnockoutBlood GlucoseApoproteinsChromatography, Agarosealpha-MacroglobulinsScavenger Receptors, Class BHypolipoproteinemiasPlant OilsProtaminesHeparitin SulfateCHO CellsAntigens, CD36Receptors, ImmunologicGene Expression Regulation, EnzymologicMolecular WeightApolipoprotein C-IEsterasesSodium ChlorideMice, Inbred C57BLRabbitsObesityIndolizinesGlycoproteinsGenotypeGlycerolReference ValuesAortaPerfusionApolipoprotein E3Gene ExpressionEnzyme ActivationReceptors, ScavengerSepharoseMice, TransgenicRecombinant ProteinsStructure-Activity RelationshipDiet, AtherogenicRhizopusPhosphatidylcholinesApoprotein(a)DyslipidemiasLactonesBlotting, NorthernSulfur OxidesChromatography, GelPhospholipid Transfer ProteinsCoronary DiseaseLDL-Receptor Related ProteinsSterol O-AcyltransferaseFoodLipid Metabolism, Inborn ErrorsGeotrichumStarvationIodine RadioisotopesTransfectionHydroxymethylglutaryl CoA ReductasesMuscle, SkeletalElectrophoresis, Agar GelInsulin ResistanceGene Expression RegulationRats, Sprague-DawleyEatingRisk Factors
Lipoprotein Lipase: An enzyme of the hydrolase class that catalyzes the reaction of triacylglycerol and water to yield diacylglycerol and a fatty acid anion. The enzyme hydrolyzes triacylglycerols in chylomicrons, very-low-density lipoproteins, low-density lipoproteins, and diacylglycerols. It occurs on capillary endothelial surfaces, especially in mammary, muscle, and adipose tissue. Genetic deficiency of the enzyme causes familial hyperlipoproteinemia Type I. (Dorland, 27th ed) EC 3.1.1.34.Lipase: An enzyme of the hydrolase class that catalyzes the reaction of triacylglycerol and water to yield diacylglycerol and a fatty acid anion. It is produced by glands on the tongue and by the pancreas and initiates the digestion of dietary fats. (From Dorland, 27th ed) EC 3.1.1.3.Lipoproteins: 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.Lipoproteins, LDL: 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.Lipoproteins, VLDL: 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.Lipoproteins, HDL: 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.Hyperlipoproteinemia Type I: 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.TriglyceridesApolipoprotein C-II: 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.Lipoprotein(a): 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.Chylomicrons: 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.Triolein: (Z)-9-Octadecenoic acid 1,2,3-propanetriyl ester.Heparin: 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.Apolipoproteins C: 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.Apolipoproteins: 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.Receptors, Lipoprotein: 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.Lipolysis: 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.Adipose Tissue: 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.Cholesterol: The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils.Lipids: 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)Hypertriglyceridemia: A condition of elevated levels of TRIGLYCERIDES in the blood.Apolipoproteins B: 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, LDL: 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, HDL: Cholesterol which is contained in or bound to high-density lipoproteins (HDL), including CHOLESTEROL ESTERS and free cholesterol.Lipoproteins, IDL: 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.Lipoprotein Lipase Activators: 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.Liver: A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.Apolipoproteins E: 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.Lipid Metabolism: Physiological processes in biosynthesis (anabolism) and degradation (catabolism) of LIPIDS.Lipoproteins, HDL2: Low-density subclass of the high-density lipoproteins, with particle sizes between 8 to 13 nm.Lipoproteins, HDL3: 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.Cholesterol Esters: 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.Hyperlipoproteinemias: 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.Sterol Esterase: An enzyme that catalyzes the hydrolysis of CHOLESTEROL ESTERS and some other sterol esters, to liberate cholesterol plus a fatty acid anion.Angiopoietins: A family of structurally-related angiogenic proteins of approximately 70 kDa in size. They have high specificity for members of the TIE RECEPTOR FAMILY.Low Density Lipoprotein Receptor-Related Protein-1: A LDL-receptor related protein involved in clearance of chylomicron remnants and of activated ALPHA-MACROGLOBULINS from plasma.Cholesterol, LDL: Cholesterol which is contained in or bound to low density lipoproteins (LDL), including CHOLESTEROL ESTERS and free cholesterol.Monoacylglycerol Lipases: An enzyme that catalyzes the hydrolysis of glycerol monoesters of long-chain fatty acids EC 3.1.1.23.Hyperlipidemias: Conditions with excess LIPIDS in the blood.Apolipoprotein C-III: 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).Apolipoproteins A: 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.Milk: The white liquid secreted by the mammary glands. It contains proteins, sugar, lipids, vitamins, and minerals.Fatty Acids, Nonesterified: FATTY ACIDS found in the plasma that are complexed with SERUM ALBUMIN for transport. These fatty acids are not in glycerol ester form.Cholesterol, VLDL: 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.Dietary Fats: 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.Apolipoprotein B-100: 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.Heparin Lyase: 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 4.2.2.7.Fatty Acids: 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)Kinetics: The rate dynamics in chemical or physical systems.Fasting: Abstaining from all food.Arteriosclerosis: 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.Hyperlipoproteinemia Type IV: 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.Molecular Sequence Data: 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.Emulsions: 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.Hyperlipidemia, Familial Combined: 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.Apolipoprotein A-II: 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.Fat Emulsions, Intravenous: Emulsions of fats or lipids used primarily in parenteral feeding.Hydrolysis: The process of cleaving a chemical compound by the addition of a molecule of water.Cells, Cultured: 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, Messenger: 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.Apolipoprotein B-48: 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.Cattle: 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.Cholesterol Ester Transfer Proteins: Proteins that bind to and transfer CHOLESTEROL ESTERS between LIPOPROTEINS such as LOW-DENSITY LIPOPROTEINS and HIGH-DENSITY LIPOPROTEINS.Macrophages: 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.)Colipases: 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.Ultracentrifugation: 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)Insulin: 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).Hypercholesterolemia: 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.Phospholipids: 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.Carrier Proteins: Transport proteins that carry specific substances in the blood or across cell membranes.Base Sequence: The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.Adipocytes: 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.Amino Acid Sequence: 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.Lipid Mobilization: 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.Hyperlipoproteinemia Type III: 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.Phosphatidylcholine-Sterol O-Acyltransferase: An enzyme secreted from the liver into the plasma of many mammalian species. It catalyzes the esterification of the hydroxyl group of lipoprotein cholesterol by the transfer of a fatty acid from the C-2 position of lecithin. In familial lecithin:cholesterol acyltransferase deficiency disease, the absence of the enzyme results in an excess of unesterified cholesterol in plasma. EC 2.3.1.43.Cholesterol, Dietary: Cholesterol present in food, especially in animal products.Myocardium: 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.Hyperlipoproteinemia Type V: 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 .Rats, Inbred Strains: 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.Lymph: The interstitial fluid that is in the LYMPHATIC SYSTEM.Esterification: 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.Polysaccharide-Lyases: 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.Hyperlipoproteinemia Type II: 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).Hypolipidemic Agents: Substances that lower the levels of certain LIPIDS in the BLOOD. They are used to treat HYPERLIPIDEMIAS.Postprandial Period: The time frame after a meal or FOOD INTAKE.Protein Binding: 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.Heterozygote: An individual having different alleles at one or more loci regarding a specific character.Apolipoprotein E2: 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.Adipose Tissue, Brown: 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.Oleic Acid: 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)Particle Size: Relating to the size of solids.Body Weight: The mass or quantity of heaviness of an individual. It is expressed by units of pounds or kilograms.Mutation: 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.Time Factors: Elements of limited time intervals, contributing to particular results or situations.Electrophoresis, Polyacrylamide Gel: Electrophoresis in which a polyacrylamide gel is used as the diffusion medium.Glycerides: GLYCEROL esterified with FATTY ACIDS.Oleic Acids: A group of fatty acids that contain 18 carbon atoms and a double bond at the omega 9 carbon.Chromatography, Affinity: 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)Biological Transport: 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.LDL-Receptor Related Protein-Associated Protein: 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.Pancreas: 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.Deoxyribonuclease HindIII: One of the Type II site-specific deoxyribonucleases (EC 3.1.21.4). 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.-.Cricetinae: A subfamily in the family MURIDAE, comprising the hamsters. Four of the more common genera are Cricetus, CRICETULUS; MESOCRICETUS; and PHODOPUS.Foam Cells: Lipid-laden macrophages originating from monocytes or from smooth muscle cells.Homozygote: An individual in which both alleles at a given locus are identical.Oxidation-Reduction: 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).Cell Line: Established cell cultures that have the potential to propagate indefinitely.Atherosclerosis: A thickening and loss of elasticity of the walls of ARTERIES that occurs with formation of ATHEROSCLEROTIC PLAQUES within the ARTERIAL INTIMA.Heparan Sulfate Proteoglycans: 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)Binding Sites: The parts of a macromolecule that directly participate in its specific combination with another molecule.Carboxylic Ester Hydrolases: Enzymes which catalyze the hydrolysis of carboxylic acid esters with the formation of an alcohol and a carboxylic acid anion.Mice, Knockout: 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.Blood Glucose: Glucose in blood.Apoproteins: The protein components of a number of complexes, such as enzymes (APOENZYMES), ferritin (APOFERRITINS), or lipoproteins (APOLIPOPROTEINS).Chromatography, Agarose: 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.alpha-Macroglobulins: 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.Scavenger Receptors, Class B: A family of scavenger receptors that are predominately localized to CAVEOLAE of the PLASMA MEMBRANE and bind HIGH DENSITY LIPOPROTEINS.Hypolipoproteinemias: 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).Plant Oils: Oils derived from plants or plant products.Protamines: 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)Heparitin Sulfate: A heteropolysaccharide that is similar in structure to HEPARIN. It accumulates in individuals with MUCOPOLYSACCHARIDOSIS.CHO Cells: 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.Antigens, CD36: 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.Receptors, Immunologic: 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.Gene Expression Regulation, Enzymologic: Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in enzyme synthesis.Molecular Weight: The sum of the weight of all the atoms in a molecule.Apolipoprotein C-I: 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.EsterasesSodium Chloride: A ubiquitous sodium salt that is commonly used to season food.Mice, Inbred C57BLRabbits: 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.Obesity: 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).IndolizinesGlycoproteins: Conjugated protein-carbohydrate compounds including mucins, mucoid, and amyloid glycoproteins.Genotype: The genetic constitution of the individual, comprising the ALLELES present at each GENETIC LOCUS.Glycerol: 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.Reference Values: 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.Aorta: The main trunk of the systemic arteries.Perfusion: Treatment process involving the injection of fluid into an organ or tissue.Apolipoprotein E3: 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.Gene Expression: The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.Enzyme Activation: 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.Receptors, Scavenger: 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.SepharoseMice, Transgenic: Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.Recombinant Proteins: Proteins prepared by recombinant DNA technology.Structure-Activity Relationship: 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.Diet, Atherogenic: A diet that contributes to the development and acceleration of ATHEROGENESIS.Rhizopus: 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.Phosphatidylcholines: 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.Apoprotein(a): 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.Dyslipidemias: 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.Lactones: Cyclic esters of hydroxy carboxylic acids, containing a 1-oxacycloalkan-2-one structure. Large cyclic lactones of over a dozen atoms are MACROLIDES.Blotting, Northern: 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.Sulfur Oxides: Inorganic oxides of sulfur.Chromatography, Gel: Chromatography on non-ionic gels without regard to the mechanism of solute discrimination.Phospholipid Transfer Proteins: 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.Coronary Disease: 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.LDL-Receptor Related Proteins: A family of proteins that share sequence similarity with the low density lipoprotein receptor (RECEPTORS, LDL).Sterol O-Acyltransferase: An enzyme that catalyzes the formation of cholesterol esters by the direct transfer of the fatty acid group from a fatty acyl CoA derivative. This enzyme has been found in the adrenal gland, gonads, liver, intestinal mucosa, and aorta of many mammalian species. EC 2.3.1.26.Food: Any substances taken in by the body that provide nourishment.Lipid Metabolism, Inborn Errors: Errors in the metabolism of LIPIDS resulting from inborn genetic MUTATIONS that are heritable.Geotrichum: A mitosporic Saccharomycetales fungal genus, various species of which have been isolated from pulmonary lesions. Teleomorphs include Dipodascus and Galactomyces.Starvation: Lengthy and continuous deprivation of food. (Stedman, 25th ed)Iodine Radioisotopes: Unstable isotopes of iodine that decay or disintegrate emitting radiation. I atoms with atomic weights 117-139, except I 127, are radioactive iodine isotopes.Transfection: 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.Hydroxymethylglutaryl CoA Reductases: Enzymes that catalyze the reversible reduction of alpha-carboxyl group of 3-hydroxy-3-methylglutaryl-coenzyme A to yield MEVALONIC ACID.Muscle, Skeletal: 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, Agar Gel: Electrophoresis in which agar or agarose gel is used as the diffusion medium.Insulin Resistance: 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.Gene Expression Regulation: 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.Rats, Sprague-Dawley: 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.Eating: The consumption of edible substances.Risk Factors: 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)

Association of Backfat Thickness with Postheparin Lipoprotein Lipase Activity and Very Low Density Lipoprotein-Subfractions in...Association of Backfat Thickness with Postheparin Lipoprotein Lipase Activity and Very Low Density Lipoprotein-Subfractions in...
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 ...
Inhibition of lipoprotein lipase activity by high density lipoprotein & apolipoproteins C, E & A in rhesus monkeys. - Semantic...Inhibition of lipoprotein lipase activity by high density lipoprotein & apolipoproteins C, E & A in rhesus monkeys. - Semantic...
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...Effects of a Six Month Training Program on Serum Lipids, Glucose, Insulin and Adipose Tissue Lipoprotein Lipase in Young...
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 ...
Lipoprotein Lipase Mass and Activity in Plasma and Their Increase After Heparin Are Separate Parameters With Different...Lipoprotein Lipase Mass and Activity in Plasma and Their Increase After Heparin Are Separate Parameters With Different...
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 ...
Further Observations on the Activation and Inhibition of Lipoprotein Lipase by Apolipoproteins | Circulation ResearchFurther Observations on the Activation and Inhibition of Lipoprotein Lipase by Apolipoproteins | Circulation Research
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 ...
Clearing-factor lipase in adipose tissue. Distinction of different states of the enzyme and the possible role of the fat cell...Clearing-factor lipase in adipose tissue. Distinction of different states of the enzyme and the possible role of the fat cell...
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 ...
Adenovirus-mediated rescue of lipoprotein lipase-deficient mice. Lipolysis of triglyceride-rich lipoproteins is essential for...Adenovirus-mediated rescue of lipoprotein lipase-deficient mice. Lipolysis of triglyceride-rich lipoproteins is essential for...
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 - ...
Lipoprotein Lipase Expression in Chronic Lymphocytic Leukemia - Full Text View - ClinicalTrials.govLipoprotein Lipase Expression in Chronic Lymphocytic Leukemia - Full Text View - ClinicalTrials.gov
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 ...
Differential effects of lipoprotein lipase on tumor necrosis factor-α and interferon-γ-mediated gene expression in human...Differential effects of lipoprotein lipase on tumor necrosis factor-α and interferon-γ-mediated gene expression in human...
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 ...
JCI - Lipoprotein lipase (LpL) on the surface of cardiomyocytes increases lipid uptake and produces a cardiomyopathyJCI - Lipoprotein lipase (LpL) on the surface of cardiomyocytes increases lipid uptake and produces a cardiomyopathy
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 ...
A frequently occurring mutation in the lipoprotein lipase gene (Asn291Ser) results in altered postprandial chylomicron...A frequently occurring mutation in the lipoprotein lipase gene (Asn291Ser) results in altered postprandial chylomicron...
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% ...
Lipoprotein particle distribution and skeletal muscle lipoprotein lipase activity after acute exercise | Lipids in Health and...Lipoprotein particle distribution and skeletal muscle lipoprotein lipase activity after acute exercise | Lipids in Health and...
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
Maternal expression of functional lipoprotein lipase and effects on body fat mass and body condition scores of mature cats with...Maternal expression of functional lipoprotein lipase and effects on body fat mass and body condition scores of mature cats with...
TY - JOUR. T1 - Maternal expression of functional lipoprotein lipase and effects on body fat mass and body condition scores of mature cats with lipoprotein lipase deficiency. AU - Backus, Robert C.. AU - Ginzinger, David G.. AU - Ashbourne Excoffon, Katherine J.D.. AU - Clee, Susanne M.. AU - Hayden, Michael R.. AU - Eckel, Robert H.. AU - Hickman, M. Anne. AU - Rogers, Quinton. PY - 2001/1/1. Y1 - 2001/1/1. N2 - Objective - To assess effects of deficiency of lipoprotein lipase (LPL) on body condition scores and lean and fat body masses of adult cats. Animals - 12 cats without LPL mutations and 23 cats that were heterozygous or homozygous carriers of the Gly412Arg LPL mutation. Procedure - Lean and fat body masses were estimated by use of body condition scores and change in enrichment of serum after IV administration of deuterium oxide. Mass spectroscopy and infrared absorbance methods were used to determine deuterium enrichment. Results - Fat body mass (mean ± SD; 0.2 ± 0.1 kg) and percentage ...
Lipoprotein lipase gene expression: physiological regulators at the transcriptional and post-transcriptional level. - PubMed -...Lipoprotein lipase gene expression: physiological regulators at the transcriptional and post-transcriptional level. - PubMed -...
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Efficacy and Safety of Human Lipoprotein Lipase (LPL)[S447X] Expressed by an Adeno-Associated Viral Vector in LPL-deficient...Efficacy and Safety of Human Lipoprotein Lipase (LPL)[S447X] Expressed by an Adeno-Associated Viral Vector in LPL-deficient...
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 ...
The characterization of lipoprotein lipase isolated from the post-heparin plasma of the rainbow trout, Salmo gairdneri...The characterization of lipoprotein lipase isolated from the post-heparin plasma of the rainbow trout, Salmo gairdneri...
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. ...
Free fatty acids: the possible regulators of muscle lipoprotein lipase | Biochemical Society TransactionsFree fatty acids: the possible regulators of muscle lipoprotein lipase | Biochemical Society Transactions
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Hepatic regeneration induces changes in lipoprotein lipase activity in several tissues and its re-expression in the liver |...Hepatic regeneration induces changes in lipoprotein lipase activity in several tissues and its re-expression in the liver |...
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 ...
Intravascular Free Tissue Factor Pathway Inhibitor Is Inversely Correlated With HDL Cholesterol and Postheparin Lipoprotein...Intravascular Free Tissue Factor Pathway Inhibitor Is Inversely Correlated With HDL Cholesterol and Postheparin Lipoprotein...
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 ...
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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 ...
Feeding studies of dietary diacylglycerol oil in normal and lipoprotein lipase-deficient catsFeeding studies of dietary diacylglycerol oil in normal and lipoprotein lipase-deficient cats
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, ...
Reduced kidney lipoprotein lipase and renal tubule triglyceride accumulation in cisplatin-mediated acute kidney injuryReduced kidney lipoprotein lipase and renal tubule triglyceride accumulation in cisplatin-mediated acute kidney injury
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 ...
Hippocampal lipoprotein lipase regulates energy balance in rodents<...Hippocampal lipoprotein lipase regulates energy balance in rodents<...
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 ...
Lipoprotein Lipase Important for Fat Burning | androseriesLipoprotein Lipase Important for Fat Burning | androseries
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…
Influence of PvuII (Intron 6) polymorphism of the lipoprotein lipase gene on cord plasma lipid and apolipoprotein levels in...Influence of PvuII (Intron 6) polymorphism of the lipoprotein lipase gene on cord plasma lipid and apolipoprotein levels in...
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 ...
Adipose Tissue, Brown | The Chopra LibraryAdipose Tissue, Brown | The Chopra Library
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 | Open-iRelative LPL expression of Group C compared to B. Fold | Open-i
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
Advice | Josh Bezoni | FitnessAdvice | Josh Bezoni | Fitness
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 ...
CiNii 論文 - Chylomicronemia Caused by Lipoprotein Lipase Gene Mutation Related to a Hyper...CiNii 論文 - Chylomicronemia Caused by Lipoprotein Lipase Gene Mutation Related to a Hyper...
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). ...
Lpl ELISA Kit| Rat Lipoprotein lipase ELISA Kit [EF017174] - $566.00 : Plasmid,ELISA Kits,antibodies,strains, - Nova lifetech...Lpl ELISA Kit| Rat Lipoprotein lipase ELISA Kit [EF017174] - $566.00 : Plasmid,ELISA Kits,antibodies,strains, - Nova lifetech...
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
Association between lipoprotein lipase (LPL) gene and blood lipids: A common variant for a common trait? - Morabia - 2003 -...Association between lipoprotein lipase (LPL) gene and blood lipids: A common variant for a common trait? - Morabia - 2003 -...
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. ...
A Common Mutation in the Lipoprotein Lipase Gene (N291S) Alters the Lipoprotein Phenotype and Risk for Cardiovascular Disease...A Common Mutation in the Lipoprotein Lipase Gene (N291S) Alters the Lipoprotein Phenotype and Risk for Cardiovascular Disease...
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, ...
Lipoprotein Lipase/LPL Antibody Pair (H00004023-PW1): Novus BiologicalsLipoprotein Lipase/LPL Antibody Pair (H00004023-PW1): Novus Biologicals
Lipoprotein Lipase/LPL Antibody Pair. Matched antibody pairs validated for ELISA or IP-Western Blot. Backed by our 100% Guarantee.
Lipoprotein Lipase & Insulin | Healthy Eating | SF GateLipoprotein Lipase & Insulin | Healthy Eating | SF Gate
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.
重组人Lipoprotein lipase (ab115500)| Abcam中国重组人Lipoprotein lipase (ab115500)| Abcam中国
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Suchergebnis: Picard, F.Suchergebnis: Picard, F.
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 ...
Nerdy FCS | Nerdy NateNerdy FCS | Nerdy Nate
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 ...
THE LIPOPROTEIN LIPASE S447X GENETIC POLYMORPHISM RELATES TO POLYUNSATURATED FATTY ACID IN PATIENTS WITH CORONARY ARTERY DISEASETHE LIPOPROTEIN LIPASE S447X GENETIC POLYMORPHISM RELATES TO POLYUNSATURATED FATTY ACID IN PATIENTS WITH CORONARY ARTERY DISEASE
عنوان کنگره : 2nd international and 14th iranian nutrition congress in tehran (inc-ir2016), ایران,tehran,1395/06/14-1395/06/17 ...
Design, synthesis and evaluation of photoaffinity chemical probe to study Lipoprotein lipase - small molecule interactionsDesign, synthesis and evaluation of photoaffinity chemical probe to study Lipoprotein lipase - small molecule interactions
The number of downloads is the sum of all downloads of full texts. It may include eg previous versions that are now no longer ...
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Ovarian cancer is a disease associated with a high mortality mainly because it currently escapes detection at early stages. Identification of an effective biomarker for early detection would improve survival. This study reports statistically significant differences in LPL levels between preoperative samples of ovarian cancer patients and those of healthy controls. The study also confirms that statistically significant elevations in LPL levels are present in patients with early-stage disease. Thus, the findings support the utility of LPL, especially LPA, as biomarkers for early detection of ovarian cancer. The study is the first to report significant postoperative changes in specific LPL levels. Further study is needed to determine whether some LPLs may return to baseline after successful treatment and/or have utility as biomarkers of recurrence. The study also contributes data toward determination of the best combinations of markers and cutoff values for clinical use.. Although our conclusions ...
JoVE Author Search: Lafond JJoVE Author Search: Lafond J
Human, Time, Pregnancy, Fetal Growth, Growth, mRNA, Trophoblasts, Acids, Affects, Apolipoprotein, Blood, Body Mass Index, Cholesterol, Cord Blood, Diseases, Fatty Acids, Fetus, Lipase, Lipoprotein, Lipoprotein Lipase
Dynein mutation reverts the systemic and molecular alte | Open-iDynein mutation reverts the systemic and molecular alte | Open-i
Dynein mutation reverts the systemic and molecular alterations associated with energy deficit in SOD1(G93A) mice. A- mRNA levels of lipoprotein lipase (LPL) in
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The Increase Activity of Lipoprotein Lipase (LPL) Enzyme and Histophatological Changes of Liver of Hypercholesterolemic Rat (Rattus norvegicus) Induced by Ethanolic Extract of Ant Plant (Myrmecodia sp.) Journal Article published 15 Mar 2016 in Jurnal Kedokteran Hewan - Indonesian Journal of Veterinary Sciences volume 10 issue 1 Authors: Roslizawaty R, Rusli R, Nazaruddin N, Syafruddin S, Indahlia Syahfitri Bangun, Jumaidar J. ...
Rapid Fat Loss With Carb RotatingRapid Fat Loss With Carb Rotating
Do you want a much more effective and realistic method of rapid fat loss? Try a much safer and healthier approach to quick weight loss called Carb Rotation. There are two general approaches to Carb Rotating. The first approach is to follow a "no, no, no, high carb" program. This means no carbohydrates for the first three days at all and then you eat a "high" amount of carbohydrates for the fourth day. The fifth day you are back to eating "no carbs" again.. This plan can be effective, but you have to be very strict. It is an aggressive approach that may trigger your starvation response. Yes, the very same starvation response which causes elevation of a hormone called lipoprotein lipase. When this hormone becomes elevated your metabolism begins to slow down.. And since that is the last thing anyone who is trying to get rid of unwanted pounds wants, it is not the approach I recommend. Additionally, when people deprive themselves completely of "carbs" for three days they have a tendency to: 1) Go ...
The Mind-full Motivator, LLC: Moving More and Sitting Less is Critical for HealthThe Mind-full Motivator, LLC: Moving More and Sitting Less is Critical for Health
P.T. Katzmarzyk studied over 17,000 Canadians and found that sitting is an independent risk factor of exercise. As the amount of sitting increased, so did the risk of cancer, heart disease, metabolic syndrome, and overall mortality from all causes. For every 2 hours of sitting, the risk for developing diabetes increases by 7%, along with heart disease and depression. Sitting still for long periods of time tells the muscle fibers to chill out, metabolic rate goes down, and fat burning enzymes such as lipoprotein lipase start switching off. Sitting all day can reduce fat burning by 50%. So, even if you are exercising 5 days each week, if you are sitting still the rest of the time, these risk factors still creep up. Ouch ...
6 Warning Signs That Indicates A Heart Attack Is Coming Your Way - ArtikuloUno6 Warning Signs That Indicates A Heart Attack Is Coming Your Way - ArtikuloUno
Research claimed that people who watch TV or work on a computer for four or more hours a day increase their risk of an event associated with cardiovascular disease, like a heart attack. Long periods of sitting deplete the bodys supply of lipoprotein lipase, an enzyme that breaks down fat and prevents clogged arteries ...
Inactivation of lipoprotein lipase occurs on the surface of THP-1 macrophages where oligomers of angiopoietin-like protein 4...Inactivation of lipoprotein lipase occurs on the surface of THP-1 macrophages where oligomers of angiopoietin-like protein 4...
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 ...
Adipose tissue fatty acid composition in humans with lipoprotein lipase deficiency<...Adipose tissue fatty acid composition in humans with lipoprotein lipase deficiency<...
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 ...
LPL | SelfDecode | Genome AnalysisLPL | SelfDecode | Genome Analysis
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 ...
Lipoprotein lipase deficiency - WikipediaLipoprotein lipase deficiency - Wikipedia
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 ...
Triglyceride-induced diabetes associated with familial lipoprotein lipase deficiency. | DiabetesTriglyceride-induced diabetes associated with familial lipoprotein lipase deficiency. | Diabetes
Raised plasma triglycerides (TGs) and nonesterified fatty acid (NEFA) concentrations are thought to play a role in the pathogenesis of insulin-resistant diabetes. We report on two sisters with extreme hypertriglyceridemia and overt diabetes, in whom surgical normalization of TGs cured the diabetes. 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. In addition, GC-clamped polymerase chain reaction-amplified DNA from the promoter region and the 10 coding LPL gene exons were screened for nucleotide substitution. Two silent mutations were found in the fathers exon 4 (Glu118 Glu) and in the mothers exon 8 (Thr361 Thr), while a nonsense mutation (Ser447 ...
Association of lipoprotein lipase gene with coronary heart disease in Sudanese populationAssociation of lipoprotein lipase gene with coronary heart disease in Sudanese population
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 ...
北京大学医学部机构知识库(IR@PKUHSC): Comparative Analyses of Lipoprotein Lipase, Hepatic Lipase, and Endothelial Lipase, and Their Binding...北京大学医学部机构知识库([email protected]): Comparative Analyses of Lipoprotein Lipase, Hepatic Lipase, and Endothelial Lipase, and Their Binding...
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 ...
Differential effects of angiopoietin-like 4 in brain and muscle on regulation of lipoprotein lipase activityDifferential effects of angiopoietin-like 4 in brain and muscle on regulation of lipoprotein lipase activity
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 ...
Familial lipoprotein lipase inhibitor: Definition with Familial lipoprotein lipase inhibitor Pictures and PhotosFamilial lipoprotein lipase inhibitor: Definition with Familial lipoprotein lipase inhibitor Pictures and Photos
Definition of Familial lipoprotein lipase inhibitor with photos and pictures, translations, sample usage, and additional links for more information.
Association between skeletal muscle mass and serum concentrations of lipoprotein lipase, GPIHBP1, and hepatic triglyceride...Association between skeletal muscle mass and serum concentrations of lipoprotein lipase, GPIHBP1, and hepatic triglyceride...
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 - WikipediaLipoprotein lipase - Wikipedia
Lipoprotein lipase (LPL) (EC 3.1.1.34) 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 ...
The gut microbiota as an environmental factor that regulates fat storage | PNASThe gut microbiota as an environmental factor that regulates fat storage | PNAS
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 = ...
Plus itPlus it
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 ...
Volanesorsen Active Not Recruiting Phase 3 Trials for Lipoprotein Lipase Deficiency / Hyperlipoproteinemia Type 1 / Familial...Volanesorsen Active Not Recruiting Phase 3 Trials for Lipoprotein Lipase Deficiency / Hyperlipoproteinemia Type 1 / Familial...
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. ...
Recent Articles | Lipoprotein Lipase Deficiency, Genetics & Genomics And Ecology | The Scientist Magazine®| Page 34Recent Articles | Lipoprotein Lipase Deficiency, Genetics & Genomics And Ecology | The Scientist Magazine®| Page 34
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.. ...
Recent Articles | Lipoprotein Lipase Deficiency, Evolution And Microbiology | The Scientist Magazine®Recent Articles | Lipoprotein Lipase Deficiency, Evolution And Microbiology | The Scientist Magazine®
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. ...
List of OMIM disorder codesList of OMIM disorder codes
IbrolipimIbrolipim
Apolipoprotein C3Apolipoprotein C3
Omega-3 acid ethyl estersOmega-3 acid ethyl esters
GPIHBP1GPIHBP1
Omega-3 carboxylic acidsOmega-3 carboxylic acids
Ethyl eicosapentaenoic acidEthyl eicosapentaenoic acid
ChylomicronChylomicron
ExoenzymeExoenzyme
Sortilin 1Sortilin 1
Claire WeekesClaire Weekes
PlacentationPlacentation
LactealLacteal
Southern grass skinkSouthern grass skink
Carbonyl cyanide m-chlorophenyl hydrazoneCarbonyl cyanide m-chlorophenyl hydrazone
ANGPTL4ANGPTL4
Familial hypercholesterolemiaFamilial hypercholesterolemia
Alipogene tiparvovecAlipogene tiparvovec
Robert H. EckelRobert H. Eckel
David J. GaltonDavid J. Galton
POU2F1POU2F1
LRP2LRP2
Leukemia inhibitory factorLeukemia inhibitory factor
StarvationStarvation
Starvation responseStarvation response
Waist-hip ratioWaist-hip ratio
ANGPTL8ANGPTL8
Nephrotic syndromeNephrotic syndrome
ANGPTL3ANGPTL3
Medication-induced hyperlipoproteinemiaMedication-induced hyperlipoproteinemia
Apolipoprotein C2Apolipoprotein C2
Reverse cholesterol transportReverse cholesterol transport
TryptophanTryptophan
APOA4APOA4
FenofibrateFenofibrate
LRP1LRP1
ClofibrateClofibrate
LDL-receptor-related protein-associated proteinLDL-receptor-related protein-associated protein
Absorptive stateAbsorptive state
Apovitellenin-1Apovitellenin-1
4-Nonylphenylboronic acid4-Nonylphenylboronic acid
HyperlipidemiaHyperlipidemia
LDL receptorLDL receptor
APOA5APOA5
TriglycerideTriglyceride
Macular degenerationMacular degeneration
Adipose tissueAdipose tissue
HypertriglyceridemiaHypertriglyceridemia
SittingSitting
Asim DuttaroyAsim Duttaroy
Yerba mateYerba mate
Wolfgang PatschWolfgang Patsch
GlycocalyxGlycocalyx
List of enzymesList of enzymes
LPLLPL
Pentosan polysulfatePentosan polysulfate
Chromosome 8 (human)Chromosome 8 (human)
Liver X receptorLiver X receptor
ApolipoproteinApolipoprotein
Fatty acid metabolismFatty acid metabolism
List of MeSH codes (D08)List of MeSH codes (D08)
List of MeSH codes (C18)List of MeSH codes (C18)
List of MeSH codes (C16)List of MeSH codes (C16)
Neonatal jaundiceNeonatal jaundice
GlycosaminoglycanGlycosaminoglycan
List of EC numbers (EC 3)List of EC numbers (EC 3)
Standing deskStanding desk
Adeno-associated virusAdeno-associated virus
List of cutaneous conditionsList of cutaneous conditions
Serine hydrolaseSerine hydrolase
LipoproteinLipoprotein
LipaseLipase
Lipoprotein lipaseLipoprotein lipase
Hepatic lipaseHepatic lipase
Monoacylglycerol lipaseMonoacylglycerol lipase
Lipoprotein lipase deficiencyLipoprotein lipase deficiency
Pancreatic lipase familyPancreatic lipase family
Acid lipase diseaseAcid lipase disease
High-density lipoproteinHigh-density lipoprotein
Low-density lipoproteinLow-density lipoprotein
Intermediate-density lipoproteinIntermediate-density lipoprotein
Bile salt-dependent lipaseBile salt-dependent lipase
Very low-density lipoproteinVery low-density lipoprotein
List of biomoleculesList of biomolecules
RetinaRetina
SCARB1SCARB1
Angiostrongylus cantonensisAngiostrongylus cantonensis
Insulin, den frie encyklopædiInsulin, den frie encyklopædi
Apolipoprotein C2Apolipoprotein C2
Index of biochemistry articlesIndex of biochemistry articles
Lysosomal acid lipase deficiencyLysosomal acid lipase deficiency
Lecithin-cholesterol acyltransferaseLecithin-cholesterol acyltransferase
LipolysisLipolysis
Lysosomal acid lipase deficiencyLysosomal acid lipase deficiency
ProtamineProtamine
1-Lysophosphatidylcholine1-Lysophosphatidylcholine
Foam cellFoam cell
肥胖症 - 维基百科，自由的百科全书肥胖症 - 维基百科，自由的百科全书
Familial hypercholesterolemiaFamilial hypercholesterolemia
Human digestive systemHuman digestive system
APOA2APOA2
SecretionSecretion
MonoglycerideMonoglyceride
Hormone-sensitive lipaseHormone-sensitive lipase
Adipose tissueAdipose tissue
چربی‌های خون - ویکی‌پدیا، دانشنامهٔ آزادچربی‌های خون - ویکی‌پدیا، دانشنامهٔ آزاد
Liosta Bithmhóilíní - VicipéidLiosta Bithmhóilíní - Vicipéid
Glucose 6-phosphataseGlucose 6-phosphatase
VirotherapyVirotherapy
Waist-hip ratioWaist-hip ratio
LipidLipid
Phosphoserine phosphatasePhosphoserine phosphatase
Blood testBlood test
TriptofaanTriptofaan
LipolysisLipolysis
List of enzymesList of enzymes
Lipid, den frie encyklopædiLipid, den frie encyklopædi
Lipoproteína de alta densidade, a enciclopedia libreLipoproteína de alta densidade, a enciclopedia libre
Arachidonic acidArachidonic acid
PDE11PDE11
PLCG1PLCG1
Eosinophil-derived neurotoxinEosinophil-derived neurotoxin
Deoxyribonuclease IIDeoxyribonuclease II
Phosphodiesterase 2Phosphodiesterase 2
EnterocyteEnterocyte
Protein serine/threonine phosphataseProtein serine/threonine phosphatase
mTOR inhibitorsmTOR inhibitors
Restriction enzymeRestriction enzyme
Lipid signalingLipid signaling
HalobacteriumHalobacterium
PAFAH2PAFAH2
AbetalipoproteinemiaAbetalipoproteinemia
Nutritional genomicsNutritional genomics
Pirinixic acidPirinixic acid
Alpha-CyclodextrinAlpha-Cyclodextrin
EnterocyteEnterocyte
LipoxygenaseLipoxygenase
Lipid metabolismLipid metabolism
IDFPIDFP
AnatomyOrganismsDiseasesChemicals and DrugsAnalytical, Diagnostic and Therapeutic Techniques and EquipmentPsychiatry and PsychologyPhenomena and ProcessesTechnology, Industry, AgricultureInformation ScienceHealth Care
Lipoprotein LipaseLipaseLipoproteinsLipoproteins, LDLLipoproteins, VLDLLipoproteins, HDLHyperlipoproteinemia Type ITriglyceridesApolipoprotein C-IILipoprotein(a)ChylomicronsTrioleinHeparinApolipoproteins CApolipoproteinsReceptors, LipoproteinLipolysisAdipose TissueCholesterolLipidsHypertriglyceridemiaApolipoproteins BReceptors, LDLCholesterol, HDLLipoproteins, IDLLipoprotein Lipase ActivatorsLiverApolipoproteins ELipid MetabolismLipoproteins, HDL2Lipoproteins, HDL3Cholesterol EstersHyperlipoproteinemiasSterol EsteraseAngiopoietinsLow Density Lipoprotein Receptor-Related Protein-1Cholesterol, LDLMonoacylglycerol LipasesHyperlipidemiasApolipoprotein C-IIIApolipoproteins AMilkFatty Acids, NonesterifiedCholesterol, VLDLDietary FatsApolipoprotein B-100Heparin LyaseFatty AcidsKineticsFastingArteriosclerosisHyperlipoproteinemia Type IVMolecular Sequence DataEmulsionsHyperlipidemia, Familial CombinedApolipoprotein A-IIFat Emulsions, IntravenousHydrolysisCells, CulturedRNA, MessengerApolipoprotein B-48CattleCholesterol Ester Transfer ProteinsMacrophagesColipasesUltracentrifugationInsulinHypercholesterolemiaPhospholipidsCarrier ProteinsBase SequenceAdipocytesAmino Acid SequenceLipid MobilizationHyperlipoproteinemia Type IIIPhosphatidylcholine-Sterol O-AcyltransferaseCholesterol, DietaryMyocardiumHyperlipoproteinemia Type VRats, Inbred StrainsLymphEsterificationPolysaccharide-LyasesHyperlipoproteinemia Type IIHypolipidemic AgentsPostprandial PeriodProtein BindingHeterozygoteApolipoprotein E2Adipose Tissue, BrownOleic AcidParticle SizeBody WeightMutationTime FactorsElectrophoresis, Polyacrylamide GelGlyceridesOleic AcidsChromatography, AffinityBiological TransportLDL-Receptor Related Protein-Associated ProteinPancreasDeoxyribonuclease HindIIICricetinaeFoam CellsHomozygoteOxidation-ReductionCell LineAtherosclerosisHeparan Sulfate ProteoglycansBinding SitesCarboxylic Ester HydrolasesMice, KnockoutBlood GlucoseApoproteinsChromatography, Agarosealpha-MacroglobulinsScavenger Receptors, Class BHypolipoproteinemiasPlant OilsProtaminesHeparitin SulfateCHO CellsAntigens, CD36Receptors, ImmunologicGene Expression Regulation, EnzymologicMolecular WeightApolipoprotein C-IEsterasesSodium ChlorideMice, Inbred C57BLRabbitsObesityIndolizinesGlycoproteinsGenotypeGlycerolReference ValuesAortaPerfusionApolipoprotein E3Gene ExpressionEnzyme ActivationReceptors, ScavengerSepharoseMice, TransgenicRecombinant ProteinsStructure-Activity RelationshipDiet, AtherogenicRhizopusPhosphatidylcholinesApoprotein(a)DyslipidemiasLactonesBlotting, NorthernSulfur OxidesChromatography, GelPhospholipid Transfer ProteinsCoronary DiseaseLDL-Receptor Related ProteinsSterol O-AcyltransferaseFoodLipid Metabolism, Inborn ErrorsGeotrichumStarvationIodine RadioisotopesTransfectionHydroxymethylglutaryl CoA ReductasesMuscle, SkeletalElectrophoresis, Agar GelInsulin ResistanceGene Expression RegulationRats, Sprague-DawleyEatingRisk Factors
Search of: familial lipoprotein lipase deficiency - List Results - ClinicalTrials.govSearch of: 'familial lipoprotein lipase deficiency' - List Results - ClinicalTrials.gov
Lipoprotein Lipase Expression in Chronic Lymphocytic Leukemia - Full Text View - ClinicalTrials.govLipoprotein Lipase Expression in Chronic Lymphocytic Leukemia - Full Text View - ClinicalTrials.gov
Lipoprotein Lipase/LPL Antibody Pair (H00004023-PW1): Novus BiologicalsLipoprotein Lipase/LPL Antibody Pair (H00004023-PW1): Novus Biologicals
Lipoprotein Lipase & Insulin | Healthy Eating | SF GateLipoprotein Lipase & Insulin | Healthy Eating | SF Gate
Design, synthesis and evaluation of photoaffinity chemical probe to study Lipoprotein lipase - small molecule interactionsDesign, synthesis and evaluation of photoaffinity chemical probe to study Lipoprotein lipase - small molecule interactions
Association between lipoprotein lipase (LPL) gene and blood lipids: A common variant for a common trait? - Morabia - 2003 -...Association between lipoprotein lipase (LPL) gene and blood lipids: A common variant for a common trait? - Morabia - 2003 -...
Reduced kidney lipoprotein lipase and renal tubule triglyceride accumulation in cisplatin-mediated acute kidney injuryReduced kidney lipoprotein lipase and renal tubule triglyceride accumulation in cisplatin-mediated acute kidney injury
A Common Mutation in the Lipoprotein Lipase Gene (N291S) Alters the Lipoprotein Phenotype and Risk for Cardiovascular Disease...A Common Mutation in the Lipoprotein Lipase Gene (N291S) Alters the Lipoprotein Phenotype and Risk for Cardiovascular Disease...
CiNii 論文 - Chylomicronemia Caused by Lipoprotein Lipase Gene Mutation Related to a Hyper...CiNii 論文 - Chylomicronemia Caused by Lipoprotein Lipase Gene Mutation Related to a Hyper...
The heterogeneity of the lipoprotein lipase of rat epididymal adipose tissue | Biochemical JournalThe heterogeneity of the lipoprotein lipase of rat epididymal adipose tissue | Biochemical Journal
Further Observations on the Activation and Inhibition of Lipoprotein Lipase by Apolipoproteins | Circulation ResearchFurther Observations on the Activation and Inhibition of Lipoprotein Lipase by Apolipoproteins | Circulation Research
Intravascular Free Tissue Factor Pathway Inhibitor Is Inversely Correlated With HDL Cholesterol and Postheparin Lipoprotein...Intravascular Free Tissue Factor Pathway Inhibitor Is Inversely Correlated With HDL Cholesterol and Postheparin Lipoprotein...
Feeding studies of dietary diacylglycerol oil in normal and lipoprotein lipase-deficient catsFeeding studies of dietary diacylglycerol oil in normal and lipoprotein lipase-deficient cats
The characterization of lipoprotein lipase isolated from the post-heparin plasma of the rainbow trout, Salmo gairdneri...The characterization of lipoprotein lipase isolated from the post-heparin plasma of the rainbow trout, Salmo gairdneri...
Lipoprotein particle distribution and skeletal muscle lipoprotein lipase activity after acute exercise | Lipids in Health and...Lipoprotein particle distribution and skeletal muscle lipoprotein lipase activity after acute exercise | Lipids in Health and...
Maternal expression of functional lipoprotein lipase and effects on body fat mass and body condition scores of mature cats with...Maternal expression of functional lipoprotein lipase and effects on body fat mass and body condition scores of mature cats with...
Influence of PvuII (Intron 6) polymorphism of the lipoprotein lipase gene on cord plasma lipid and apolipoprotein levels in...Influence of PvuII (Intron 6) polymorphism of the lipoprotein lipase gene on cord plasma lipid and apolipoprotein levels in...
Lipoprotein Lipase Important for Fat Burning | androseriesLipoprotein Lipase Important for Fat Burning | androseries
重组人Lipoprotein lipase (ab115500)| Abcam中国重组人Lipoprotein lipase (ab115500)| Abcam中国
Hippocampal lipoprotein lipase regulates energy balance in rodents<...Hippocampal lipoprotein lipase regulates energy balance in rodents<...
JCI - Lipoprotein lipase (LpL) on the surface of cardiomyocytes increases lipid uptake and produces a cardiomyopathyJCI - Lipoprotein lipase (LpL) on the surface of cardiomyocytes increases lipid uptake and produces a cardiomyopathy
THE LIPOPROTEIN LIPASE S447X GENETIC POLYMORPHISM RELATES TO POLYUNSATURATED FATTY ACID IN PATIENTS WITH CORONARY ARTERY DISEASETHE LIPOPROTEIN LIPASE S447X GENETIC POLYMORPHISM RELATES TO POLYUNSATURATED FATTY ACID IN PATIENTS WITH CORONARY ARTERY DISEASE
Lpl ELISA Kit| Rat Lipoprotein lipase ELISA Kit [EF017174] - $566.00 : Plasmid,ELISA Kits,antibodies,strains, - Nova lifetech...Lpl ELISA Kit| Rat Lipoprotein lipase ELISA Kit [EF017174] - $566.00 : Plasmid,ELISA Kits,antibodies,strains, - Nova lifetech...
Association of Backfat Thickness with Postheparin Lipoprotein Lipase Activity and Very Low Density Lipoprotein-Subfractions in...Association of Backfat Thickness with Postheparin Lipoprotein Lipase Activity and Very Low Density Lipoprotein-Subfractions in...
Adenovirus-mediated rescue of lipoprotein lipase-deficient mice. Lipolysis of triglyceride-rich lipoproteins is essential for...Adenovirus-mediated rescue of lipoprotein lipase-deficient mice. Lipolysis of triglyceride-rich lipoproteins is essential for...
Effects of a Six Month Training Program on Serum Lipids, Glucose, Insulin and Adipose Tissue Lipoprotein Lipase in Young...Effects of a Six Month Training Program on Serum Lipids, Glucose, Insulin and Adipose Tissue Lipoprotein Lipase in Young...
A frequently occurring mutation in the lipoprotein lipase gene (Asn291Ser) results in altered postprandial chylomicron...A frequently occurring mutation in the lipoprotein lipase gene (Asn291Ser) results in altered postprandial chylomicron...
KEGG ENZYME: 3.1.1.71KEGG ENZYME: 3.1.1.71
Jana Klauer M.D. >> monthly...Jana Klauer M.D. >> monthly...
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6 Warning Signs That Indicates A Heart Attack Is Coming Your Way - ArtikuloUno6 Warning Signs That Indicates A Heart Attack Is Coming Your Way - ArtikuloUno
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Lipoprotein LipaseLipaseLipoproteinsLipoproteins, LDLLipoproteins, VLDLLipoproteins, HDLHyperlipoproteinemia Type ITriglyceridesApolipoprotein C-IILipoprotein(a)ChylomicronsTrioleinHeparinApolipoproteins CApolipoproteinsReceptors, LipoproteinLipolysisAdipose TissueCholesterolLipidsHypertriglyceridemiaApolipoproteins BReceptors, LDLCholesterol, HDLLipoproteins, IDLLipoprotein Lipase ActivatorsLiverApolipoproteins ELipid MetabolismLipoproteins, HDL2Lipoproteins, HDL3Cholesterol EstersHyperlipoproteinemiasSterol EsteraseAngiopoietinsLow Density Lipoprotein Receptor-Related Protein-1Cholesterol, LDLMonoacylglycerol LipasesHyperlipidemiasApolipoprotein C-IIIApolipoproteins AMilkFatty Acids, NonesterifiedCholesterol, VLDLDietary FatsApolipoprotein B-100Heparin LyaseFatty AcidsKineticsFastingArteriosclerosisHyperlipoproteinemia Type IVMolecular Sequence DataEmulsionsHyperlipidemia, Familial CombinedApolipoprotein A-IIFat Emulsions, IntravenousHydrolysisCells, CulturedRNA, MessengerApolipoprotein B-48CattleCholesterol Ester Transfer ProteinsMacrophagesColipasesUltracentrifugationInsulinHypercholesterolemiaPhospholipidsCarrier ProteinsBase SequenceAdipocytesAmino Acid SequenceLipid MobilizationHyperlipoproteinemia Type IIIPhosphatidylcholine-Sterol O-AcyltransferaseCholesterol, DietaryMyocardiumHyperlipoproteinemia Type VRats, Inbred StrainsLymphEsterificationPolysaccharide-LyasesHyperlipoproteinemia Type IIHypolipidemic AgentsPostprandial PeriodProtein BindingHeterozygoteApolipoprotein E2Adipose Tissue, BrownOleic AcidParticle SizeBody WeightMutationTime FactorsElectrophoresis, Polyacrylamide GelGlyceridesOleic AcidsChromatography, AffinityBiological TransportLDL-Receptor Related Protein-Associated ProteinPancreasDeoxyribonuclease HindIIICricetinaeFoam CellsHomozygoteOxidation-ReductionCell LineAtherosclerosisHeparan Sulfate ProteoglycansBinding SitesCarboxylic Ester HydrolasesMice, KnockoutBlood GlucoseApoproteinsChromatography, Agarosealpha-MacroglobulinsScavenger Receptors, Class BHypolipoproteinemiasPlant OilsProtaminesHeparitin SulfateCHO CellsAntigens, CD36Receptors, ImmunologicGene Expression Regulation, EnzymologicMolecular WeightApolipoprotein C-IEsterasesSodium ChlorideMice, Inbred C57BLRabbitsObesityIndolizinesGlycoproteinsGenotypeGlycerolReference ValuesAortaPerfusionApolipoprotein E3Gene ExpressionEnzyme ActivationReceptors, ScavengerSepharoseMice, TransgenicRecombinant ProteinsStructure-Activity RelationshipDiet, AtherogenicRhizopusPhosphatidylcholinesApoprotein(a)DyslipidemiasLactonesBlotting, NorthernSulfur OxidesChromatography, GelPhospholipid Transfer ProteinsCoronary DiseaseLDL-Receptor Related ProteinsSterol O-AcyltransferaseFoodLipid Metabolism, Inborn ErrorsGeotrichumStarvationIodine RadioisotopesTransfectionHydroxymethylglutaryl CoA ReductasesMuscle, SkeletalElectrophoresis, Agar GelInsulin ResistanceGene Expression RegulationRats, Sprague-DawleyEatingRisk Factors
TriglyceridesDeficiencyGeneLipidsHepaticInsulinProteinVLDLPostheparin plasmaChylomicronsFatty acidsEndothelial cellsActivityMiceGlycosylphosphatidylinositolPlasmaAdipose tissue lipoprotein lipase activityCholesterolMutationsParticlesAntibodyProcessing of triglyceride-rich lipoproteinsRegulationUptakeGeneticSkeletalPancreatic lipaseHumansActivity Assay KitHydrolysis of TG-rich lipoproteinsAtherosclerosisHyperlipoproteinemiaCardiovascular diseaseCatabolismMediatesTriglyceride lipase activitiesRegulatesMonoclonal
Triglycerides5
Deficiency3
Gene1
Lipids1
Hepatic1
Insulin5
Protein1
  • Hearts of transgenic mice expressed the altered lipoprotein lipase, and the protein localized to the surface of cardiomyocytes. (jci.org)
VLDL2
Postheparin plasma1
Chylomicrons1
Fatty acids1
Endothelial cells1
  • 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. (jci.org)
Activity3
Mice1
Glycosylphosphatidylinositol1
Plasma2
  • Selective measurement of two lipase activities in post heparin plasma from normal subjects and patients with hyperlipoproteinemia. (nii.ac.jp)
  • Rat Lpl ELISA Kit is a Sandwich ELISA KIT detecting the concentration of Lipoprotein lipase in Rat serum, plasma, tissue homogenates and other biological fluids. (lifescience-market.com)
Adipose tissue lipoprotein lipase activity4
Cholesterol18
Mutations3
Particles7
Antibody3
Processing of triglyceride-rich lipoproteins1
Regulation1
Uptake6
Genetic1
  • 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. (clinsci.org)
Skeletal4
Pancreatic lipase1
  • Yes research has suggested that fluorinated water may be responsible for the decreased activity of both pancreatic lipase protease. (natrilha.info)
Humans3
Activity Assay Kit1
  • 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. (cellbiolabs.com)
Hydrolysis of TG-rich lipoproteins1
  • Major functions of LPL include the hydrolysis of TG-rich lipoproteins and release of non-esterified fatty acid (NEFA), which are taken up and used for metabolic energy in peripheral tissue such as muscle, or are re-esterified into TG and stored in adipose tissue. (omicsonline.org)
Atherosclerosis3
  • 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. (hindawi.com)
  • Lipoprotein lipase for treating Atherosclerosis. (edoctoronline.com)
  • 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. (edoctoronline.com)
Hyperlipoproteinemia1
Cardiovascular disease1
Catabolism1
Mediates1
Triglyceride lipase activities1
Regulates2
Monoclonal1
Lipoprotein Lipase & Insulin | Healthy Eating | SF Gate
Lipoprotein Lipase & Insulin | Healthy Eating | SF Gate (healthyeating.sfgate.com)
Lipoprotein particle distribution and skeletal muscle lipoprotein lipase activity after acute exercise | Lipids in Health and...
Lipoprotein particle distribution and skeletal muscle lipoprotein lipase activity after acute exercise | Lipids in Health and... (lipidworld.biomedcentral.com)
Jana Klauer M.D. >> monthly...
Jana Klauer M.D. >> monthly... (janaklauermd.com)
Advice | Josh Bezoni | Fitness
Advice | Josh Bezoni | Fitness (joshbezonifitness.com)
Structure of the lipoprotein lipase-GPIHBP1 complex that mediates plasma triglyceride hydrolysis | PNAS
Structure of the lipoprotein lipase-GPIHBP1 complex that mediates plasma triglyceride hydrolysis | PNAS (pnas.org)
Plasmapheresis News, Research
Plasmapheresis News, Research (news-medical.net)
Frontiers | Hypothalamic Fatty Acids and Ketone Bodies Sensing and Role of FAT/CD36 in the Regulation of Food Intake |...
Frontiers | Hypothalamic Fatty Acids and Ketone Bodies Sensing and Role of FAT/CD36 in the Regulation of Food Intake |... (frontiersin.org)
LPL gene: MedlinePlus Genetics
LPL gene: MedlinePlus Genetics (medlineplus.gov)
Progress of Genomics in Atherosclerosis-Coronary Heart Disease and Myocardial Infarction | SpringerLink
Progress of Genomics in Atherosclerosis-Coronary Heart Disease and Myocardial Infarction | SpringerLink (link.springer.com)
Microbiota and metabolic diseases | SpringerLink
Microbiota and metabolic diseases | SpringerLink (link.springer.com)
June 1998 - Volume 9 - Issue 3 : Current Opinion in Lipidology
June 1998 - Volume 9 - Issue 3 : Current Opinion in Lipidology (journals.lww.com)
Factors Contributing to the Efficacy-Effectiveness Gap in the Case of Orphan Drugs for Metabolic Diseases | SpringerLink
Factors Contributing to the Efficacy-Effectiveness Gap in the Case of Orphan Drugs for Metabolic Diseases | SpringerLink (link.springer.com)
The gut microbiota as an environmental factor that regulates fat storage | PNAS
The gut microbiota as an environmental factor that regulates fat storage | PNAS (pnas.org)
Insights into the role of gut microbiota in obesity: pathogenesis, mechanisms, and therapeutic perspectives | SpringerLink
Insights into the role of gut microbiota in obesity: pathogenesis, mechanisms, and therapeutic perspectives | SpringerLink (link.springer.com)
Cholesterol deposits in the eyes: Causes and how to get rid of them
Cholesterol deposits in the eyes: Causes and how to get rid of them (medicalnewstoday.com)
Familial lipoprotein lipase deficiency: MedlinePlus Medical Encyclopedia
Familial lipoprotein lipase deficiency: MedlinePlus Medical Encyclopedia (medlineplus.gov)
Evidence that oestrogen receptor-α plays an important role in the regulation of glucose homeostasis in mice: insulin...
Evidence that oestrogen receptor-α plays an important role in the regulation of glucose homeostasis in mice: insulin... (link.springer.com)
Gut Microbioma Population: An Indicator Really Sensible to Any Change in Age, Diet, Metabolic Syndrome, and Life-Style
Gut Microbioma Population: An Indicator Really Sensible to Any Change in Age, Diet, Metabolic Syndrome, and Life-Style (hindawi.com)
MEDLINE/PubMed Data Element (Field) Descriptions
MEDLINE/PubMed Data Element (Field) Descriptions (nlm.nih.gov)
Digestion of Proteins, Lipids, and Starches in Ca... (Example) - MindMeister
Digestion of Proteins, Lipids, and Starches in Ca... (Example) - MindMeister (mindmeister.com)
Clinical Chemistry and Laboratory Medicine
Clinical Chemistry and Laboratory Medicine (degruyter.com)
Search of: Recruiting, Not yet recruiting, Available Studies | 'Hyperlipoproteinemia Type II' - List Results - ClinicalTrials...
Search of: Recruiting, Not yet recruiting, Available Studies | 'Hyperlipoproteinemia Type II' - List Results - ClinicalTrials... (clinicaltrials.gov)
Lipoprotein Lipase/LPL Mouse anti-Human, Alexa Fluor 405, Clone: OTI3A10, | Fisher Scientific
Lipoprotein Lipase/LPL Mouse anti-Human, Alexa Fluor 405, Clone: OTI3A10, | Fisher Scientific (fishersci.com)
Lipid Metabolism Disorders: MedlinePlus
Lipid Metabolism Disorders: MedlinePlus (medlineplus.gov)
A Polyglucuronic Acid to Target the FIAF Adipokine for Slimming Effects
A Polyglucuronic Acid to Target the FIAF Adipokine for Slimming Effects (cosmeticsandtoiletries.com)
Metabolic fuel kinetics in fish: swimming, hypoxia and muscle membranes | Journal of Experimental Biology
Metabolic fuel kinetics in fish: swimming, hypoxia and muscle membranes | Journal of Experimental Biology (jeb.biologists.org)