Chylomicron Remnants
Metabolic products of chylomicron particles in which TRIGLYCERIDES have been selectively removed by the LIPOPROTEIN LIPASE. These remnants carry dietary lipids in the blood and are cholesterol-rich. Their interactions with MACROPHAGES; ENDOTHELIAL CELLS; and SMOOTH MUSCLE CELLS in the artery wall can lead to ATHEROSCLEROSIS.
Chylomicrons
Apolipoprotein B-48
A 241-kDa protein synthesized only in the INTESTINES. It serves as a structural protein of CHYLOMICRONS. Its exclusive association with chylomicron particles provides an indicator of intestinally derived lipoproteins in circulation. Apo B-48 is a shortened form of apo B-100 and lacks the LDL-receptor region.
Lipoproteins, VLDL
A class of lipoproteins of very light (0.93-1.006 g/ml) large size (30-80 nm) particles with a core composed mainly of TRIGLYCERIDES and a surface monolayer of PHOSPHOLIPIDS and CHOLESTEROL into which are imbedded the apolipoproteins B, E, and C. VLDL facilitates the transport of endogenously made triglycerides to extrahepatic tissues. As triglycerides and Apo C are removed, VLDL is converted to INTERMEDIATE-DENSITY LIPOPROTEINS, then to LOW-DENSITY LIPOPROTEINS from which cholesterol is delivered to the extrahepatic tissues.
Receptors, LDL
Receptors on the plasma membrane of nonhepatic cells that specifically bind LDL. The receptors are localized in specialized regions called coated pits. Hypercholesteremia is caused by an allelic genetic defect of three types: 1, receptors do not bind to LDL; 2, there is reduced binding of LDL; and 3, there is normal binding but no internalization of LDL. In consequence, entry of cholesterol esters into the cell is impaired and the intracellular feedback by cholesterol on 3-hydroxy-3-methylglutaryl CoA reductase is lacking.
Lipoproteins
Lipid-protein complexes involved in the transportation and metabolism of lipids in the body. They are spherical particles consisting of a hydrophobic core of TRIGLYCERIDES and CHOLESTEROL ESTERS surrounded by a layer of hydrophilic free CHOLESTEROL; PHOSPHOLIPIDS; and APOLIPOPROTEINS. Lipoproteins are classified by their varying buoyant density and sizes.
Vitamin A
Retinol and derivatives of retinol that play an essential role in metabolic functioning of the retina, the growth of and differentiation of epithelial tissue, the growth of bone, reproduction, and the immune response. Dietary vitamin A is derived from a variety of CAROTENOIDS found in plants. It is enriched in the liver, egg yolks, and the fat component of dairy products.
Apolipoproteins E
A class of protein components which can be found in several lipoproteins including HIGH-DENSITY LIPOPROTEINS; VERY-LOW-DENSITY LIPOPROTEINS; and CHYLOMICRONS. Synthesized in most organs, Apo E is important in the global transport of lipids and cholesterol throughout the body. Apo E is also a ligand for LDL receptors (RECEPTORS, LDL) that mediates the binding, internalization, and catabolism of lipoprotein particles in cells. There are several allelic isoforms (such as E2, E3, and E4). Deficiency or defects in Apo E are causes of HYPERLIPOPROTEINEMIA TYPE III.
Liver
Low Density Lipoprotein Receptor-Related Protein-1
Fetuins
Apolipoproteins
Protein components on the surface of LIPOPROTEINS. They form a layer surrounding the hydrophobic lipid core. There are several classes of apolipoproteins with each playing a different role in lipid transport and LIPID METABOLISM. These proteins are synthesized mainly in the LIVER and the INTESTINES.
Cholesterol
Emulsions
Colloids formed by the combination of two immiscible liquids such as oil and water. Lipid-in-water emulsions are usually liquid, like milk or lotion. Water-in-lipid emulsions tend to be creams. The formation of emulsions may be aided by amphiphatic molecules that surround one component of the system to form MICELLES.
Lipase
Apolipoproteins B
Major structural proteins of triacylglycerol-rich LIPOPROTEINS. There are two forms, apolipoprotein B-100 and apolipoprotein B-48, both derived from a single gene. ApoB-100 expressed in the liver is found in low-density lipoproteins (LIPOPROTEINS, LDL; LIPOPROTEINS, VLDL). ApoB-48 expressed in the intestine is found in CHYLOMICRONS. They are important in the biosynthesis, transport, and metabolism of triacylglycerol-rich lipoproteins. Plasma Apo-B levels are high in atherosclerotic patients but non-detectable in ABETALIPOPROTEINEMIA.
Cholesterol Esters
Lipoprotein Lipase
An enzyme of the hydrolase class that catalyzes the reaction of triacylglycerol and water to yield diacylglycerol and a fatty acid anion. The enzyme hydrolyzes triacylglycerols in chylomicrons, very-low-density lipoproteins, low-density lipoproteins, and diacylglycerols. It occurs on capillary endothelial surfaces, especially in mammary, muscle, and adipose tissue. Genetic deficiency of the enzyme causes familial hyperlipoproteinemia Type I. (Dorland, 27th ed) EC 3.1.1.34.
Receptors, Lipoprotein
Cell surface proteins that bind lipoproteins with high affinity. Lipoprotein receptors in the liver and peripheral tissues mediate the regulation of plasma and cellular cholesterol metabolism and concentration. The receptors generally recognize the apolipoproteins of the lipoprotein complex, and binding is often a trigger for endocytosis.
Lactoferrin
An iron-binding protein that was originally characterized as a milk protein. It is widely distributed in secretory fluids and is found in the neutrophilic granules of LEUKOCYTES. The N-terminal part of lactoferrin possesses a serine protease which functions to inactivate the TYPE III SECRETION SYSTEM used by bacteria to export virulence proteins for host cell invasion.
alpha-Macroglobulins
Glycoproteins with a molecular weight of approximately 620,000 to 680,000. Precipitation by electrophoresis is in the alpha region. They include alpha 1-macroglobulins and alpha 2-macroglobulins. These proteins exhibit trypsin-, chymotrypsin-, thrombin-, and plasmin-binding activity and function as hormonal transporters.
Chyle
Fetuin-B
Hyperlipoproteinemia Type IV
A hypertriglyceridemia disorder, often with autosomal dominant inheritance. It is characterized by the persistent elevations of plasma TRIGLYCERIDES, endogenously synthesized and contained predominantly in VERY-LOW-DENSITY LIPOPROTEINS (pre-beta lipoproteins). In contrast, the plasma CHOLESTEROL and PHOSPHOLIPIDS usually remain within normal limits.
Apolipoprotein C-I
A 6.6-kDa protein component of VERY-LOW-DENSITY LIPOPROTEINS; INTERMEDIATE-DENSITY LIPOPROTEINS; and HIGH-DENSITY LIPOPROTEINS. Apo C-I displaces APO E from lipoproteins, modulate their binding to receptors (RECEPTORS, LDL), and thereby decrease their clearance from plasma. Elevated Apo C-I levels are associated with HYPERLIPOPROTEINEMIA and ATHEROSCLEROSIS.
Apolipoprotein B-100
Dietary Fats
Lipoproteins, LDL
A class of lipoproteins of small size (18-25 nm) and light (1.019-1.063 g/ml) particles with a core composed mainly of CHOLESTEROL ESTERS and smaller amounts of TRIGLYCERIDES. The surface monolayer consists mostly of PHOSPHOLIPIDS, a single copy of APOLIPOPROTEIN B-100, and free cholesterol molecules. The main LDL function is to transport cholesterol and cholesterol esters to extrahepatic tissues.
LDL-Receptor Related Protein-Associated Protein
Lipolysis
The metabolic process of breaking down LIPIDS to release FREE FATTY ACIDS, the major oxidative fuel for the body. Lipolysis may involve dietary lipids in the DIGESTIVE TRACT, circulating lipids in the BLOOD, and stored lipids in the ADIPOSE TISSUE or the LIVER. A number of enzymes are involved in such lipid hydrolysis, such as LIPASE and LIPOPROTEIN LIPASE from various tissues.
Rats, Inbred Strains
Metabolic Clearance Rate
Iodine Radioisotopes
Asialoglycoproteins
Endogenous glycoproteins from which SIALIC ACID has been removed by the action of sialidases. They bind tightly to the ASIALOGLYCOPROTEIN RECEPTOR which is located on hepatocyte plasma membranes. After internalization by adsorptive ENDOCYTOSIS they are delivered to LYSOSOMES for degradation. Therefore receptor-mediated clearance of asialoglycoproteins is an important aspect of the turnover of plasma glycoproteins. They are elevated in serum of patients with HEPATIC CIRRHOSIS or HEPATITIS.
Hyperlipoproteinemias
Lipids
A generic term for fats and lipoids, the alcohol-ether-soluble constituents of protoplasm, which are insoluble in water. They comprise the fats, fatty oils, essential oils, waxes, phospholipids, glycolipids, sulfolipids, aminolipids, chromolipids (lipochromes), and fatty acids. (Grant & Hackh's Chemical Dictionary, 5th ed)
Fish Oils
Lipid Metabolism
Ethinyl Estradiol
Lipoproteins, HDL
A class of lipoproteins of small size (4-13 nm) and dense (greater than 1.063 g/ml) particles. HDL lipoproteins, synthesized in the liver without a lipid core, accumulate cholesterol esters from peripheral tissues and transport them to the liver for re-utilization or elimination from the body (the reverse cholesterol transport). Their major protein component is APOLIPOPROTEIN A-I. HDL also shuttle APOLIPOPROTEINS C and APOLIPOPROTEINS E to and from triglyceride-rich lipoproteins during their catabolism. HDL plasma level has been inversely correlated with the risk of cardiovascular diseases.
Apolipoproteins C
A group of apolipoproteins that can readily exchange among the various classes of lipoproteins (HDL; VLDL; CHYLOMICRONS). After lipolysis of TRIGLYCERIDES on VLDL and chylomicrons, Apo-C proteins are normally transferred to HDL. The subtypes can modulate remnant binding to receptors, LECITHIN CHOLESTEROL ACYLTRANSFERASE, or LIPOPROTEIN LIPASE.
Phospholipids
Lipids containing one or more phosphate groups, particularly those derived from either glycerol (phosphoglycerides see GLYCEROPHOSPHOLIPIDS) or sphingosine (SPHINGOLIPIDS). They are polar lipids that are of great importance for the structure and function of cell membranes and are the most abundant of membrane lipids, although not stored in large amounts in the system.
Binding, Competitive
Rabbits
Carbon Radioisotopes
Receptors, Immunologic
Heparin
A highly acidic mucopolysaccharide formed of equal parts of sulfated D-glucosamine and D-glucuronic acid with sulfaminic bridges. The molecular weight ranges from six to twenty thousand. Heparin occurs in and is obtained from liver, lung, mast cells, etc., of vertebrates. Its function is unknown, but it is used to prevent blood clotting in vivo and vitro, in the form of many different salts.
Hydroxymethylglutaryl CoA Reductases
Cholesterol, VLDL
Cholesterol which is contained in or bound to very low density lipoproteins (VLDL). High circulating levels of VLDL cholesterol are found in HYPERLIPOPROTEINEMIA TYPE IIB. The cholesterol on the VLDL is eventually delivered by LOW-DENSITY LIPOPROTEINS to the tissues after the catabolism of VLDL to INTERMEDIATE-DENSITY LIPOPROTEINS, then to LDL.
Receptors, Cell Surface
Cell surface proteins that bind signalling molecules external to the cell with high affinity and convert this extracellular event into one or more intracellular signals that alter the behavior of the target cell (From Alberts, Molecular Biology of the Cell, 2nd ed, pp693-5). Cell surface receptors, unlike enzymes, do not chemically alter their ligands.
Fatty Acids, Omega-3
A group of fatty acids, often of marine origin, which have the first unsaturated bond in the third position from the omega carbon. These fatty acids are believed to reduce serum triglycerides, prevent insulin resistance, improve lipid profile, prolong bleeding times, reduce platelet counts, and decrease platelet adhesiveness.
Apolipoprotein C-II
A 9-kDa protein component of VERY-LOW-DENSITY LIPOPROTEINS. It contains a cofactor for LIPOPROTEIN LIPASE and activates several triacylglycerol lipases. The association of Apo C-II with plasma CHYLOMICRONS; VLDL, and HIGH-DENSITY LIPOPROTEINS is reversible and changes rapidly as a function of triglyceride metabolism. Clinically, Apo C-II deficiency is similar to lipoprotein lipase deficiency (HYPERLIPOPROTEINEMIA TYPE I) and is therefore called hyperlipoproteinemia type IB.
Fatty Acids
Endocytosis
Fatty Acids, Unsaturated
Biological Transport
Hyperlipoproteinemia Type II
Fatty Acids, Omega-6
alpha-Fetoproteins
Rats, Sprague-Dawley
Bile
Macrophages
The relatively long-lived phagocytic cell of mammalian tissues that are derived from blood MONOCYTES. Main types are PERITONEAL MACROPHAGES; ALVEOLAR MACROPHAGES; HISTIOCYTES; KUPFFER CELLS of the liver; and OSTEOCLASTS. They may further differentiate within chronic inflammatory lesions to EPITHELIOID CELLS or may fuse to form FOREIGN BODY GIANT CELLS or LANGHANS GIANT CELLS. (from The Dictionary of Cell Biology, Lackie and Dow, 3rd ed.)
Poloxalene
Butter
Microscopy, Electron
Microscopy using an electron beam, instead of light, to visualize the sample, thereby allowing much greater magnification. The interactions of ELECTRONS with specimens are used to provide information about the fine structure of that specimen. In TRANSMISSION ELECTRON MICROSCOPY the reactions of the electrons that are transmitted through the specimen are imaged. In SCANNING ELECTRON MICROSCOPY an electron beam falls at a non-normal angle on the specimen and the image is derived from the reactions occurring above the plane of the specimen.
Cells, Cultured
Hyperlipoproteinemia Type III
An autosomal recessively inherited disorder characterized by the accumulation of intermediate-density lipoprotein (IDL or broad-beta-lipoprotein). IDL has a CHOLESTEROL to TRIGLYCERIDES ratio greater than that of VERY-LOW-DENSITY LIPOPROTEINS. This disorder is due to mutation of APOLIPOPROTEINS E, a receptor-binding component of VLDL and CHYLOMICRONS, resulting in their reduced clearance and high plasma levels of both cholesterol and triglycerides.
Electrophoresis, Polyacrylamide Gel
Hepatocytes
Rats, Wistar
Arteriosclerosis
Poloxamer
A nonionic polyoxyethylene-polyoxypropylene block co-polymer with the general formula HO(C2H4O)a(-C3H6O)b(C2H4O)aH. It is available in different grades which vary from liquids to solids. It is used as an emulsifying agent, solubilizing agent, surfactant, and wetting agent for antibiotics. Poloxamer is also used in ointment and suppository bases and as a tablet binder or coater. (Martindale The Extra Pharmacopoeia, 31st ed)
Hypercholesterolemia
Biological Transport, Active
Carrier Proteins
Cholesterol, HDL
Antibodies
Dogs
Apoproteins
Cell Membrane
Oleic Acids
Mice, Knockout
Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.
Plasma levels of remnant particles are determined in part by variation in the APOC3 gene insulin response element and the APOCI-APOE cluster. (1/40)
Remnant particles of triglyceride-rich lipoproteins (RLP) are known to be a strong predictor of atherogenicity. The serum concentrations of remnant-like particle triglyceride (RLPTG) and remnant-like particle cholesterol (RLPC) have been determined in a representative sample of the Czech MONICA study (n = 285). The relationship was investigated between remnant particle triglyceride/cholesterol concentrations and polymorphisms in the genes APOC3 (-482C-->T/3238C-->G), APOE (epsilon2/epsilon3/epsilon4), APOCI (-317-321ins), APOB (signal peptide), hepatic lipase (LIPE, -480C-->T), and lipoprotein lipase (LPL, S447X). Univariate analysis showed significant effects on RLPTG associated only with the APOE genotype (P = 0.009), the APOC3 -482C-->T genotype (P = 0.018), and the APOCI -317-321ins (P = 0.014) genotype and significant effects on RLPC with APOE (P = 0.01) and APOCI -317-321ins (P = 0.021). The raising effect of the APOE genotype for both remnant cholesterol and triglyceride was confined to the epsilon2/4 (n = 6) and varepsilon4/4 (n = 3) groups, and thus when the epsilon2/4 group was omitted in order to analyze by allele (epsilon2+/epsilon3+/epsilon4+), significance was lost (P = 0.6). There was strong linkage disequilibrium between the APOE and APOCI alleles (chi(2), P < 0.001) and a multivariate ANOVA of RLPTG with all three significantly associated variants as factors demonstrated that while the APOC3 -482C-->T effect was independent of the others (P = 0.003), the APOCI -317-321ins and APOE effects were not. This was also true for the APOCI -317-321ins and APOE effects on RLPC. To assess whether APOE-CI effects on RLPC were independent of their effects on total cholesterol and triglyceride levels, multiple linear regression was used. Using multiple linear regression, it appeared that the APOE-CI effects on RLPC were independent of their effects on plasma cholesterol, but the effects of APOC3 and APOE-CI on RLPTG could not be separated from their effects on plasma Tg levels. Further characterization of this remnant particle phenotype and its genetic determinants may lead to a better understanding of its metabolism and contribution to atherosclerosis. (+info)Transcriptional regulation of apolipoprotein C-III gene expression by the orphan nuclear receptor RORalpha. (2/40)
Triglyceride-rich remnant lipoproteins are considered as major risk factors contributing to the pathogenesis of atherosclerosis. Because apolipoprotein (apo) C-III is a major determinant of plasma triglyceride and remnant lipoprotein metabolism, it is important to understand how the expression of this gene is regulated. In the present study, we identified the orphan nuclear receptor RORalpha1 as a regulator of human and mouse apo C-III gene expression. Plasma triglyceride and apo C-III protein concentrations in staggerer (sg/sg) mice, homozygous for a deletion in the RORalpha gene, were significantly lower than in wild type littermates. The lowered plasma apo C-III levels were associated with reduced apo C-III mRNA levels in liver and intestine of sg/sg mice. Transient transfection experiments in human hepatoma HepG2, human colonic CaCO2, and rabbit kidney RK13 cells demonstrated that overexpression of the human RORalpha1 isoform specifically increases human apo C-III promoter activity, indicating that RORalpha1 enhances human apo C-III gene transcription. RORalpha1 response elements were mapped by promoter deletion analysis and gel shift experiments to two AGGTCA half-sites located at positions -83/-78 (within the C3P site) and -23/-18 (downstream of the TATA box) in the human apo C-III promoter, with the -23/-18 site exhibiting the highest binding affinity. Transfection of site-directed mutated constructs in HepG2 cells indicated that the RORalpha1 effect is predominantly mediated by the -23/-18 site. This site is conserved in the mouse apo C-III gene promoter. Moreover, RORalpha binds to the equivalent mouse site and activates constructs containing three copies of the mouse site cloned in front of an heterologous promoter. Taken together, our data identify RORalpha as a transcriptional regulator of apo C-III gene expression, providing a novel, physiological role for RORalpha1 in the regulation of genes controlling triglyceride metabolism. (+info)Chylomicron remnant metabolism in familial dyslipidemias studied with a remnant-like emulsion breath test. (3/40)
We have developed a stable isotope breath test for the assessment of chylomicron remnant metabolism and report the results from the breath test in human subjects selected for disorders of chylomicron or remnant metabolism. In type I hyperlipemia, the phenotype is extreme hypertriglyceridemia due to a lack of lipoprotein lipase activity, which causes the failure of remnant formation. The type III dyslipidemia phenotype is caused by the inefficient removal of chylomicron remnants from plasma, generally because of homozygosity for apolipoprotein E2 alleles. The breath test was predicted to be abnormal in type III hyperlipemia, whereas a priori in type I hyperlipemia defective remnant clearance was not anticipated. Subjects were injected with lipid emulsions prepared with a composition similar to normal chylomicron remnants. The emulsions contained cholesteryl ester incorporating the stable nonradioactive isotope (13)C in the fatty acid moiety. End exhalation breath was collected at intervals after intravenous injection of the remnant-like emulsions and analyzed for (13)C enrichment by isotope-ratio mass spectrometry. Compared with the group of normolipemic men, the fractional catabolic rate of remnants measured by the breath test was significantly decreased (P = 0.006) in subjects with type III dyslipidemia. In the group with type I hyperlipemia, the fractional catabolic rate was not different (P = 0.233) from the control group. Therefore, the underlying capacity for remnant catabolism was normal in this group of markedly hypertriglyceridemic subjects. By short-circuiting the step of lipolysis, the remnant-like emulsion breath test provides direct information about remnant clearance and metabolism, which should assist in investigations of postprandial lipid metabolism. (+info)LDL receptor-related protein mediates cell-surface clustering and hepatic sequestration of chylomicron remnants in LDLR-deficient mice. (4/40)
It has been proposed that in the liver, chylomicron remnants (lipoproteins carrying dietary lipid) may be sequestered before being internalized by hepatocytes. To study this, chylomicron remnants labeled with a fluorescent dye were perfused into isolated livers of LDL receptor-deficient (LDLR-deficient) mice (Ldlr(-/-)) and examined by confocal microscopy. In contrast to livers from normal mice, there was clustering of the chylomicron remnants on the cell surface in the space of DISSE: These remnant clusters colocalized with clusters of LDLR-related protein (LRP) and could be eliminated by low concentrations of receptor-associated protein, an inhibitor of LRP. When competed with ligands of heparan sulfate proteoglycans (HSPGs), the remnant clusters still appeared but were fewer in number, although syndecans (membrane HSPGs) colocalized with the remnant clusters. This suggests that the clustering of remnants is not dependent on syndecans but that the syndecans may modify the binding of remnants. These results establish that sequestration is a novel process, the clustering of remnants in the space of DISSE: The clustering involves remnants binding to the LRP, and this may be stabilized by binding with syndecans, eventually followed by endocytosis. (+info)Lipid synthesis in macrophages derived from the human cell line THP-1: modulation of the effects of native and oxidized chylomicron-remnant-like particles by oestrogen. (5/40)
The effects of native and oxidized chylomicron remnants on the synthesis of cholesteryl ester and triacylglycerol in macrophages, and the way that this is influenced by exposure of the cells to oestrogen, was investigated using the human monocyte cell line THP-1 and chylomicron-remnant-like particles containing human apolipoprotein E (CRLPs). Synthesis of the lipids was measured by the incorporation of [(3)H]oleate into cholesteryl ester and triacylglycerol. CRLPs (5-40 microgram of cholesterol/ml) containing either trilinolein or triolein as the triacylglycerol component caused a dose-dependent decrease in cholesteryl ester formation, while triacylglycerol production was unchanged. After oxidation of the CRLPs, the level of thiobarbituric acid-reactive substances was increased by 6.3-fold and 2.2-fold in particles containing trilinolein and triolein respectively. Furthermore, CRLPs containing oxidized trilinolein lost their ability to down-regulate cholesterol esterification, while CRLPs containing oxidized triolein did not. Both types of oxidized CRLPs decreased triacylglycerol synthesis. Treatment of the macrophages with 17beta-oestradiol caused increases of approx. 94% and 34% in the synthesis of cholesteryl ester and triacylglycerol respectively in the absence of CRLPs. The differences between control and oestrogen-treated cells were abolished, however, when CRLPs (40 microgram of cholesterol/ml) were added to the incubations. In addition, in contrast with their lack of effect in control cells, CRLPs containing oxidized trilinolein decreased cholesterol esterification in oestrogen-treated cells by approx. 48%. These findings with CRLPs suggest that chylomicron remnants have significant effects on cholesteryl ester and triacylglycerol synthesis in macrophages, which may be modulated both by the oxidation state of the particles and by oestrogen. (+info)Preliminary experience with a new stable isotope breath test for chylomicron remnant metabolism: a study in central obesity. (6/40)
We aimed to investigate the metabolism of chylomicron remnants in the postabsorptive state employing a new stable isotope breath test in centrally obese men without overt hyperlipidaemia. Groups of 12 centrally obese and 12 non-obese men of similar age and with similar plasma cholesterol and triacylglycerol (triglyceride) levels were studied. The catabolism of chylomicron remnants was measured using an intravenous injection of a remnant-like emulsion containing cholesteryl [(13)C]oleate. Isotopic enrichment of (13)CO(2) in breath was determined using isotope-ratio mass spectrometry, and a multi-compartmental model (SAAM II program) was used to estimate the fractional catabolic rate (FCR) of the chylomicron remnant-like particles. The plasma concentrations of low-density lipoprotein (LDL)-cholesterol, non-high-density lipoprotein (HDL)-cholesterol and insulin were significantly higher (P<0.05) in the obese than the control subjects. The obese subjects had significantly lower HDL-cholesterol (P<0.05) and, in particular, a decreased FCR of the remnant-like particles compared with lean subjects (0.061+/-0.014 and 0.201+/-0.048 pools/h respectively; P=0.016). In the obese group, the FCR of remnant-like particles was inversely associated with the waist/hip ratio, and with plasma triacylglycerol, cholesterol, LDL-cholesterol and non-HDL-cholesterol levels. In multiple regression analysis, the waist/hip ratio was the best predictor of the FCR of the emulsion. In conclusion, this new test suggests that postabsorptive chylomicron remnant catabolism is impaired in centrally obese subjects without overt hyperlipidaemia. This defect may be due to the degree of adiposity. (+info)Food restriction normalizes chylomicron remnant metabolism in murine models of obesity as assessed by a novel stable isotope breath test. (7/40)
Evidence is increasing that defective metabolism of postprandial remnants of triglyceride-rich lipoproteins contributes to atherogenesis. In obesity, postprandial lipemia is increased by mechanisms that are not currently established. In the present study, a recently developed (13)CO(2) breath test was used to assess the metabolism of chylomicron remnants (CR) in obese mice. Six murine obese models ob/ob, fat/fat, New Zealand Obese (NZO), db/db, gold thioglucose (GTG)-treated and agouti (A(y)) were studied. All obese mice were hyperphagic and their breath test metabolism was markedly impaired (P < 0.01) compared with control, nonobese mice. The breath test was also impaired (P < 0.01) in all obese mice except A(y) mice after 24-h food deprivation. However, after restriction to the food intake of paired control mice for 6 wk, the breath test in all obese mice improved to values of control, nonobese mice. The obese NZO, fat/fat and ob/ob mice had significant (P < 0.02) weight loss when food restricted, whereas A(y), GTG, and db/db mice did not. In all obese mice, plasma cholesterol levels decreased (P < 0.02) after the 6-wk period of food restriction. Plasma triglyceride levels significantly decreased (P < 0.02) in NZO, GTG and db/db mice, but not in other obese mice. Plasma glucose levels were significantly decreased (P < 0.02) after the 6-wk period in the obese mice except for the A(y) and NZO mice; levels were greater in food-restricted db/db mice. Although some of the obese models such as db/db were diabetic, our data suggest that the defective breath test was independent of diabetes because all obese and diabetic models responded similarly to food restriction. Impaired hepatic catabolism of CR was excluded as a cause of the abnormal breath tests. In summary, the impairment (P < 0.05) in remnant metabolism as assessed by the breath test in obese mice was corrected by food restriction, associated with improvements in plasma glucose, triglyceride and cholesterol levels. (+info)Effect of atorvastatin on chylomicron remnant metabolism in visceral obesity: a study employing a new stable isotope breath test. (8/40)
Elevated plasma concentration of chylomicron remnants may be causally related to atherosclerosis in obesity. We examined the effect of atorvastatin on chylomicron remnant metabolism in 25 obese men with dyslipidaemia. A remnant-like emulsion labeled with cholesteryl [(13)C]oleate was injected intravenously into patients; the fractional catabolic rate (FCR) of the remnant-like emulsion was determined by measurement of (13)CO(2) in the breath and analyzed using compartmental modelling. Compared with placebo, atorvastatin significantly decreased the plasma concentrations of total cholesterol, triglycerides, LDL cholesterol, apolipoprotein B (apoB), and lathosterol (P < 0.001). ApoB-48 and remnant-like particle-cholesterol (RLP-C) both decreased significantly by 23% (P = 0.002) and 33% (P = 0.045), respectively. The FCR of the remnant-like emulsion increased significantly from 0.054 +/- 0.008 to 0.090 +/- 0.010 pools/h (P = 0.002). The decrease in RLP-C was associated with the decrease in plasma triglycerides (r = 0.750, P = 0.003). Furthermore, the change in FCR of remnant-like emulsions was inversely associated with the change in LDL-C (r = -0.575, P = 0.040), suggesting removal of LDL and chylomicron remnants by similar hepatic receptor pathways. We conclude that in obese subjects, inhibition of cholesterol synthesis with atorvastatin decreases the plasma concentrations of both LDL-C and triglyceride-rich remnants and that this may be partially due to an enhancement in hepatic clearance of these lipoproteins. (+info)
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Remnant lipoproteins induce proatherothrombogenic molecules in endothelial cells through a redox-sensitive mechanism. -...
Penile Implants Grafts or Remnants Reconstructive Micro Surgery Rio de Janeiro.
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remnant facts, information, pictures | Encyclopedia.com articles about remnant
Study of the Absorption of Vitamin E Water-soluble Form (Pegylated) in the Familial Hypocholesterolemia With Chylomicron...
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Lipoprotein
The hydrolyzed chylomicrons are now called chylomicron remnants. The chylomicron remnants continue circulating the bloodstream ... This interaction causes the endocytosis of the chylomicron remnants, which are subsequently hydrolyzed within lysosomes. ... The chylomicron at this stage is then considered mature. Via apolipoprotein C-II, mature chylomicrons activate lipoprotein ... The hydrolyzed VLDL particles are now called VLDL remnants or intermediate-density lipoproteins (IDLs). VLDL remnants can ...
Chylomicron
... becomes a chylomicron remnant, now only 30-50 nm. ApoB48 and APOE are important to identify the chylomicron remnant in the ... chylomicron remnants are formed and are taken up by the liver, thereby also transferring dietary fat to the liver. Chylomicrons ... to the nascent chylomicron and, thus, converts it to a mature chylomicron (often referred to simply as "chylomicron"). APOC2 is ... The three stages of the chylomicron are nascent, mature, and remnant. Triglycerides are emulsified by bile and hydrolyzed by ...
LDL-receptor-related protein-associated protein
Willnow TE, Sheng Z, Ishibashi S, Herz J (1994). "Inhibition of hepatic chylomicron remnant uptake by gene transfer of a ...
Hepatocyte
The liver receives many lipids from the systemic circulation and metabolizes chylomicron remnants. It also synthesizes ...
LDL receptor
The receptor also recognizes apolipoprotein E (ApoE) which is found in chylomicron remnants and IDL. In humans, the LDL ... their remnants-i.e. intermediate-density lipoprotein (IDL), and LDL particles. ...
Apolipoprotein B
After most of the lipids in the chylomicron have been absorbed, ApoB48 returns to the liver as part of the chylomicron remnant ... Intestinal proteins containing ApoB48 are metabolized to chylomicron remnant particles which are taken up by remnant receptors ... assembly and secretion of chylomicrons. These chylomicrons transport dietary lipids to tissues while the remaining chylomicrons ... Apolipoprotein B is the primary apolipoprotein of chylomicrons, VLDL, Lp(a), IDL, and LDL particles (LDL-commonly known as "bad ...
Remnant cholesterol
However, remnant cholesterol is primarily chylomicron and VLDL, and each remnant particle contains about 40 times more ... Remnant cholesterol is associated with chronic inflammation, whereas LDL cholesterol is not. Chylomicron remnant Lipid profile ... Remnant cholesterol, also known as remnant lipoprotein, is a very atherogenic lipoprotein composed primarily of very low- ... Remnant cholesterol has about twice the association with ischemic heart disease as LDL cholesterol. Although remnant ...
LRP1
In the liver LRP1 is important for the removal of atherogenic lipoproteins (Chylomicron remnants, VLDL) and other ... inactivation of hepatic LRP gene by cre-mediated recombination confirms role of LRP in clearance of chylomicron remnants". The ... Chylomicron, Circumsporozoite protein, Collectin, Complement C3, CTGF, DLG4, Elastase, Factor IXa, Factor VIIa, Fibronectin, ...
Hyperlipidemia
The receptor defect causes levels of chylomicron remnants and IDL to be higher than normal in the blood stream. The receptor ... which is normally required for clearance of chylomicron remnants and IDL from the circulation. ... Remnant hyperlipidemia occurs as a result of abnormal function of the ApoE receptor, ... resulting in elevated chylomicrons, the particles that transfer fatty acids from the digestive tract to the liver Familial ...
Cholesterol
Unused cholesterol remains in more cholesterol-rich chylomicron remnants, and taken up from here to the bloodstream by the ... Chylomicrons carry fats from the intestine to muscle and other tissues in need of fatty acids for energy or fat production. ... Chylomicrons, the least dense cholesterol transport molecules, contain apolipoprotein B-48, apolipoprotein C, and ... In order of increasing density, they are chylomicrons, very-low-density lipoprotein (VLDL), intermediate-density lipoprotein ( ...
Liver sinusoidal endothelial cell
The size of circulating chylomicrons is gradually reduced to chylomicron remnants by lipoprotein lipase on endothelial cells of ... When the chylomicron remnants become small enough (30-80 nm), they pass through the LSEC fenestrations, leading to their ... Chylomicrons produced by the intestinal epithelial cells from dietary lipids have diameter up to 1000 nm which prevents them ... Naito, M; Wisse, E (10 July 1978). "Filtration effect of endothelial fenestrations on chylomicron transport in neonatal rat ...
Diacylglycerol oil
Dynamics of post-prandial remnant-like lipoprotein particles in serum after loading of diacylglycerols. Clin Chim Acta. 2001; ... Double-blind controlled study on the effects of dietary diacylglycerol on post-prandial serum and chylomicron triacylglycerol ...
Apolipoprotein E
In the circulation, it is present as part of several classes of lipoprotein particles, including chylomicron remnants, VLDL, ... Mahley RW, Ji ZS (January 1999). "Remnant lipoprotein metabolism: key pathways involving cell-surface heparan sulfate ... in which increased plasma cholesterol and triglycerides are the consequence of impaired clearance of chylomicron, VLDL and LDL ...
Cholesterol absorption inhibitor
By reducing the cholesterol content in chylomicrons and chylomicron remnants, cholesterol absorption inhibitors effectively ... These chylomicrons are then secreted into the lymphatics and circulated to the liver. These cholesterol particles are then ... Once absorbed by the enterocyte, cholesterol is reassembled into intestinal lipoproteins called chylomicrons. ... thereby reducing the incorporation of cholesterol esters into chylomicron particles. ...
LRP5
... to increased plasma cholesterol levels on a high-fat diet because of the decreased hepatic clearance of chylomicron remnants. ...
Lacteal
... now referred to as a chylomicron remnant) can be taken up by the liver. From the liver, the fat released from chylomicron ... At this point, the fats are in the bloodstream in the form of chylomicrons. Once in the blood, chylomicrons are subject to ... These chylomicrons then pass into the lacteals, forming a milky substance known as chyle. The lacteals merge to form larger ... The triglyceride is then combined with phospholipids, cholesterol ester, and apolipoprotein B48 to form chylomicrons. ...
Fatty acid metabolism
... partially digests the chylomicrons into free fatty acids, glycerol and chylomicron remnants. The fatty acids are absorbed by ... These VLDL droplets are processed in exactly the same manner as chylomicrons, except that the VLDL remnant is known as an ... but the glycerol and chylomicron remnants remain in the blood plasma, ultimately to be removed from the circulation by the ... The chylomicrons circulate throughout the body, giving the blood plasma a milky or creamy appearance after a fatty meal.[ ...
Lipoprotein lipase
... a carboxylate It is also involved in promoting the cellular uptake of chylomicron remnants, cholesterol-rich lipoproteins, and ... It is a water-soluble enzyme that hydrolyzes triglycerides in lipoproteins, such as those found in chylomicrons and very low- ... Beisiegel U, Weber W, Bengtsson-Olivecrona G (October 1991). "Lipoprotein lipase enhances the binding of chylomicrons to low ... high-density lipoprotein-binding protein 1 plays a critical role in the lipolytic processing of chylomicrons". Cell Metabolism ...
Apolipoprotein C-III
... and is found on triglyceride-rich lipoproteins such as chylomicrons, very low density lipoprotein (VLDL), and remnant ...
Familial dysbetalipoproteinemia
This defect prevents the normal metabolism of chylomicrons, IDL and VLDL, otherwise known as remnants, and therefore leads to ... that serves as a ligand for the liver receptor for chylomicrons, IDL and VLDL, also known as very-low-density-lipoprotein ...
APOA5
Finally, the third possibility relates to the acceleration of the hepatic uptake of lipoprotein remnants and it has been shown ... It is a component of several lipoprotein fractions including VLDL, HDL, chylomicrons. It is believed that apoA-V affects ... APOA5 is associated predominantly with TG-rich lipoproteins (chylomicrons and VLDL) and has also been detected on HDL particles ... and chylomicrons, and circulates at very low concentrations compared with other apolipoproteins". Clinical Chemistry. 51 (2): ...
Hypertriglyceridemia: Practice Essentials, Pathophysiology, Etiology
Lipoprotein lipase (LPL) releases free fatty acids (FFAs) from chylomicrons (chylo) and produces chylomicron remnants that are ... Lipoprotein lipase (LPL) releases free fatty acids (FFAs) from chylomicrons (chylo) and produces chylomicron remnants that are ... a VLDL remnant, to LDL particles in the blood and because of a decreased clearance of chylomicron remnants. [4] Typically, ... Chylomicron remnants are taken up by the LDL receptor or the LDL receptor-related protein. [14] ...
Ola Myklebost | Universitetet i Bergen
Sources of Arachidonic Acid in Platelets, Bone, Marrow and Gastrointestinal Tract | Lund University Publications
Chylomicron remnant, Chylomicron, Arachidonic acid, Bone marrow, Platelets, Protein S, Prothrombin, Triglycerides., ... Chylomicron remnant; Chylomicron; Arachidonic acid; Bone marrow; Platelets; Protein S; Prothrombin; Triglycerides.; ... but do not exhibit any receptor mediated uptake and degradation of chylomicron remnants (CMR). Although CM, CMR and Intralipid ... but do not exhibit any receptor mediated uptake and degradation of chylomicron remnants (CMR). Although CM, CMR and Intralipid ...
Questions & Answers
Lipoprotein lipase (LPL) releases free fatty acids (FFAs) from chylomicrons (chylo) and produces chylomicron remnants that are ... Once very low-density lipoprotein (VLDL) has been metabolized by lipoprotein lipase, VLDL remnants in the form of intermediate- ... What is the role of chylomicron and VLDL metabolism in the pathophysiology of hypertriglyceridemia (high triglyceride levels)? ... How is the presence of chylomicrons confirmed in hypertriglyceridemia (high triglyceride levels)? ...
Reactome | APOE [extracellular region]
Chylomicron remodeling (Homo sapiens) * chylomicron remnant + apoE => chylomicron remnant:apoE complex (Homo sapiens) * APOE [ ... chylomicron remnant + apoE => chylomicron remnant:apoE complex (Homo sapiens) * Spherical HDL binds C and E apolipoproteins ( ... chylomicron remnant:apoE complex [extracellular region] (Homo sapiens) * chylomicron remnant [extracellular region] (Homo ...
Hypertriglyceridaemia: an update | Journal of Clinical Pathology
Metformin enhances clearance of chylomicrons and chylomicron remnants in nondiabetic mildly overweight glucose-intolerant ... Remnant hyperlipidaemia. Remnant hyperlipidaemias are associated with polymorphisms in apoE.75 Homozygosity for apoE2 (familial ... Regulation of chylomicron production in humans. Biochim Biophys Acta 2012;1821:736-46.doi:10.1016/j.bbalip.2011.09.019 pmid: ... Remnants of the triglyceride-rich lipoproteins, diabetes, and cardiovascular disease. Diabetes 2020;69:508-16. ...
Thematic Reviews
Which JAX mouse model is best for atherosclerosis studies: Apoe or Ldlr knockout mice?
Nonfasting lipid testing: the new standard for cardiovascular risk assessment | CMAJ
... including intermediate density lipoproteins and chylomicron remnants, which cross the vascular endothelium like LDL and become ... Use of non-HDL cholesterol in a nonfasting plasma sample captures the atherogenic effect of remnant lipoproteins and is a ... 7 One study suggested that this is due to the added atherogenic effect of cholesterol in remnant lipoproteins, ... inclusion of the risk associated with postprandial remnant lipoproteins in the test for non-HDL cholesterol, a better ...
Anti-Apolipoprotein E antibody [D6E10] - BSA and Azide free (ab1906) | Abcam
The most important thing you probably don't know about cholesterol
... increase chylomicron and chylomicron remnant apoE and ApoCIII content (both of which inhibit lipoprotein lipase, thereby ... and to have higher levels of chylomicrons and chylomicron remnants, which are also cleared more slowly (Bergeron 1995; ... saturated fats provoke twice the chylomicron triglyceride response and several-fold greater VLDL response." ...
WikiGenes
Newly absorbed chylomicron remnant retinyl ester is endocytosed by parenchymal liver cells, and retinol is subsequently ... These findings indicate that following uptake of chylomicron remnant retinyl ester in parenchymal cells, the retinyl ester is ... In one series of experiments, chylomicrons labeled with [3H]retinyl palmitate or with retinyl [3H]palmitate were injected ...
9 questions on Lipid transport and the nutrition quiz by Bill Lamb the nutrition man
Chylomicron remnants bind to specific receptors in the liver through which apolipoprotein?. Select the correct answer(s). (0/0) ... Chylomicron remnants bind to specific receptors in the liver through which apolipoprotein?,questionTimeSeconds:0, ... Chylomicrons transport dietary fats and cholesterol. Select the correct answer(s). (0/0). ... Which apolipoproteins are transferred from HDL to chylomicrons?. Select the correct answer(s). (0/0). ...
Combination of curcumin and piperine prevents formation of gallstones in C57BL6 mice fed on lithogenic diet: whether NPC1L1...
Clinical heterogeneity in monogenic chylomicronaemia | BMJ Case Reports
... from the circulation rapidly because TGs are efficiently removed by lipolysis that processes chylomicrons and VLDL to remnant ... Severe hypertriglyceridaemia is usually caused by the pathological presence of chylomicrons in the fasting state.2 Both mild to ... 1 TGs from the diet are incorporated in chylomicrons and the liver secretes TG in very low-density lipoproteins (VLDLs). These ... Chylomicrons are the largest lipoproteins with the highest TG content, but are cleared ...
OUH - Group members
Donna Vine, PhD - [email protected]
... to determine the permeability of intestinal chylomicron-remnants into arterial vessels. * We have pioneered the development of ... We have made extensive contributions to the study of intestinal chylomicrons, which has lead to the discovery that the ... chylomicrons). Dr. Vine and her team (together with Dr. Proctor, Nutrition, UofA) has been one of the first to contribute to ... are incorporated into intestinal chylomicrons and transported to the circulation. ...
etx-lipid-ch37-fig1 - Endotext
... apoC-III delays receptor-mediated hepatic uptake of VLDL and chylomicron remnants resulting in formation of intermediate ... Chylomicrons and VLDL production originating from the intestine and liver are increased. Mobilization of free fatty acids (FFA ... Dietary intake of fat provides the intestine with TG for chylomicron formation, which is upregulated in insulin resistance. ...
DeCS
Chylomicron Remnants - Preferred Concept UI. M0365537. Scope note. Metabolic products of chylomicron particles in which ... Résidus de chylomicrons Entry term(s):. Chylomicron Remnant. Remnant, Chylomicron. Remnants, Chylomicron. ... These remnants carry dietary lipids in the blood and are cholesterol-rich. Their interactions with MACROPHAGES; ENDOTHELIAL ... Metabolic products of chylomicron particles in which TRIGLYCERIDES have been selectively removed by the LIPOPROTEIN LIPASE. ...
Code System Concept
Life Extension What's Hot Archive February 2009 - Life Extension
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DeCS 2007 - New terms
Conference Proceedings - Metabolic and Cardiovascular Diseases Laboratory
Oxysterols alter the apolipoprotein complement of chylomicrons and chylomicron remnants effecting their metabolism in-vivo. ... The contribution of chylomicron-remnants and LDL to the accumulation of cholesterol in the arterial wall following in-situ ... The contribution of chylomicron-remnants and LDL to the accumulation of cholesterol in the arterial wall following in-situ ... Proctor SD, Yu K.C.W and Mamo J.C.L Chylomicron Remnants can penetrate arterial subendothelium and are Cytotoxic to surrounding ...
Effects of Evolocumab on the Postprandial Kinetics of Apo (Apolipoprotein) B100-and B48-Containing Lipoproteins in Subjects...
chylomicrons evolocumab kinetics TRIGLYCERIDE-RICH LIPOPROTEINS PCSK9 INHIBITOR EVOLOCUMAB SUBTILISIN/KEXIN TYPE 9 ... disease in subjects with type 2 diabetes is linked to elevated levels of triglyceride-rich lipoproteins and their remnants. The ... Kinetic parameters were determined for the following: apoB48 in chylomicrons; triglyceride in VLDL1 (very low-density ... CONCLUSIONS: Evolocumab had only minor effects on lipoproteins that are involved in triglyceride transport (chylomicrons and ...
PromoSimple
Plasma Lipids and Lipoproteins | Basicmedical Key
from chylomicron remnants via the exogenous pathway or synthesized locally. These lipids are transported from the liver as VLDL ... Like chylomicrons, VLDL is hydrolysed by lipoprotein lipase in the peripheral tissues, albeit more slowly. The resulting VLDL ... If a lipaemic plasma sample, for example after a meal, is left overnight at 4°C, the larger and less dense chylomicrons form a ... Chylomicrons are the largest and least dense lipoproteins and transport exogenous lipid from the intestine to all cells. ...
Lipoproteins19
- APOE is a plasma glycoprotein constituent on the surface of most lipoproteins including very low density lipoprotein (VLDL), intermediate-density lipoprotein (IDL) and chylomicron remnant lipoprotein particles. (jax.org)
- Use of non-HDL cholesterol in a nonfasting plasma sample captures the atherogenic effect of remnant lipoproteins and is a better indicator of cardiovascular risk than LDL cholesterol. (cmaj.ca)
- 6 , 7 One study suggested that this is due to the added atherogenic effect of cholesterol in remnant lipoproteins, including intermediate density lipoproteins and chylomicron remnants, which cross the vascular endothelium like LDL and become trapped in the artery wall, contributing to plaque formation. (cmaj.ca)
- 10 mmol/L. 1 TGs from the diet are incorporated in chylomicrons and the liver secretes TG in very low-density lipoproteins (VLDLs). (bmj.com)
- These lipoproteins and their lipolytic remnants that vary in size and density are collectively called triglyceride-rich lipoproteins (TRLs). (bmj.com)
- Chylomicrons are the largest lipoproteins with the highest TG content, but are cleared from the circulation rapidly because TGs are efficiently removed by lipolysis that processes chylomicrons and VLDL to remnant lipoproteins. (bmj.com)
- apoC-III delays receptor-mediated hepatic uptake of VLDL and chylomicron remnants resulting in formation of intermediate density lipoproteins (IDL, not shown) and smaller and denser low-density lipoproteins (LDL). (endotext.org)
- Proctor SD, Pabla C.K. and Mamo J.C.L. Arterial uptake of chylomicrons and low density lipoproteins in insulin deficient rats and rabbits. (ualberta.ca)
- Accumulation of intestinal cholesterol-rich remnant lipoproteins within arterial vessels may be exacerbated by advanced glycation endproducts and the co-localisation of proteoglycans in diabetes. (ualberta.ca)
- OBJECTIVE: Increased risk of atherosclerotic cardiovascular disease in subjects with type 2 diabetes is linked to elevated levels of triglyceride-rich lipoproteins and their remnants. (helsinki.fi)
- CONCLUSIONS: Evolocumab had only minor effects on lipoproteins that are involved in triglyceride transport (chylomicrons and VLDL1) but, in contrast, had a profound impact on lipoproteins that carry cholesterol (VLDL2, IDL, LDL). (helsinki.fi)
- The key features I would like to focus on in the next few slides are the action on lipoprotein assembly and secretion in the liver and intestine, alterations in the plasma lipid profile in remnant lipoproteins LDL and HDL, potential anti-inflammatory effects of EPA and antithrombotic effects in the artery wall, then perturbations in cell membrane cholesterol metabolism. (ipccs.org)
- These lipoproteins are neither LDL-C or high density lipoprotein cholesterol (HDL-C), but rather consist of the cholesterol-rich remnants of triglyceride-rich lipoproteins produced by the liver (VLDL) and the small intestine (chylomicrons)(1). (nutritioneducationstore.com)
- Both genetic factors and dietary factors influence the amount of these triglyceride-rich lipoproteins produced and also the amount of cholesterol-rich remnant particles derived from each of them in the blood. (nutritioneducationstore.com)
- As such, APOE associates with chylomicrons, chylomicron remnants, very low density lipoproteins (VLDL) and intermediate density lipoproteins (IDL) but shows a preferential binding to high-density lipoproteins (HDL). (acrobiosystems.com)
- These studies have provided important information on the major serum lipoprotein fractions found in dog serum or plasma, namely chylomicrons, very low density lipoproteins (VLDL), low density lipoproteins (LDL), and high density lipoproteins (HDL). (biomedcentral.com)
- ARO-APOC3 is a subcutaneously administered RNAi therapeutic that targets apolipoprotein C-III (apoC-III), and reduces VLDL synthesis and assembly, enhances the breakdown of triglyceride rich lipoproteins, and improve clearance of VLDL and chylomicron remnants. (thedaytimereport.com)
- Interchange of apolipoproteins between chylomicrons and high density lipoproteins during alimentary lipemia in man. (nih.gov)
- Production of cholesterol-rich particles such as VLDL (very low density lipoproteins) and chylomicrons is increased. (cyclingplantbasedgranny.com)
VLDL6
- Enterocytes secrete chylomicron (CM) particles containing a short form (48%) of apolipoprotein (apo) B (apoB 48 ), while hepatocytes secrete very low-density lipoprotein (VLDL) with full length apoB (apoB 100 ). (bmj.com)
- Chylomicrons and VLDL production originating from the intestine and liver are increased. (endotext.org)
- It's been known for many years through metabolic investigations, that high doses of EPA and DHA decrease the production of large triglyceride-rich VLDL from the liver and chylomicrons from the intestine following a fat meal. (ipccs.org)
- The net effect is the reduction in postprandial alimentary lipemia and a reduction in the level of apoB containing VLDL particles and their remnants in the circulation and apoB-48 containing chylomicrons and their remnants in the circulation. (ipccs.org)
- we can see the major changes were seen in chylomicron VLDL remnants with smaller changes in LDL and HDL. (ipccs.org)
- Type III hyperlipidemia or dysbetalipoproteinemia is characterized by an individual's decreased ability to convert VLDL and intermediate-density lipoprotein (IDL), a VLDL remnant, to LDL particles in the blood and because of a decreased clearance of chylomicron remnants. (medscape.com)
Uptake3
- 1. Platelets take up chylomicrons (CM) in vitro, the main part being sequestered in open canalicular system and not degraded, but do not exhibit any receptor mediated uptake and degradation of chylomicron remnants (CMR). (lu.se)
- It's interaction with specific ApoE receptor enables uptake of chylomicron remnants by liver cells, which is an essential step during normal lipid metabolism. (immunetics.com)
- Proctor SD, and Mamo J.C.L Arterial fatty lesions have increased uptake of chylomicron remnants but not low density lipoprotein. (ualberta.ca)
Incorporated into intes1
- We have been the first to provide evidence that dietary derived cholesterol oxidation products are rapidly absorbed by the intestine, are incorporated into intestinal chylomicrons and transported to the circulation. (ualberta.ca)
Lipoprotein1
- Metabolic products of chylomicron particles in which TRIGLYCERIDES have been selectively removed by the LIPOPROTEIN LIPASE . (bvsalud.org)
Penetrate arterial2
- Proctor SD, Yu K.C.W and Mamo J.C.L Chylomicron Remnants can penetrate arterial subendothelium and are Cytotoxic to surrounding cells. (ualberta.ca)
- We have been the first to provide visual evidence that intestinally derived cholesterol particles (chylomicrons) penetrate arterial tissue after hydrolysis to their smaller remnant form, and therefore contribute to the atherogenic process. (ualberta.ca)
Particles in the b1
- Of course, we now know HDL-C particles can actually become proinflammatory and proatherogenic "bad" HDL particles, perhaps partly in response to biochemical changes in the HDL particles triggered in part by chylomicrons and other remnant cholesterol particles in the blood. (nutritioneducationstore.com)
Atherogenic1
- And these remnants are highly atherogenic with a high cholesterol to apo-B ratio, decrease particle fluidity, and partial lipolysis products from the lipolytic reaction and possibly these were different in the two treatment regimens. (ipccs.org)
Lipids1
- These remnants carry dietary lipids in the blood and are cholesterol-rich. (bvsalud.org)
Apolipoprotein3
- The genetic causes of hypertriglyceridaemia range from familial combined hyperlipidaemia through the autosomal recessive remnant hyperlipidaemia (related to apolipoprotein E variants) and familial chylomicronaemia syndromes. (bmj.com)
- Chylomicron remnants bind to specific receptors in the liver through which apolipoprotein? (topgradeapp.com)
- We continue to contribute to studies that correlate raised levels of chylomicron particles (measured as apolipoprotein-B48) and risk of heart disease in numerous clinical conditions. (ualberta.ca)
Intestine3
- Dietary intake of fat provides the intestine with TG for chylomicron formation, which is upregulated in insulin resistance. (endotext.org)
- Chylomicrons are small fat globules that help transport fat after digestion from great intestine to tissues of the body. (promosimple.com)
- Protetox Chylomicrons are small fat globules that help transport fat after digestion from the small intestine to tissues systems Protetox Abdominal fat increases until liver function is increased significantly Protetox So, detox your liver for Weight Loss Protetox Turn it back in the fat metabolizing and toxin eliminating power house Weight Loss 24/7. (techplanet.today)
Elevations1
- Type I is a rare disorder characterized by severe elevations in chylomicrons and extremely elevated triglycerides, always reaching well above 1000 mg/dL and not infrequently rising as high as 10,000 mg/dL or more. (medscape.com)
Metabolism3
- We have made extensive contributions to the study of intestinal chylomicrons, which has lead to the discovery that the impairment of intestinal chylomicron metabolism leads to an accumulation of these particles in the circulation. (ualberta.ca)
- Dane-Stewart CA, Watts GF, Barrett PH, Stuckey BG, Mamo JC, Martins IJ, Redgrave TG (2003) Chylomicron remnant metabolism studied with a new breath test in postmenopausal women with and without type 2 diabetes mellitus. (sapub.org)
- Martins IJ, Tran JML Redgrave TG (2002) Food restriction normalizes chylomicron remnant metabolism in murine models of obesity as assessed by a novel stable isotope breath test. (sapub.org)
Accumulation1
- The contribution of chylomicron-remnants and LDL to the accumulation of cholesterol in the arterial wall following in-situ arterial perfusion. (ualberta.ca)
Severe1
- Severe hypertriglyceridaemia is usually caused by the pathological presence of chylomicrons in the fasting state. (bmj.com)
Experiments1
- And experiments have shown that particle oxidation of remnants, or LDL particles can be interrupted by EPA to a great extent with DHA, and therefore there is an oxidation benefit in terms of EPA ingestion. (ipccs.org)
Artery1
- Proctor SD, and Mamo J.C.L. In situ perfusion of fluorescent labeled chylomicron-remnants in rabbit carotid artery visualised by 3D-confocal microscopy. (ualberta.ca)
Blood1
- Fat and cholesterol-rich meals can dramatically increase the production of chylomicrons and lead to greater amounts of cholesterol-rich chlyomicron remnants in the blood for several hours after each fat-rich meal (2). (nutritioneducationstore.com)
Levels2
- Dr. Borge Nordestgaard's recent study followed nearly 12,000 people with established CAD in Denmark and found that each 1 mmol (38.7 mg/dl) increase in non-fasting remnant cholesterol caused 2.8 times greater risk of a CAD event that was independent of HDL-C levels. (nutritioneducationstore.com)
- The increased causal risk of CAD from elevated cholesterol remnant particles appeared much stronger than for changes in either LDL-C or HDL-C levels (3). (nutritioneducationstore.com)
Level1
- 7 Remnant cholesterol is captured along with LDL cholesterol in the non-HDL cholesterol level regardless of the time since eating. (cmaj.ca)