Lipoprotein lipase. Medical search

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.

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.

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

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

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

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

An inherited condition due to a deficiency of either LIPOPROTEIN LIPASE or APOLIPOPROTEIN C-II (a lipase-activating protein). The lack of lipase activities results in inability to remove CHYLOMICRONS and TRIGLYCERIDES from the blood which has a creamy top layer after standing.

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

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

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

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

A highly acidic mucopolysaccharide formed of equal parts of sulfated D-glucosamine and D-glucuronic acid with sulfaminic bridges. The molecular weight ranges from six to twenty thousand. Heparin occurs in and is obtained from liver, lung, mast cells, etc., of vertebrates. Its function is unknown, but it is used to prevent blood clotting in vivo and vitro, in the form of many different salts.

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

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

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

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

Specialized connective tissue composed of fat cells (ADIPOCYTES). It is the site of stored FATS, usually in the form of TRIGLYCERIDES. In mammals, there are two types of adipose tissue, the WHITE FAT and the BROWN FAT. Their relative distributions vary in different species with most adipose tissue being white.

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

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

A condition of elevated levels of TRIGLYCERIDES in the blood.

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

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

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

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

Compounds that increase the enzymatic activity of LIPOPROTEIN LIPASE. Lipoprotein lipase activators have a potential role in the treatment of OBESITY by increasing LIPID METABOLISM. Note that substances that increase the synthesis of lipoprotein lipase are not included here.

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

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

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

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

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

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

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

An enzyme that catalyzes the hydrolysis of CHOLESTEROL ESTERS and some other sterol esters, to liberate cholesterol plus a fatty acid anion.

A family of structurally-related angiogenic proteins of approximately 70 kDa in size. They have high specificity for members of the TIE RECEPTOR FAMILY.

A LDL-receptor related protein involved in clearance of chylomicron remnants and of activated ALPHA-MACROGLOBULINS from plasma.

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

An enzyme that catalyzes the hydrolysis of glycerol monoesters of long-chain fatty acids EC 3.1.1.23.

Conditions with excess LIPIDS in the blood.

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

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

The white liquid secreted by the mammary glands. It contains proteins, sugar, lipids, vitamins, and minerals.

FATTY ACIDS found in the plasma that are complexed with SERUM ALBUMIN for transport. These fatty acids are not in glycerol ester form.

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

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

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

An enzyme of the isomerase class that catalyzes the eliminative cleavage of polysaccharides containing 1,4-linked D-glucuronate or L-iduronate residues and 1,4-alpha-linked 2-sulfoamino-2-deoxy-6-sulfo-D-glucose residues to give oligosaccharides with terminal 4-deoxy-alpha-D-gluc-4-enuronosyl groups at their non-reducing ends. (From Enzyme Nomenclature, 1992) EC 4.2.2.7.

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

The rate dynamics in chemical or physical systems.

Abstaining from all food.

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

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

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

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

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

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

Emulsions of fats or lipids used primarily in parenteral feeding.

The process of cleaving a chemical compound by the addition of a molecule of water.

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

RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.

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

Domesticated bovine animals of the genus Bos, usually kept on a farm or ranch and used for the production of meat or dairy products or for heavy labor.

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

The relatively long-lived phagocytic cell of mammalian tissues that are derived from blood MONOCYTES. Main types are PERITONEAL MACROPHAGES; ALVEOLAR MACROPHAGES; HISTIOCYTES; KUPFFER CELLS of the liver; and OSTEOCLASTS. They may further differentiate within chronic inflammatory lesions to EPITHELIOID CELLS or may fuse to form FOREIGN BODY GIANT CELLS or LANGHANS GIANT CELLS. (from The Dictionary of Cell Biology, Lackie and Dow, 3rd ed.)

Colipase I and II, consisting of 94-95 and 84-85 amino acid residues, respectively, have been isolated from porcine pancreas. Their role is to prevent the inhibitory effect of bile salts on the lipase-catalyzed intraduodenal hydrolysis of dietary long-chain triglycerides.

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

A 51-amino acid pancreatic hormone that plays a major role in the regulation of glucose metabolism, directly by suppressing endogenous glucose production (GLYCOGENOLYSIS; GLUCONEOGENESIS) and indirectly by suppressing GLUCAGON secretion and LIPOLYSIS. Native insulin is a globular protein comprised of a zinc-coordinated hexamer. Each insulin monomer containing two chains, A (21 residues) and B (30 residues), linked by two disulfide bonds. Insulin is used as a drug to control insulin-dependent diabetes mellitus (DIABETES MELLITUS, TYPE 1).

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

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

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

The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.

Cells in the body that store FATS, usually in the form of TRIGLYCERIDES. WHITE ADIPOCYTES are the predominant type and found mostly in the abdominal cavity and subcutaneous tissue. BROWN ADIPOCYTES are thermogenic cells that can be found in newborns of some species and hibernating mammals.

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

LIPOLYSIS of stored LIPIDS in the ADIPOSE TISSUE to release FREE FATTY ACIDS. Mobilization of stored lipids is under the regulation of lipolytic signals (CATECHOLAMINES) or anti-lipolytic signals (INSULIN) via their actions on the hormone-sensitive LIPASE. This concept does not include lipid transport.

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

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

Cholesterol present in food, especially in animal products.

The muscle tissue of the HEART. It is composed of striated, involuntary muscle cells (MYOCYTES, CARDIAC) connected to form the contractile pump to generate blood flow.

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

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

The interstitial fluid that is in the LYMPHATIC SYSTEM.

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

A group of carbon-oxygen lyases. These enzymes catalyze the breakage of a carbon-oxygen bond in polysaccharides leading to an unsaturated product and the elimination of an alcohol. EC 4.2.2.

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

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

The time frame after a meal or FOOD INTAKE.

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

An individual having different alleles at one or more loci regarding a specific character.

One of three major isoforms of apolipoprotein E. In humans, Apo E2 differs from APOLIPOPROTEIN E3 at one residue 158 where arginine is replaced by cysteine (R158--C). In contrast to Apo E3, Apo E2 displays extremely low binding affinity for LDL receptors (RECEPTORS, LDL) which mediate the internalization and catabolism of lipoprotein particles in liver cells. ApoE2 allelic homozygosity is associated with HYPERLIPOPROTEINEMIA TYPE III.

A thermogenic form of adipose tissue composed of BROWN ADIPOCYTES. It is found in newborns of many species including humans, and in hibernating mammals. Brown fat is richly vascularized, innervated, and densely packed with MITOCHONDRIA which can generate heat directly from the stored lipids.

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

Relating to the size of solids.

The mass or quantity of heaviness of an individual. It is expressed by units of pounds or kilograms.

Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.

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

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

GLYCEROL esterified with FATTY ACIDS.

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

A chromatographic technique that utilizes the ability of biological molecules to bind to certain ligands specifically and reversibly. It is used in protein biochemistry. (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)

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

A membrane protein found in the rough endoplasm reticulum (ENDOPLASMIC RETICULUM, ROUGH) that binds to LDL-RECEPTOR RELATED PROTEINS. It may function to prevent ligand binding of receptors during protein processing events within endosomal compartments.

A nodular organ in the ABDOMEN that contains a mixture of ENDOCRINE GLANDS and EXOCRINE GLANDS. The small endocrine portion consists of the ISLETS OF LANGERHANS secreting a number of hormones into the blood stream. The large exocrine portion (EXOCRINE PANCREAS) is a compound acinar gland that secretes several digestive enzymes into the pancreatic ductal system that empties into the DUODENUM.

One of the Type II site-specific deoxyribonucleases (EC 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.-.

A subfamily in the family MURIDAE, comprising the hamsters. Four of the more common genera are Cricetus, CRICETULUS; MESOCRICETUS; and PHODOPUS.

Lipid-laden macrophages originating from monocytes or from smooth muscle cells.

An individual in which both alleles at a given locus are identical.

A chemical reaction in which an electron is transferred from one molecule to another. The electron-donating molecule is the reducing agent or reductant; the electron-accepting molecule is the oxidizing agent or oxidant. Reducing and oxidizing agents function as conjugate reductant-oxidant pairs or redox pairs (Lehninger, Principles of Biochemistry, 1982, p471).

Established cell cultures that have the potential to propagate indefinitely.

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

Ubiquitous macromolecules associated with the cell surface and extracellular matrix of a wide range of cells of vertebrate and invertebrate tissues. They are essential cofactors in cell-matrix adhesion processes, in cell-cell recognition systems, and in receptor-growth factor interactions. (From Cancer Metastasis Rev 1996; 15(2): 177-86; Hepatology 1996; 24(3): 524-32)

The parts of a macromolecule that directly participate in its specific combination with another molecule.

Enzymes which catalyze the hydrolysis of carboxylic acid esters with the formation of an alcohol and a carboxylic acid anion.

Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.

Glucose in blood.

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

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

Glycoproteins with a molecular weight of approximately 620,000 to 680,000. Precipitation by electrophoresis is in the alpha region. They include alpha 1-macroglobulins and alpha 2-macroglobulins. These proteins exhibit trypsin-, chymotrypsin-, thrombin-, and plasmin-binding activity and function as hormonal transporters.

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

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

Oils derived from plants or plant products.

A group of simple proteins that yield basic amino acids on hydrolysis and that occur combined with nucleic acid in the sperm of fish. Protamines contain very few kinds of amino acids. Protamine sulfate combines with heparin to form a stable inactive complex; it is used to neutralize the anticoagulant action of heparin in the treatment of heparin overdose. (From Merck Index, 11th ed; Martindale, The Extra Pharmacopoeia, 30th ed, p692)

A heteropolysaccharide that is similar in structure to HEPARIN. It accumulates in individuals with MUCOPOLYSACCHARIDOSIS.

CELL LINE derived from the ovary of the Chinese hamster, Cricetulus griseus (CRICETULUS). The species is a favorite for cytogenetic studies because of its small chromosome number. The cell line has provided model systems for the study of genetic alterations in cultured mammalian cells.

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

Cell surface molecules on cells of the immune system that specifically bind surface molecules or messenger molecules and trigger changes in the behavior of cells. Although these receptors were first identified in the immune system, many have important functions elsewhere.

Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in enzyme synthesis.

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

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

A ubiquitous sodium salt that is commonly used to season food.

The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.

A status with BODY WEIGHT that is grossly above the acceptable or desirable weight, usually due to accumulation of excess FATS in the body. The standards may vary with age, sex, genetic or cultural background. In the BODY MASS INDEX, a BMI greater than 30.0 kg/m2 is considered obese, and a BMI greater than 40.0 kg/m2 is considered morbidly obese (MORBID OBESITY).

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

The genetic constitution of the individual, comprising the ALLELES present at each GENETIC LOCUS.

A trihydroxy sugar alcohol that is an intermediate in carbohydrate and lipid metabolism. It is used as a solvent, emollient, pharmaceutical agent, and sweetening agent.

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

The main trunk of the systemic arteries.

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

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

The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.

Conversion of an inactive form of an enzyme to one possessing metabolic activity. It includes 1, activation by ions (activators); 2, activation by cofactors (coenzymes); and 3, conversion of an enzyme precursor (proenzyme or zymogen) to an active enzyme.

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

Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.

Proteins prepared by recombinant DNA technology.

The relationship between the chemical structure of a compound and its biological or pharmacological activity. Compounds are often classed together because they have structural characteristics in common including shape, size, stereochemical arrangement, and distribution of functional groups.

A diet that contributes to the development and acceleration of ATHEROGENESIS.

A genus of zygomycetous fungi of the family Mucoraceae, order MUCORALES, a common saprophyte and facultative parasite of mature fruits and vegetables. It may cause cerebral mycoses in diabetes and cutaneous infection in severely burned patients.

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

A large and highly glycosylated protein constituent of LIPOPROTEIN (A). It has very little affinity for lipids but forms disulfide-linkage to APOLIPOPROTEIN B-100. Apoprotein(a) has SERINE PROTEINASE activity and can be of varying sizes from 400- to 800-kDa. It is homologous to PLASMINOGEN and is known to modulate THROMBOSIS and FIBRINOLYSIS.

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

Cyclic esters of hydroxy carboxylic acids, containing a 1-oxacycloalkan-2-one structure. Large cyclic lactones of over a dozen atoms are MACROLIDES.

Detection of RNA that has been electrophoretically separated and immobilized by blotting on nitrocellulose or other type of paper or nylon membrane followed by hybridization with labeled NUCLEIC ACID PROBES.

Inorganic oxides of sulfur.

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

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

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

A family of proteins that share sequence similarity with the low density lipoprotein receptor (RECEPTORS, LDL).

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

Any substances taken in by the body that provide nourishment.

Errors in the metabolism of LIPIDS resulting from inborn genetic MUTATIONS that are heritable.

A mitosporic Saccharomycetales fungal genus, various species of which have been isolated from pulmonary lesions. Teleomorphs include Dipodascus and Galactomyces.

Lengthy and continuous deprivation of food. (Stedman, 25th ed)

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

The uptake of naked or purified DNA by CELLS, usually meaning the process as it occurs in eukaryotic cells. It is analogous to bacterial transformation (TRANSFORMATION, BACTERIAL) and both are routinely employed in GENE TRANSFER TECHNIQUES.

Enzymes that catalyze the reversible reduction of alpha-carboxyl group of 3-hydroxy-3-methylglutaryl-coenzyme A to yield MEVALONIC ACID.

A subtype of striated muscle, attached by TENDONS to the SKELETON. Skeletal muscles are innervated and their movement can be consciously controlled. They are also called voluntary muscles.

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

Diminished effectiveness of INSULIN in lowering blood sugar levels: requiring the use of 200 units or more of insulin per day to prevent HYPERGLYCEMIA or KETOSIS.

Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.

A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.

The consumption of edible substances.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

The condition is caused by mutations in the genes that code for proteins involved in cholesterol transport and metabolism, particularly the low-density lipoprotein receptor gene. This leads to a deficiency of functional LDL receptors on the surface of liver cells, resulting in excessive accumulation of LDL cholesterol in the bloodstream.

Symptoms of hyperlipoproteinemia Type I can include xanthomas (yellowish deposits of cholesterol in the skin), corneal arcus (a white deposit on the edge of the cornea), and early-onset cardiovascular disease, such as heart attacks or strokes.

Treatment for hyperlipoproteinemia Type I typically involves a combination of dietary changes, such as reducing intake of saturated and trans fats and cholesterol, and medications, such as statins, to lower LDL cholesterol levels. In some cases, medical procedures such as liver transplantation or gene therapy may be necessary to treat the condition.

There are several causes of hypertriglyceridemia, including:

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

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

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

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

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

There are several types of hyperlipidemia, including:

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

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

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

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

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

There are several types of arteriosclerosis, including:

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

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

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

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

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

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

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

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

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

There are several types of hypercholesterolemia, including:

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

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

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

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

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

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

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

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

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

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

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

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

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

Body weight is an important health indicator, as it can affect an individual's risk for certain medical conditions, such as obesity, diabetes, and cardiovascular disease. Maintaining a healthy body weight is essential for overall health and well-being, and there are many ways to do so, including a balanced diet, regular exercise, and other lifestyle changes.

There are several ways to measure body weight, including:

1. Scale: This is the most common method of measuring body weight, and it involves standing on a scale that displays the individual's weight in kg or lb.
2. Body fat calipers: These are used to measure body fat percentage by pinching the skin at specific points on the body.
3. Skinfold measurements: This method involves measuring the thickness of the skin folds at specific points on the body to estimate body fat percentage.
4. Bioelectrical impedance analysis (BIA): This is a non-invasive method that uses electrical impulses to measure body fat percentage.
5. Dual-energy X-ray absorptiometry (DXA): This is a more accurate method of measuring body composition, including bone density and body fat percentage.

It's important to note that body weight can fluctuate throughout the day due to factors such as water retention, so it's best to measure body weight at the same time each day for the most accurate results. Additionally, it's important to use a reliable scale or measuring tool to ensure accurate measurements.

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

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

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

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

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

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

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

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

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

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

There are several different types of obesity, including:

1. Central obesity: This type of obesity is characterized by excess fat around the waistline, which can increase the risk of health problems such as type 2 diabetes and cardiovascular disease.
2. Peripheral obesity: This type of obesity is characterized by excess fat in the hips, thighs, and arms.
3. Visceral obesity: This type of obesity is characterized by excess fat around the internal organs in the abdominal cavity.
4. Mixed obesity: This type of obesity is characterized by both central and peripheral obesity.

Obesity can be caused by a variety of factors, including genetics, lack of physical activity, poor diet, sleep deprivation, and certain medications. Treatment for obesity typically involves a combination of lifestyle changes, such as increased physical activity and a healthy diet, and in some cases, medication or surgery may be necessary to achieve weight loss.

Preventing obesity is important for overall health and well-being, and can be achieved through a variety of strategies, including:

1. Eating a healthy, balanced diet that is low in added sugars, saturated fats, and refined carbohydrates.
2. Engaging in regular physical activity, such as walking, jogging, or swimming.
3. Getting enough sleep each night.
4. Managing stress levels through relaxation techniques, such as meditation or deep breathing.
5. Avoiding excessive alcohol consumption and quitting smoking.
6. Monitoring weight and body mass index (BMI) on a regular basis to identify any changes or potential health risks.
7. Seeking professional help from a healthcare provider or registered dietitian for personalized guidance on weight management and healthy lifestyle choices.

There are several types of dyslipidemias, including:

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

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

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

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

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

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

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

Preventative measures for coronary disease include:

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

There are several types of inborn errors of lipid metabolism, each with its own unique set of symptoms and characteristics. Some of the most common include:

* Familial hypercholesterolemia: A condition that causes high levels of low-density lipoprotein (LDL) cholesterol in the blood, which can lead to heart disease and other health problems.
* Fabry disease: A rare genetic disorder that affects the body's ability to break down certain fats, leading to a buildup of toxic substances in the body.
* Gaucher disease: Another rare genetic disorder that affects the body's ability to break down certain lipids, leading to a buildup of toxic substances in the body.
* Lipoid cerebral degeneration: A condition that causes fatty deposits to accumulate in the brain, leading to cognitive decline and other neurological problems.
* Tangier disease: A rare genetic disorder that affects the body's ability to break down certain lipids, leading to a buildup of toxic substances in the body.

Inborn errors of lipid metabolism can be diagnosed through a variety of tests, including blood tests and genetic analysis. Treatment options vary depending on the specific disorder and its severity, but may include dietary changes, medication, and other therapies. With proper treatment and management, many individuals with inborn errors of lipid metabolism can lead active and fulfilling lives.

Starvation is a condition where an individual's body does not receive enough nutrients to maintain proper bodily functions and growth. It can be caused by a lack of access to food, poverty, poor nutrition, or other factors that prevent the intake of sufficient calories and essential nutrients. Starvation can lead to severe health consequences, including weight loss, weakness, fatigue, and even death.

Types of Starvation:

There are several types of starvation, each with different causes and effects. These include:

1. Acute starvation: This occurs when an individual suddenly stops eating or has a limited access to food for a short period of time.
2. Chronic starvation: This occurs when an individual consistently does not consume enough calories and nutrients over a longer period of time, leading to gradual weight loss and other health problems.
3. Malnutrition starvation: This occurs when an individual's diet is deficient in essential nutrients, leading to malnutrition and other health problems.
4. Marasmus: This is a severe form of starvation that occurs in children, characterized by extreme weight loss, weakness, and wasting of muscles and organs.
5. Kwashiorkor: This is a form of malnutrition caused by a diet lacking in protein, leading to edema, diarrhea, and other health problems.

Effects of Starvation on the Body:

Starvation can have severe effects on the body, including:

1. Weight loss: Starvation causes weight loss, which can lead to a decrease in muscle mass and a loss of essential nutrients.
2. Fatigue: Starvation can cause fatigue, weakness, and a lack of energy, making it difficult to perform daily activities.
3. Weakened immune system: Starvation can weaken the immune system, making an individual more susceptible to illnesses and infections.
4. Nutrient deficiencies: Starvation can lead to a deficiency of essential nutrients, including vitamins and minerals, which can cause a range of health problems.
5. Increased risk of disease: Starvation can increase the risk of diseases such as tuberculosis, pellagra, and other infections.
6. Mental health issues: Starvation can lead to mental health issues such as depression, anxiety, and irritability.
7. Reproductive problems: Starvation can cause reproductive problems, including infertility and miscarriage.
8. Hair loss: Starvation can cause hair loss, which can be a sign of malnutrition.
9. Skin problems: Starvation can cause skin problems, such as dryness, irritation, and infections.
10. Increased risk of death: Starvation can lead to increased risk of death, especially in children and the elderly.

It is important to note that these effects can be reversed with proper nutrition and care. If you or someone you know is experiencing starvation, it is essential to seek medical attention immediately.

There are several factors that can contribute to the development of insulin resistance, including:

1. Genetics: Insulin resistance can be inherited, and some people may be more prone to developing the condition based on their genetic makeup.
2. Obesity: Excess body fat, particularly around the abdominal area, can contribute to insulin resistance.
3. Physical inactivity: A sedentary lifestyle can lead to insulin resistance.
4. Poor diet: Consuming a diet high in refined carbohydrates and sugar can contribute to insulin resistance.
5. Other medical conditions: Certain medical conditions, such as polycystic ovary syndrome (PCOS) and Cushing's syndrome, can increase the risk of developing insulin resistance.
6. Medications: Certain medications, such as steroids and some antipsychotic drugs, can increase insulin resistance.
7. Hormonal imbalances: Hormonal changes during pregnancy or menopause can lead to insulin resistance.
8. Sleep apnea: Sleep apnea can contribute to insulin resistance.
9. Chronic stress: Chronic stress can lead to insulin resistance.
10. Aging: Insulin resistance tends to increase with age, particularly after the age of 45.

There are several ways to diagnose insulin resistance, including:

1. Fasting blood sugar test: This test measures the level of glucose in the blood after an overnight fast.
2. Glucose tolerance test: This test measures the body's ability to regulate blood sugar levels after consuming a sugary drink.
3. Insulin sensitivity test: This test measures the body's ability to respond to insulin.
4. Homeostatic model assessment (HOMA): This is a mathematical formula that uses the results of a fasting glucose and insulin test to estimate insulin resistance.
5. Adiponectin test: This test measures the level of adiponectin, a protein produced by fat cells that helps regulate blood sugar levels. Low levels of adiponectin are associated with insulin resistance.

There is no cure for insulin resistance, but it can be managed through lifestyle changes and medication. Lifestyle changes include:

1. Diet: A healthy diet that is low in processed carbohydrates and added sugars can help improve insulin sensitivity.
2. Exercise: Regular physical activity, such as aerobic exercise and strength training, can improve insulin sensitivity.
3. Weight loss: Losing weight, particularly around the abdominal area, can improve insulin sensitivity.
4. Stress management: Strategies to manage stress, such as meditation or yoga, can help improve insulin sensitivity.
5. Sleep: Getting adequate sleep is important for maintaining healthy insulin levels.

Medications that may be used to treat insulin resistance include:

1. Metformin: This is a commonly used medication to treat type 2 diabetes and improve insulin sensitivity.
2. Thiazolidinediones (TZDs): These medications, such as pioglitazone, improve insulin sensitivity by increasing the body's ability to use insulin.
3. Sulfonylureas: These medications stimulate the release of insulin from the pancreas, which can help improve insulin sensitivity.
4. DPP-4 inhibitors: These medications, such as sitagliptin, work by reducing the breakdown of the hormone incretin, which helps to increase insulin secretion and improve insulin sensitivity.
5. GLP-1 receptor agonists: These medications, such as exenatide, mimic the action of the hormone GLP-1 and help to improve insulin sensitivity.

It is important to note that these medications may have side effects, so it is important to discuss the potential benefits and risks with your healthcare provider before starting treatment. Additionally, lifestyle modifications such as diet and exercise can also be effective in improving insulin sensitivity and managing blood sugar levels.

NIH/UW entry on Familial Lipoprotein Lipase Deficiency Gene therapy for lipoprotein lipase deficiency Lipoprotein+lipase at the ... "Entrez Gene: LPL lipoprotein lipase". Wang H, Eckel RH (2009). "Lipoprotein lipase: from gene to obesity". Am J Physiol ... lipoprotein-dependent)) is a member of the lipase gene family, which includes pancreatic lipase, hepatic lipase, and ... Zechner R (1997). "The tissue-specific expression of lipoprotein lipase: implications for energy and lipoprotein metabolism". ...

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

... is a genetic disorder in which a person has a defective gene for lipoprotein lipase, which leads ... More than 220 mutations in the LPL gene have been found to cause familial lipoprotein lipase deficiency so far.[citation needed ... "Familial lipoprotein lipase deficiency: MedlinePlus Medical Encyclopedia". medlineplus.gov. Retrieved 17 April 2019. Burnett, ... "Familial Lipoprotein Lipase Deficiency". In Adam, MP; Ardinger, HH; Pagon, RA; et al. (eds.). GeneReviews. Seattle: University ...

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

ECM1 Lipoprotein glomerulopathy; 611771; APOE Lipoprotein lipase deficiency; 238600; LPL Lissencephaly 3; 611603; TUBA1A ... TP63 Lipase deficiency, combined; 246650; LMF1 Lipodystrophy, congenital generalized, type 1; 608594; AGPAT2 Lipodystrophy, ...

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

"Structural features of lipoprotein lipase. Lipase family relationships, binding interactions, non-equivalence of lipase ... These lipases are closely related to each other and to lipoprotein lipase (EC 3.1.1.34), which hydrolyses triglycerides of ... Triglyceride lipases (EC 3.1.1.3) are a family of lipolytic enzymes that hydrolyse ester linkages of triglycerides. Lipases are ... Pancreatic lipase, also known as pancreatic triacylglycerol lipase or steapsin, is an enzyme secreted from the pancreas. As the ...

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

... (NO-1886) is a cholesterol lowering drug from the statin family, which acts as a lipoprotein lipase activator. The ... Yin W, Tsutsumi K (2003). "Lipoprotein lipase activator NO-1886". Cardiovascular Drug Reviews. 21 (2): 133-42. doi:10.1111/j. ...

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

Korn ED, Quigley TW (June 1957). "Lipoprotein lipase of chicken adipose tissue". The Journal of Biological Chemistry. 226 (2): ... triglyceride lipase, liver lipase, hepatic monoacylglycerol acyltransferase). Pancreatic lipase Gastric lipase Lingual lipase ... meito Sangyo OF lipase, hepatic lipase, lipazin, post-heparin plasma protamine-resistant lipase, salt-resistant post-heparin ... This family was also called class 3 lipases as they are only distantly related to other lipase families. DAGLA; DAGLB; ...

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

Lipoprotein lipase has an important role. Once the chylomicrons (or other lipoproteins) travel through the tissues, these ... Chemicals from the pancreas (pancreatic lipase family and bile salt-dependent lipase) are secreted into the small intestines to ... For example, very-low-density lipoproteins (VLDL) carry the synthesized triglycerides by our body and low-density lipoproteins ... they require special transport proteins known as lipoproteins. The amphipathic structure of lipoproteins allows the ...

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

APOC3 inhibits lipoprotein lipase and hepatic lipase; it is thought to inhibit hepatic uptake of triglyceride-rich particles. ... "Metabolism of very-low-density lipoprotein and low-density lipoprotein containing apolipoprotein C-III and not other small ... Apo-CIII is secreted by the liver as well as the small intestine, and is found on triglyceride-rich lipoproteins such as ... "A human APOC3 missense variant and monoclonal antibody accelerate apoC-III clearance and lower triglyceride-rich lipoprotein ...

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

... and increased activity of lipoprotein lipase in blood. The synthesis of triglycerides is reduced in the liver because EPA and ... of triglycerides in the liver and to enhance clearance of triglycerides from circulating very low-density lipoprotein (VLDL) ...

https://en.wikipedia.org/wiki/Omega-3_acid_ethyl_esters

The triglycerides in chylomicrons are hydrolyzed by lipoprotein lipase (LPL) along the luminal surface of capillaries, mainly ... "GPIHBP1 stabilizes lipoprotein lipase and prevents its inhibition by angiopoietin-like 3 and angiopoietin-like 4". The Journal ... That Cannot Bind Lipoprotein Lipase". Arteriosclerosis, Thrombosis, and Vascular Biology. 29 (6): 956-962. doi:10.1161/ATVBAHA. ... "The Acidic Domain of GPIHBP1 is Important for the Binding of Lipoprotein Lipase and Chylomicrons". Journal of Biological ...

https://en.wikipedia.org/wiki/GPIHBP1

... and increased activity of lipoprotein lipase in blood. Omega-3 carboxylic acids are derived from fish oil and are a purified ... of triglycerides in the liver and to enhance clearance of triglycerides from circulating very low-density lipoprotein (VLDL) ... carboxylic acids in statin-treated patients with high levels of triglycerides and low levels of high-density lipoprotein ...

https://en.wikipedia.org/wiki/Omega-3_carboxylic_acids

... and increased activity of lipoprotein lipase in blood. Ethyl eicosapentaenoic acid (E-EPA) is an ethyl ester of ... DHA alone appears to raise low-density lipoprotein (the variant which drives atherosclerosis; sometimes very inaccurately ... of triglycerides in the liver and to enhance clearance of triglycerides from circulating very low-density lipoprotein (VLDL) ...

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

... where their triglyceride components are hydrolyzed by the activity of the lipoprotein lipase, allowing the released free fatty ... APOC2 is the coenzyme for lipoprotein lipase (LPL) activity. Once triglyceride stores are distributed, the chylomicron returns ... also known as ultra low-density lipoproteins (ULDL), are lipoprotein particles that consist of triglycerides (85-92%), ... ULDLs, if in the region of 1,000 nm or more, are the only lipoprotein particles that can be seen using a light microscope, at ...

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

Lipoprotein lipase (LPL) is a type of digestive enzyme that helps regulate the uptake of triacylglycerols from chylomicrons and ... Lipoprotein lipase is downregulated by high levels of insulin, and upregulated by high levels of glucagon and adrenaline. ... Lipase assays are done using a lipid agar with a spirit blue dye. If the bacteria has lipase, a clear streak will form in the ... Kiens B, Lithell H, Mikines KJ, Richter EA (October 1989). "Effects of insulin and exercise on muscle lipoprotein lipase ...

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

"Human genes involved in lipolysis of plasma lipoproteins: mapping of loci for lipoprotein lipase to 8p22 and hepatic lipase to ... Hepatic lipase (HL), also called hepatic triglyceride lipase (HTGL) or LIPC (for "lipase, hepatic"), is a form of lipase, ... and evolutionary relationships with lipoprotein lipase and pancreatic lipase". The Journal of Biological Chemistry. 263 (3): ... Hepatic lipase deficiency is a rare, autosomal recessive disorder that results in elevated high density lipoprotein (HDL) ...

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

It shares with ANGPTL4 and ANGPTL8 the ability to inhibit the enzyme Lipoprotein lipase (LPL), and its hepatic overexpression ... with its interacting partner lipoprotein lipase". Computational Biology and Chemistry. 61: 210-20. doi:10.1016/j.compbiolchem. ... antibody lowers mouse serum triglycerides involving increased postprandial activity of the cardiac lipoprotein lipase". ... mice lacking ANGPTL8 exhibit markedly decreased uptake of Very low-density lipoprotein-derived fatty acids into white adipose ...

https://en.wikipedia.org/wiki/ANGPTL8

Other processes involving sortilin include endocytosis, negative regulation of lipoprotein lipase activity, myotube ... "Sortilin/neurotensin receptor-3 binds and mediates degradation of lipoprotein lipase". The Journal of Biological Chemistry. 274 ... "Sortilin/neurotensin receptor-3 binds and mediates degradation of lipoprotein lipase". The Journal of Biological Chemistry. 274 ... September 2010). "Sort1, encoded by the cardiovascular risk locus 1p13.3, is a regulator of hepatic lipoprotein export". Cell ...

https://en.wikipedia.org/wiki/Sortilin_1

"Placental lipoprotein lipase (LPL) gene expression in a placentotrophic lizard, Pseudemoia entrecasteauxii". Journal of ...

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

Griffith, O. W., Ujvari, B., Belov, K., & Thompson, M. B. (2013). Placental lipoprotein lipase (LPL) gene expression in a ... Griffith, OW; Ujvari, B; Belov, K; Thompson, MB (2013). "Placental lipoprotein lipase (LPL) gene expression in a ...

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

Griffith, OW; Ujvari, B; Belov, K; Thompson, MB (2013). "Placental lipoprotein lipase (LPL) gene expression in a ... most likely occurs through the yolk sac placenta and is facilitated in part by the production of the protein lipoprotein lipase ...

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

Glybera treats one such disease, caused by a defect in lipoprotein lipase. DNA must be administered, reach the damaged cells, ... In 2012, Glybera, a treatment for a rare inherited disorder, lipoprotein lipase deficiency, became the first treatment to be ... The treatment used Alipogene tiparvovec (Glybera) to compensate for lipoprotein lipase deficiency, which can cause severe ...

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

Very low-density lipoproteins are also subject to delipidation by vascular lipoprotein lipase, and deliver fats to tissues ... Once in the blood, chylomicrons are subject to delipidation by lipoprotein lipase. Eventually, enough lipid has been lost and ... As triglycerides are lost from very low-density lipoproteins, the lipoprotein particles become smaller and denser (since ... Triglycerides are emulsified by bile and hydrolyzed by the enzyme lipase, resulting in a mixture of fatty acids, di- and ...

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

... on the dimerization of lipoprotein lipase". Biochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism. 1344 (2): 132-8 ...

https://en.wikipedia.org/wiki/Carbonyl_cyanide_m-chlorophenyl_hydrazone

"Angiopoietin-like protein 4 converts lipoprotein lipase to inactive monomers and modulates lipase activity in adipose tissue". ... Lafferty MJ, Bradford KC, Erie DA, Neher SB (October 2013). "Angiopoietin-like protein 4 inhibition of lipoprotein lipase: ... causing elevation of serum TG levels via inhibition of the enzyme lipoprotein lipase (LPL). Biochemical studies indicate that ...

https://en.wikipedia.org/wiki/ANGPTL4

"Intramuscular Administration of AAV1-Lipoprotein LipaseS447X Lowers Triglycerides in Lipoprotein Lipase-Deficient Patients". ... The adeno-associated virus serotype 1 (AAV1) viral vector delivers an intact copy of the human lipoprotein lipase (LPL) gene to ... Alipogene tiparvovec, sold under the brand name Glybera, is a gene therapy treatment designed to reverse lipoprotein lipase ... Scott, Lesley J. (2015). "Alipogene Tiparvovec: A Review of Its Use in Adults with Familial Lipoprotein Lipase Deficiency". ...

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

He has done significant research in the biology and pathophysiology of lipoprotein lipase. Eckel was on the Scientific Advisory ...

https://en.wikipedia.org/wiki/Robert_H._Eckel

... increases the activity of extrahepatic lipoprotein lipase (LL), thereby increasing lipoprotein triglyceride ... This increase in the synthesis of lipoprotein lipase thereby increases the clearance of triglycerides. Chylomicrons are ... levels Modest reduction of low density lipoprotein (LDL) levels Moderate increase in high density lipoprotein (HDL) levels GI ... several theories exist regarding the very low density lipoprotein (VLDL) effect; it can inhibit lipolysis and decrease ...

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

Thus one extra sialyl residue on apolipoprotein C3 impairs its action on lipoprotein lipase. This can affect expression of the ... Stocks, J; Holdsworth, G; Galton, DJ (1982). "An abnormal triglyceride-rich lipoprotein containing excess sialylated ... Stocks, J; Holdsworth, G; Galton, DJ (1979). "Hypertriglyceridaemia associated with an abnormal triglyceride-rich lipoprotein ...

https://en.wikipedia.org/wiki/David_J._Galton

Inactivity of lipoprotein lipase (LPL) plays the predominant role in the development of familial hypertriglyceridemia. LPL ... Individuals with the disorder are mostly heterozygous in an inactivating mutation of the gene encoding for lipoprotein lipase ( ... 2019). "Characterization of lipoprotein profiles in patients with hypertriglyceridemic Fredrickson-Levy and Lees dyslipidemia ... is a genetic disorder characterized by the liver overproducing very-low-density lipoproteins (VLDL). As a result, an affected ...

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

The role of lipoproteins, lipases and thyroid hormones in coronary lesion growth". Atherosclerosis. 68 (1-2): 51-8. doi:10.1016 ...

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

... namely lipoprotein lipase and apolipoprotein C-III. Combined, these observations suggest that, as well as LDL cholesterol, ... The low-density lipoprotein receptor (LDL-R) is a mosaic protein of 839 amino acids (after removal of 21-amino acid signal ... "Low Density Lipoprotein Receptor". LOVD v.1.1.0 - Leiden Open Variation Database. Archived from the original on 2016-01-28. ... "LDLR low density lipoprotein receptor [Homo sapiens (human)] - Gene - NCBI". www.ncbi.nlm.nih.gov. Retrieved 2016-10-10. ...

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

... lipase - lipid - lipid anchored protein - lipid bilayer - lipoprotein - liquid - list of compounds - list of gene families - ...

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

Treatment with catalytic lipase has reportedly given coconut oil antimicrobial characteristics. Before the advent of electrical ... a saturated fat that raises total blood cholesterol levels by increasing the amounts of both high-density lipoprotein (HDL) ... cholesterol and low-density lipoprotein (LDL) cholesterol. Although lauric acid consumption may create a more favorable total ... but also high-density lipoprotein (HDL)) concentrations were elevated compared with nontropical vegetable oils. The review ...

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

2-AG can also activate both cannabinoid receptors and is inactivated by monoacylglycerol lipase. It is present at approximately ... Okajima, F. (2002). "Plasma lipoproteins behave as carriers of extracellular sphingosine 1-phosphate: is this an atherogenic ... oxidized low-density lipoproteins (oxLDL) and several immune complexes. S1P is probably formed at the inner leaflet of the ... S1P is found in high nanomolar concentrations in serum where it is bound to albumin and lipoproteins. Inside the cell, S1P can ...

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

... and to the activities of lipoprotein lipase and hepatic lipase. J Clin Invest. 1987;80:341-347. "Patsch JR, Miesenbock G, ... Coronary heart disease prediction from lipoprotein cholesterol levels, triglycerides, lipoprotein(a), apolipoproteins A-I and B ... The methods of lipoprotein isolation, developed in Innsbruck, were used by Patsch for many clinical studies at Washington ... Patsch W, Franz S, Schonfeld G. Role of insulin in lipoprotein secretion by cultured rat hepatocytes. J Clin Invest. 1983;71: ...

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

PPARα activates lipoprotein lipase and reduces apoprotein CIII, which increases lipolysis and elimination of triglyceride-rich ... It is used in addition to diet to reduce elevated low-density lipoprotein cholesterol (LDL), total cholesterol, triglycerides ( ... TG), and apolipoprotein B (apo B), and to increase high-density lipoprotein cholesterol (HDL) in adults with primary ... "Mechanism of action of fibrates on lipid and lipoprotein metabolism". Circulation. 98 (19): 2088-2093. CiteSeerX 10.1.1.1004. ...

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

Lipoprotein lipase deficiency (chylomicronemia, chylomicronemia syndrome) Macular amyloidosis Maroteaux-Lamy syndrome ( ... Familial alpha-lipoprotein deficiency (Tangier disease) Familial amyloid polyneuropathy Familial apoprotein CII deficiency ...

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

Their cell walls are also quite different from those of bacteria, as ordinary lipoprotein membranes fail in high salt ... Halophiles also produce degradative enzymes such as lipases, amylases, proteases, and xylanases that are used in various food ...

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

... is a condition that results from the decreasing of lipoprotein lipase activity ...

https://en.wikipedia.org/wiki/Medication-induced_hyperlipoproteinemia

Steatosis "Lipoproteins". Archived from the original on 2015-02-28. Retrieved 2014-11-06. "Digestion and Absorption of Fats". ... speeding up the rate of digestion by the enzyme lipase at a later point in digestion. Bile salts possess detergent properties ...

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

The triglycerides are not stable in HDL, but are degraded by hepatic lipase so that, finally, small HDL particles are left, ... High-density lipoprotein (HDL) is one of the five major groups of lipoproteins. Lipoproteins are complex particles composed of ... Kwiterovich PO (Dec 2000). "The metabolic pathways of high-density lipoprotein, low-density lipoprotein, and triglycerides: a ... Unlike the larger lipoprotein particles, which deliver fat molecules to cells, HDL particles remove fat molecules from cells. ...

https://en.wikipedia.org/wiki/High-density_lipoprotein

LDL particles are formed when triglycerides are removed from VLDL by the lipoprotein lipase enzyme (LPL) and they become ... very low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), low-density lipoprotein (LDL) and high-density ... Low-density lipoprotein (LDL) is one of the five major groups of lipoprotein that transport all fat molecules around the body ... Lipoproteins transfer lipids (fats) around the body in the extracellular fluid, making fats available to body cells for ...

https://en.wikipedia.org/wiki/Low-density_lipoprotein

Clinical features, lipoprotein characterization, lipase activity, and correction of hypertriglyceridemia after apolipoprotein C ... This protein activates the enzyme lipoprotein lipase in capillaries, which hydrolyzes triglycerides and thus provides free ... The protein encoded by this gene is secreted in plasma where it is a component of very low density lipoproteins and ...

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

Lipaemia retinalis is a white appearance of the retina, and can occur by lipid deposition in lipoprotein lipase deficiency. ...

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

Schmidt EB, Koenig W, Khuseyinova N, Christensen JH (Jan 2008). "Lipoprotein-associated phospholipase A2 concentrations in ... this lipase exhibits a broader substrate specificity than simply platelet activating factor. Two other isoforms of ... broad substrate specificity and lipoprotein binding does not modulate the catalytic properties of the plasma enzyme" (PDF). ...

https://en.wikipedia.org/wiki/PAFAH2

TNF-alpha and TNF-gamma may also lead to inhibition of lipoprotein lipase or stimulate triglyceride synthesis. Activated ...

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

Strauss, Juliane Gertrude: The role of endothelial lipase in binding and uptake of high density lipoproteins. Curricula Vitae ...

https://en.wikipedia.org/wiki/Juliane_Bogner-Strauß

... which is essential for creating beta-lipoproteins. These lipoproteins are both necessary for the absorption of fats, ... The signs and symptoms of abetalipoproteinemia appear in the first few months of life (because pancreatic lipase is not active ... New insights into lipoprotein assembly and vitamin E metabolism from a rare genetic disease". JAMA. 270 (7): 865-9. doi:10.1001 ... Often symptoms will arise that indicate the body is not absorbing or making the lipoproteins that it needs. These symptoms ...

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

They are biosynthesized by the enzymatic hydrolysis of triglycerides by lipoprotein lipase and the enzymatic hydrolysis of ... diglycerides by diacylglycerol lipase; or as an intermediate in the alkanoylation of glycerol to form fats. Several ...

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

"The very low density lipoprotein receptor mediates the cellular catabolism of lipoprotein lipase and urokinase-plasminogen ... Low density lipoprotein receptor-related protein-associated protein 1 also known as LRPAP1 or RAP is a chaperone protein which ... Encoding (Low Density Lipoprotein Receptor-Related Protein Associated protein 1) LRPAP is a largely expressed gene, and a 357 ... Willnow TE, Armstrong SA, Hammer RE, Herz J (1995). "Functional expression of low density lipoprotein receptor-related protein ...

https://en.wikipedia.org/wiki/LDL-receptor-related_protein-associated_protein

This is achieved through the increased activity of lipoprotein lipase which break down triglycerides into free fatty acids. ...

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

Angiotensin converting enzyme Antithrombin-III Lipoprotein lipase Apolipoproteins Growth factors Chemokines The enzymes and ... Initial dysfunction of the glycocalyx can be caused by hyperglycemia or oxidized low-density lipoproteins (LDLs), which then ...

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

Lipoprotein lipase (EC 3.1.1.34) Category:EC 3.1.2 Ubiquitin carboxy-terminal hydrolase L1 (EC 3.1.2.15) Category:EC 3.1.3 ...

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

The enzyme is bound to high-density lipoproteins (HDLs) (alpha-LCAT) and LDLs (beta-LCAT) in the blood plasma. LCAT deficiency ... de Vries R, Borggreve SE, Dullaart RP (2004). "Role of lipases, lecithin:cholesterol acyltransferase and cholesteryl ester ... which is then sequestered into the core of a lipoprotein particle, eventually making the newly synthesized HDL spherical and ... transfer protein in abnormal high density lipoprotein metabolism in insulin resistance and type 2 diabetes mellitus". Clin. Lab ...

https://en.wikipedia.org/wiki/Lecithin–cholesterol_acyltransferase

... lipase binds to the low density lipoprotein receptor-related protein and inhibits lipase-mediated uptake of lipoprotein in ... Hepatic lipase, ITGB1BP1, Lactoferrin, Lipoprotein lipase, LPL, MAPK8IP1, MAPK8IP2, Midkine, MMP13, MMP2, MMP9, Neuroserpin, ... "The carboxyl-terminal domain of lipoprotein lipase binds to the low density lipoprotein receptor-related protein/alpha 2- ... Yancey PG, Ding Y, Fan D, Blakemore JL, Zhang Y, Ding L, Zhang J, Linton MF, Fazio S (Jul 2011). "Low-density lipoprotein ...

https://en.wikipedia.org/wiki/LRP1

Find symptoms and other information about Familial lipoprotein lipase deficiency. ... Familial lipoprotein lipase deficiency is a rare genetic disorder is which a person lacks the enzyme lipoprotein lipase, a ... Familial lipoprotein lipase deficiency is a genetic disease, which means that it is caused by one or more genes not working ... Familial lipoprotein lipase deficiency is caused by changes in the LPL gene. It is inherited in an autosomal recessive pattern. ...

https://rarediseases.info.nih.gov/diseases/12241/familial-lipoprotein-lipase-deficiency

Familial lipoprotein lipase deficiency is a group of rare genetic disorders in which a person lacks a protein needed to break ... Familial lipoprotein lipase deficiency is a group of rare genetic disorders in which a person lacks a protein needed to break ... Familial lipoprotein lipase deficiency is caused by a defective gene that is passed down through families. ... People with this condition lack an enzyme called lipoprotein lipase. Without this enzyme, the body cannot break down fat from ...

http://www.nlm.nih.gov/medlineplus/ency/article/000408.htm

https://medlineplus.gov/ency/article/000408.htm

Familial lipoprotein lipase deficiency is an inherited condition that disrupts the normal breakdown of fats in the body, ... Mutations that cause familial lipoprotein lipase deficiency lead to a reduction or elimination of lipoprotein lipase activity, ... medlineplus.gov/genetics/condition/familial-lipoprotein-lipase-deficiency/ Familial lipoprotein lipase deficiency. ... Mutations in the LPL gene cause familial lipoprotein lipase deficiency. The LPL gene provides instructions for producing an ...

https://ghr.nlm.nih.gov/condition/familial-lipoprotein-lipase-deficiency

View Human/Mouse Lipoprotein Lipase/LPL Antibody (AF7197) datasheet. ... Background: Lipoprotein Lipase/LPL. LPL (LipoProtein Lipase; also LIPD) is a 53-56 kDa glycoprotein member of the Lipase family ... Lipoprotein Lipase/LPL in SH‑SY5Y Human Cell Line. Lipoprotein Lipase/LPL was detected in immersion fixed SH-SY5Y human ... Lipoprotein Lipase/LPL in Human Heart. Lipoprotein Lipase/LPL was detected in immersion fixed paraffin-embedded sections of ...

https://www.rndsystems.com/products/human-mouse-lipoprotein-lipase-lpl-antibody_af7197

Familial lipoprotein lipase (LPL) deficiency usually presents in childhood and is characterized by very severe ... Familial lipoprotein lipase deficiency, apo CII deficiency and hepatic lipase deficiency. In: Scriver CR, Beaudet AL, Sly WS, ... Measurement of lipoprotein lipase enzyme activity. Affected individuals have low or absent LPL enzyme activity in an assay ... Familial Lipoprotein Lipase Deficiency. Synonym: Familial LPL Deficiency. John R Burnett, MB ChB, MD, PhD, FRCPA, Amanda J ...

https://www.ncbi.nlm.nih.gov/books/n/gene/lpl/

Lipoprotein lipase (LPL; E.C. 3.1.1.34) is a key enzyme in the metabolism of lipids. Many diseases, including obesity, coronary ... Human LPL is a member of a superfamily of lipases that includes hepatic lipase and pancreatic lipase. These lipases are ... Lipoprotein lipase deficiencies]. Etienne J, Brault D. Etienne J, et al. Ann Biol Clin (Paris). 1992;50(5):299-309. Ann Biol ... Molecular pathobiology of the human lipoprotein lipase gene V Murthy 1 , P Julien, C Gagne ...

https://pubmed.ncbi.nlm.nih.gov/8843465

Comments are welcomed and encouraged. The purpose of comments on our site is to expand knowledge, engage in thoughtful discussion, and learn more from readers. Criticism and skepticism can be far more useful than praise and unflinching belief. Theres an art and science to critical thinking and how to conduct yourself. Theres a multitude of fallacious appeals we could spell out, but a good rule of thumb is not to attack the person, attack the ideas. Dont look for the flaws in the person, look for the flaws in the hypothesis. Lets keep the brawling to movies depicting minor league hockey teams and political "news" shows. Thank you for adding to the discussion ...

https://peterattiamd.com/tag/lipoproteins-lipoprotein-lipase/

Human LIPD(Lipase, Lipoprotein) ELISA Kit. Human LIPD(Lipase, Lipoprotein) ELISA Kit. To Order Contact us: [email protected] ... Lipoprotein Lipase (LPL) ELISA Kit is an enzyme immunoassay developed for the detection and quantitation of lipoprotein lipase ... Description: Lipoprotein lipase (LPL) is the key plasma lipase responsible for hydrolysis of the triglyceride core in these ... Description: A sandwich ELISA kit for detection of Lipase, Lipoprotein from Human in samples from blood, serum, plasma, cell ...

https://lscwarsaw.com/human-lipdlipase-lipoprotein-elisa-kit/

Recurrent Acute Pancreatitis Secondary to Lipoprotein Lipase Deficiency. Tropical Gastroenterology. 2021 Mar; 42(1): 47-48. ...

https://imsear.searo.who.int/handle/123456789/221091

Lipoprotein lipase (LPL) is a key regulator for TGs that hydrolyzes TGs to glycerol and free fatty acids in lipoprotein ... Lipoprotein Lipase: Is It a Magic Target for the Treatment of Hypertriglyceridemia. ... Lipoprotein Lipase: Is It a Magic Target for the Treatment of Hypertriglyceridemia. ... Angiopoietin-like protein 3; Apolipoproteins; Cardiovascular diseases; Cholesterol; Lipoprotein lipase; Oligonucleotides, ...

https://pesquisa.bvsalud.org/portal/resource/pt/mdl-36065644

... lipoprotein lipase; Lipoprotein lipase; lipoprotein lipase; lipoprotein lipase]Product Gene... ... Lipoprotein Lipase (LPL) Control Set , MBS490211 , MyBiosourceProduct Short Name: [Lipoprotein Lipase (LPL)]Product Name ...

https://biocheminfo.org/control/control-set/

In this paper, we propose that this congestion predisposes the chylomicron triglycerides to hydrolysis by lipoprotein lipase ( ... In this paper, we propose that this congestion predisposes the chylomicron triglycerides to hydrolysis by lipoprotein lipase ( ... it is crucial to understand how these lipoproteins are different between men and women. The chylomicrons in men are generally ... it is crucial to understand how these lipoproteins are different between men and women. The chylomicrons in men are generally ...

https://www.frontiersin.org/articles/10.3389/fphys.2019.01486/full

LPL: This is the enzyme lipoprotein lipase, which breaks down triglycerides (fats). ...

https://www.medicalnewstoday.com/articles/is-type-2-diabetes-genetic?utm_source=ReadNext

Haplotypes in the Lipoprotein Lipase Gene Influence High-Density Lipoprotein Cholesterol Response to Statin Therapy and ...

https://www.rand.org/pubs/authors/t/taylor_k_d.html

Lipoprotein lipase is known to be regulated by insulin. The remaining lipoprotein, enriched in cholesterol is removed primarily ... Triglycerides are readily hydrolyzed by lipoprotein lipase resulting in fatty acids for energy or storage in adipose tissue. ... A functional deficiency of lipoprotein lipase can result in very high plasma triglyceride levels and decreased high density ... or reflect changes in lipoprotein receptor function or lipoprotein metabolizing enzymes. Furthermore, it is not clear whether ...

https://grants.nih.gov/grants/guide/rfa-files/RFA-HL-00-007.html

Familial Lipoprotein Lipase Deficiency and Related Disorders of Chylomicron Metabolism. In Stanbury J.B., et al. (eds.): The ... an inhibitor of lipoprotein lipase activity). The resulting fall in triglycerides produces an alteration in the size and ... fenofibrate increases lipolysis and elimination of triglyceride-rich particles from plasma by activating lipoprotein lipase and ... In addition, treatment with fenofibrate results in increases in high density lipoprotein (HDL) and apoproteins apo AI and apo ...

https://dailymed.nlm.nih.gov/dailymed/fda/fdaDrugXsl.cfm?setid=573ffb90-61a7-4b2d-b191-13de6c01d19e&type=display

Lipoprotein Lipase/metabolism*; Mice; Mice, Inbred Strains; Receptors, Lipoprotein/analysis; Receptors, Lipoprotein/genetics*; ... Abstract: Glycosylphosphatidylinositol-anchored high density lipoprotein-binding protein 1 (GPIHBP1), the protein that shuttles ...

https://tools.niehs.nih.gov/portfolio/index.cfm?do=portfolio.publicationDetail&id=3578529

Lipoprotein lipase and diabetic cardiomyopathy].. Liu XY; Yin WD; Tang CK. Sheng Li Ke Xue Jin Zhan; 2014 Feb; 45(1):16-20. ... 4. Lipoprotein Lipase and Its Delivery of Fatty Acids to the Heart.. Shang R; Rodrigues B. Biomolecules; 2021 Jul; 11(7):. ... 1. Lipoprotein lipase mediated fatty acid delivery and its impact in diabetic cardiomyopathy.. Kim MS; Wang Y; Rodrigues B. ... 7. Cardiac lipoprotein lipase: metabolic basis for diabetic heart disease.. Pulinilkunnil T; Rodrigues B. Cardiovasc Res; 2006 ...

https://pubmedhh.nlm.nih.gov/biomarkers/search.php?id=22024251&mod=related&page=1&outid=&proj=

On the contrary, visceral fat has lower lipoprotein lipase activity and higher rates of catecholamine-induced lipolysis. This ... Regulation by obesity, weight loss, and relationship to lipoprotein lipase. The Journal of Clinical Investigation. 1995;. 95. ( ... Fried SK, Zechner R. Cachectin/tumor necrosis factor decreases human adipose tissue lipoprotein lipase mRNA levels, synthesis, ... Human recombinant TNF suppresses lipoprotein lipase activity and stimulates lipolysis in 3T3-L1 cells. Journal of Biochemistry ...

https://www.intechopen.com/chapters/61214

Metabolic characterization of a rare genetic variation within APOC3 and its lipoprotein lipase independent effects.. ...

https://bristol.ac.uk/alspac/researchers/publications/2016-a-m/

... and lipoprotein lipase (Lpl, nuclear-encoded). Nd1 levels were normalized to Lpl DNA content and expressed relative to WT (=1.0 ... were normalized to the levels of lipoprotein lipase (genomic DNA). The primer sequences are noted in Supplementary Table 2. ...

https://www.nature.com/articles/s41467-022-28557-5?error=cookies_not_supported&code=8b362637-131a-4909-8e03-7aac996e84e6

Lipoprotein lipase hydrolyzes triglycerides in chylomicrons and very low-density lipoprotein (VLDL), releasing free fatty acids ... Once very low-density lipoprotein (VLDL) has been metabolized by lipoprotein lipase, VLDL remnants in the form of intermediate- ... Once very low-density lipoprotein (VLDL) has been metabolized by lipoprotein lipase, VLDL remnants in the form of intermediate- ... IDL = intermediate-density lipoprotein; LDL = low-density lipoprotein; VLDL = very low-density lipoprotein. ...

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

And so, I, in fact, characterized the enzyme as a lipoprotein lipase. A lipase is something that hydrolyzes lipids. And this ... So the first thing I did the minute I got out of that field, which became very clinical, of lipoprotein lipase showing that it ... The first work on lipoprotein lipase, I was doing all the work. By the time we were studying myosin, Tom Pollard, Bob Weihing ... But so it was a lipoprotein lipase. And that was the first thing I worked on here. ...

https://history.nih.gov/display/history/Korn%2C+Edward+2019

Lipoprotein lipase is a very important enzyme in lipid metabolism. Found on many tissues in the body its main function is to ... 45 minutes after a meal would reveal high levels of triglycerides due to lack of function of adipose tissue lipoprotein lipase ... Increased beta-oxidation due to increased activity of hormone sensitive lipase with subsequent increase in ketone bodies in ... Some of the apoproteins have very important functions in lipoprotein metabolism. Which of the following apoproteins is an ...

https://www.proprofs.com/quiz-school/story.php?title=academic-success-week-07-lipid-metabolism-systembased-practice

... heparan sulfate mimetic Muparfostat aggravates steatohepatitis in obese mice due to its binding affinity to lipoprotein lipase ...

https://pubmed.ncbi.nlm.nih.gov/?cmd=Search&term=Ya-Ting%20Zhu

Familial lipoprotein lipase deficiency is a rare genetic disorder is which a person lacks the enzyme lipoprotein lipase, a protein needed to break down fat molecules. (nih.gov)
Familial lipoprotein lipase deficiency is caused by changes in the LPL gene. (nih.gov)
When Do Symptoms of Familial lipoprotein lipase deficiency Begin? (nih.gov)
Familial lipoprotein lipase deficiency is a genetic disease, which means that it is caused by one or more genes not working correctly. (nih.gov)
Familial lipoprotein lipase deficiency is caused by a defective gene that is passed down through families. (nih.gov)
Risk factors include a family history of lipoprotein lipase deficiency. (nih.gov)
Pancreatitis that is related to lipoprotein lipase deficiency responds to treatments for that disorder. (nih.gov)
Call your provider for screening if someone in your family has lipoprotein lipase deficiency. (nih.gov)
Familial lipoprotein lipase deficiency is an inherited condition that disrupts the normal breakdown of fats in the body, resulting in an increase of certain kinds of fats. (nih.gov)
People with familial lipoprotein lipase deficiency typically develop signs and symptoms before age 10, with one-quarter showing symptoms by age 1. (nih.gov)
Approximately half of individuals with familial lipoprotein lipase deficiency develop small yellow deposits of fat under the skin called eruptive xanthomas. (nih.gov)
The blood of people with familial lipoprotein lipase deficiency can have a milky appearance due to its high fat content. (nih.gov)
In people with familial lipoprotein lipase deficiency, increased fat levels can also cause neurological features, such as depression , memory loss, and mild intellectual decline (dementia). (nih.gov)
Mutations in the LPL gene cause familial lipoprotein lipase deficiency. (nih.gov)
Mutations that cause familial lipoprotein lipase deficiency lead to a reduction or elimination of lipoprotein lipase activity, which prevents the enzyme from effectively breaking down triglycerides. (nih.gov)
As a result, triglycerides attached to lipoproteins build up in the blood and tissues, leading to the signs and symptoms of familial lipoprotein lipase deficiency. (nih.gov)
Familial lipoprotein lipase (LPL) deficiency usually presents in childhood and is characterized by very severe hypertriglyceridemia with episodes of abdominal pain, recurrent acute pancreatitis, eruptive cutaneous xanthomata, and hepatosplenomegaly. (nih.gov)

This enzyme helps break down fats called triglycerides, which are carried by molecules called lipoproteins . (nih.gov)
Lipoprotein lipase (LPL) is a key enzyme of lipid metabolism that hydrolyses triglycerides, providing free fatty acids for cells and affecting the maturation of circulating lipoproteins. (inrae.fr)
LPL is next bound by glycosylphosphatidylinositol-anchored high-density lipoprotein-binding protein 1 (GPIHBP1) and transported into the capillary, where it acts on chylomicrons and very-low-density lipoproteins (VLDLs) to hydrolyze packaged triglycerides and release FFAs. (inrae.fr)
High levels of triglycerides (TG) and triglyceride -rich lipoproteins (TGRLs) confer a residual risk of cardiovascular disease after optimal low-density lipoprotein cholesterol (LDL-C)-lowering therapy . (bvsalud.org)
In this paper, we propose that this congestion predisposes the chylomicron triglycerides to hydrolysis by lipoprotein lipase (LPL). (frontiersin.org)
This is the enzyme lipoprotein lipase, which breaks down triglycerides (fats). (medicalnewstoday.com)
Fenofibric acid, the active metabolite of fenofibrate, produces reductions in total cholesterol, LDL cholesterol, apolipoprotein B, total triglycerides and triglyceride rich lipoprotein (VLDL) in treated patients. (nih.gov)
the triglycerides are subsequently transported throughout the circulation by triglyceride-rich lipoproteins. (medscape.com)

Human LPL is a member of a superfamily of lipases that includes hepatic lipase and pancreatic lipase. (nih.gov)
25. Lipoprotein lipase and hepatic lipase: the role of asparagine-linked glycosylation in the expression of a functional enzyme. (nih.gov)
40. Domain exchange: characterization of a chimeric lipase of hepatic lipase and lipoprotein lipase. (nih.gov)
Pregnancy effect on serum lipids.12 During pregnancy, there is an is associated with significant change in the functions of increase in the hepatic lipase activity and decrease in the normal liver. (who.int)

The lipolytic processing of triglyceride-rich lipoproteins (TRLs) by lipoprotein lipase (LPL) is crucial for the delivery of dietary lipids to the heart, skeletal muscle, and adipose tissue. (inrae.fr)
Valimaki M, Maass L, Harno K, Nikkila EA "Lipoprotein lipids and apoproteins during beta-blocker administration: comparison of penbutolol and atenolol. (drugs.com)
Effects of pindolol and metoprolol on plasma lipids and lipoproteins. (drugs.com)
Terent A, Ribacke M, Carlson LA "Long-term effect of pindolol on lipids and lipoproteins in men with newly diagnosed hypertension. (drugs.com)
Effects of pindolol on serum lipids, apolipoproteins, and lipoproteins in patients with mild to moderate essential hypertension. (drugs.com)
In clinical chemistry, over the last decade however, lipids have become associated with lipoprotein metabolism and atherosclerosis. (randox.com)

Lipoprotein lipase (LPL) is a key regulator for TGs that hydrolyzes TGs to glycerol and free fatty acids in lipoprotein particles for lipid storage and consumption in peripheral organs. (bvsalud.org)
24. Lipoprotein lipase with a defect in lipid interface recognition in a case with type I hyperlipidaemia. (nih.gov)
27. Apolipoprotein C-II39-62 activates lipoprotein lipase by direct lipid-independent binding. (nih.gov)
31. Effect of lipid composition on lipoprotein lipase activity measured by a continuous fluorescence assay: effect of cholesterol supports an interfacial surface penetration model. (nih.gov)
33. Apolipoproteins C-I and C-III inhibit lipoprotein lipase activity by displacement of the enzyme from lipid droplets. (nih.gov)
Lipid profile results showed that TG was significantly lipoproteins (LDLs) and increased triglyceride (TG) lower in the control group than in pregnant women. (who.int)
Lipoprotein lipase -- An enzyme crucial to blood lipid metabolism. (nih.gov)
Effect of metoprolol and pindolol monotherapy on plasma lipid- and lipoprotein-cholesterol levels (including the HDL subclasses) in mild hypertensive males and females. (drugs.com)
Cholesterol measurements are used in the diagnosis and treatments of lipid lipoprotein metabolism disorders. (randox.com)
Oxidised low-density lipoprotein concentration-early marker of an altered lipid metabolism in young women with PCOS. (randox.com)

Detects human Lipoprotein Lipase/LPL in direct ELISAs and less than 1% cross-reactivity with recombinant human (rh) LIPG, rhLIPI, and rhPNLIPRP1 is observed. (rndsystems.com)
Detection of Human Lipoprotein Lipase/LPL by Western Blot. (rndsystems.com)
Lipoprotein Lipase/LPL was detected in immersion fixed SH-SY5Y human neuroblastoma cell line using Goat Anti-Human Lipoprotein Lipase/LPL Antigen Affinity-purified Polyclonal Antibody (Catalog # AF7197) at 10 µg/mL for 3 hours at room temperature. (rndsystems.com)
22. Construction and functional characterization of recombinant fusion proteins of human lipoprotein lipase and apolipoprotein CII. (nih.gov)
26. Structure-function analysis of D9N and N291S mutations in human lipoprotein lipase using molecular modelling. (nih.gov)
29. Effects of substitutions of glycine and asparagine for serine132 on activity and binding of human lipoprotein lipase to very low density lipoproteins. (nih.gov)
37. Mutagenesis in four candidate heparin binding regions (residues 279-282, 291-304, 390-393, and 439-448) and identification of residues affecting heparin binding of human lipoprotein lipase. (nih.gov)

28. Post-heparin plasma hepatic triacylglycerol lipase-catalyzed hydrolysis of tributyrin. (nih.gov)
35. Severely impaired activity of lipoprotein lipase Arg243His is partially ameliorated by emulsifying phospholipids in in vitro triolein hydrolysis analysis. (nih.gov)
39. Preparation of chylomicrons and VLDL with monoacid-rich triacylglycerol and characterization of kinetic parameters in lipoprotein lipase-mediated hydrolysis in chickens. (nih.gov)
It was out of this creative, heady atmosphere that Dr. Korn began his research, first in the lab of Chris Anfinsen working on the hydrolysis of lipoproteins. (nih.gov)

Glycosylphosphatidylinositol-anchored high density lipoprotein-binding protein 1 (GPIHBP1), the protein that shuttles LPL to the capillary lumen, is essential for plasma triglyceride metabolism. (nih.gov)

Description: A sandwich quantitative ELISA assay kit for detection of Mouse Lipase, Lipoprotein (LIPD) in samples from serum, plasma, tissue homogenates, cell lysates, cell culture supernates or other biological fluids. (lscwarsaw.com)
Description: This is Double-antibody Sandwich Enzyme-linked immunosorbent assay for detection of Human Lipase, Lipoprotein (LIPD) in serum, plasma, tissue homogenates, cell lysates and other biological fluids. (lscwarsaw.com)
Description: Enzyme-linked immunosorbent assay based on the Double-antibody Sandwich method for detection of Human Lipase, Lipoprotein (LIPD) in samples from serum, plasma, tissue homogenates, cell lysates and other biological fluids with no significant corss-reactivity with analogues from other species. (lscwarsaw.com)
Rossner S, Weiner L "Atenolol and metoprolol: comparison of effects on blood pressure and serum lipoproteins, and side effects. (drugs.com)
Darga LL, Hakim MJ, Lucas CP, Franklin BA "Comparison of the effects of guanadrel sulfate and propranolol on blood pressure, functional capacity, serum lipoproteins and glucose in systemic hypertension. (drugs.com)
Carlson LA, Ribacke M, Terent A "A long-term study on the effect of pindolol on serum lipoproteins: a preliminary report. (drugs.com)
Effect of nandrolone decanoate on serum lipoprotein (a) and its isoforms in hemodialysis patients. (randox.com)
Níveis Plasmàticos Elevados de Lipoproteína(a) Correlacionados com a Gravidade da Doenca Arterial Coronariana em Pacientes Submetidos à Angiografia (Increased Serum Levels of Lipoprotein(a) Correlated with the Severity of Coronary Artery Disease in Patients Submitted to Angiography. (randox.com)

These lipases are characterized by extensive homology, both at the level of the gene and the mature protein, suggesting that they have a common evolutionary origin. (nih.gov)
Endothelial lipase (encoded by the LIPG gene) regulates the circulating level of high density lipoprotein cholesterol (HDL-C). It can also form a molecular bridge between endothelial cells and lipoproteins or circulating macrophages through interaction with heparan sulfate proteoglycans. (inrae.fr)
lipoprotein lipase]Product Gene. (biocheminfo.org)

Since dietary fat is absorbed by the enterocytes and transported to the circulation in the forms of chylomicrons and very low density lipoproteins (VLDLs), it is crucial to understand how these lipoproteins are different between men and women. (frontiersin.org)

VLDL = very low-density lipoprotein. (medscape.com)

A variety of studies have demonstrated that elevated levels of total cholesterol (total-C), low density lipoprotein cholesterol (LDL-C), and apolipoprotein B (apo B), an LDL membrane complex, are associated with human atherosclerosis. (nih.gov)
Similarly, decreased levels of high density lipoprotein cholesterol (HDL-C) and its transport complex, apolipoprotein A (apo AI and apo AII) are associated with the development of atherosclerosis. (nih.gov)

Through this mechanism, fenofibrate increases lipolysis and elimination of triglyceride-rich particles from plasma by activating lipoprotein lipase and reducing production of apoproteins C-III (an inhibitor of lipoprotein lipase activity). (nih.gov)
Hyperlipoproteinemia is a metabolic disorder characterized by abnormally elevated concentrations of specific lipoprotein particles in the plasma. (medscape.com)

It hydrolyzes, or breaks down, lipoprotein triacylglycerols. (nih.gov)

This nonenzymatic action can increase cellular lipoprotein uptake and monocyte adhesion and contribute to atherosclerosis. (inrae.fr)

PVDF membrane was probed with 1 µg/mL of Goat Anti-Human/Mouse Lipoprotein Lipase/LPL Antigen Affinity-purified Polyclonal Antibody (Catalog # AF7197) followed by HRP-conjugated Anti-Goat IgG Secondary Antibody (Catalog # HAF017 ). (rndsystems.com)
Lipoprotein Lipase/LPL was detected in immersion fixed paraffin-embedded sections of human heart using Goat Anti-Human/Mouse Lipoprotein Lipase/LPL Antigen Affinity-purified Polyclonal Antibody (Catalog # AF7197) at 3 µg/mL for 1 hour at room temperature followed by incubation with the Anti-Goat IgG VisUCyte™ HRP Polymer Antibody (Catalog # VC004 ). (rndsystems.com)
38. Identification of the epitope of a monoclonal antibody that inhibits heparin binding of lipoprotein lipase: new evidence for a carboxyl-terminal heparin-binding domain. (nih.gov)

Lipoprotein Lipase: Is It a Magic Target for the Treatment of Hypertriglyceridemia. (bvsalud.org)
Determining which lipoprotein abnormality is the cause of hypertriglyceridemia is less straightforward. (medscape.com)

The binding of LPL to glycosylphosphatidylinositol-anchored high-density lipoprotein-binding protein 1 protects against LPL unfolding. (inrae.fr)
Omega-3 fatty acids and fibrates are used to reduce TG levels, but many patients still have high TG and TGRL levels combined with low high-density lipoprotein concentration that need to be ideally treated. (bvsalud.org)
In addition, treatment with fenofibrate results in increases in high density lipoprotein (HDL) and apoproteins apo AI and apo AII. (nih.gov)

Genest J, Libby P. Lipoprotein disorders and cardiovascular disease. (nih.gov)

Lipoprotein lipase: recent contributions from molecular biology. (nih.gov)

The heparan sulfate mimetic Muparfostat aggravates steatohepatitis in obese mice due to its binding affinity to lipoprotein lipase. (nih.gov)

Cardiac-specific VEGFB overexpression minimizes lipoprotein lipase task and increases insulin actions in rat center. (topoisomerasesignaling.com)

This test looks for lipoprotein lipase activity in your blood. (nih.gov)
Because of a decrease in the activity of TG was highest in first trimester pregnancy and least lipoprotein lipase, very-LDL remains in the plasma for in the control group. (who.int)
Although the precise mechanisms un- lipoprotein lipase activity.12. (who.int)

Expression of lipoprotein lipase 1, carnitine palmitoyl transferase 1b, and 3-hydroxyacyl-CoA dehydrogenase was increased in Tg-Prkag3 225Q mice, with opposing effects in Prkag3 −/− mice after exercise. (diabetesjournals.org)

36. Alteration of chain length selectivity of a Rhizopus delemar lipase through site-directed mutagenesis. (nih.gov)

A specific band was detected for Lipoprotein Lipase/LPL at approximately 55 kDa (as indicated). (rndsystems.com)

21. The structure of helical lipoprotein lipase reveals an unexpected twist in lipase storage. (nih.gov)
It blocks fat storage (the lipoprotein lipase enzyme) and keeps fat from returning post cut. (ironmagazine.com)

People with this condition lack an enzyme called lipoprotein lipase. (nih.gov)

publish that the intrinsic instability of the hydrolase domain of lipoprotein lipase facilitates its inactivation by ANGPTL4-catalyzed unfolding. (inrae.fr)
32. Site-directed mutagenesis of a putative heparin binding domain of avian lipoprotein lipase. (nih.gov)
34. Lipoprotein lipase domain function. (nih.gov)

Anatomy15

Organisms10

Diseases20

Chemicals and Drugs89

Analytical, Diagnostic and Therapeutic Techniques and Equipment14

Psychiatry and Psychology1

Phenomena and Processes32

Technology, Industry, Agriculture3

Information Science3

Health Care1

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

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

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)

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

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

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

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

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

Lipase

Lipoproteins

Lipoproteins, LDL

Lipoproteins, VLDL

Lipoproteins, HDL

Hyperlipoproteinemia Type I

Triglycerides

Apolipoprotein C-II

Lipoprotein(a)

Chylomicrons

Triolein

Heparin

Apolipoproteins C

Apolipoproteins

Receptors, Lipoprotein

Lipolysis

Adipose Tissue

Cholesterol

Lipids

Hypertriglyceridemia

Apolipoproteins B

Receptors, LDL

Cholesterol, HDL

Lipoproteins, IDL

Lipoprotein Lipase Activators

Liver

Apolipoproteins E

Lipid Metabolism

Lipoproteins, HDL2

Lipoproteins, HDL3

Cholesterol Esters

Hyperlipoproteinemias

Sterol Esterase

Angiopoietins

Low Density Lipoprotein Receptor-Related Protein-1

Cholesterol, LDL

Monoacylglycerol Lipases

Hyperlipidemias

Apolipoprotein C-III

Apolipoproteins A

Milk

Fatty Acids, Nonesterified

Cholesterol, VLDL

Dietary Fats

Apolipoprotein B-100

Heparin Lyase

Fatty Acids

Kinetics

Fasting

Arteriosclerosis

Hyperlipoproteinemia Type IV

Molecular Sequence Data

Emulsions

Hyperlipidemia, Familial Combined

Apolipoprotein A-II

Fat Emulsions, Intravenous

Hydrolysis

Cells, Cultured

RNA, Messenger

Apolipoprotein B-48

Cattle

Cholesterol Ester Transfer Proteins

Macrophages

Colipases

Ultracentrifugation

Insulin

Hypercholesterolemia

Phospholipids

Carrier Proteins

Base Sequence

Adipocytes

Amino Acid Sequence

Lipid Mobilization

Hyperlipoproteinemia Type III

Phosphatidylcholine-Sterol O-Acyltransferase

Cholesterol, Dietary

Myocardium

Hyperlipoproteinemia Type V

Rats, Inbred Strains