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.
The interstitial fluid that is in the LYMPHATIC SYSTEM.
An opaque, milky-white fluid consisting mainly of emulsified fats that passes through the lacteals of the small intestines into the lymphatic system.
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.
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.
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.
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.
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.
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.
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.
Major structural proteins of triacylglycerol-rich LIPOPROTEINS. There are two forms, apolipoprotein B-100 and apolipoprotein B-48, both derived from a single gene. ApoB-100 expressed in the liver is found in low-density lipoproteins (LIPOPROTEINS, LDL; LIPOPROTEINS, VLDL). ApoB-48 expressed in the intestine is found in CHYLOMICRONS. They are important in the biosynthesis, transport, and metabolism of triacylglycerol-rich lipoproteins. Plasma Apo-B levels are high in atherosclerotic patients but non-detectable in ABETALIPOPROTEINEMIA.
The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils.
The largest lymphatic vessel that passes through the chest and drains into the SUBCLAVIAN VEIN.
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.
Unctuous combustible substances that are liquid or easily liquefiable on warming, and are soluble in ether but insoluble in water. Such substances, depending on their origin, are classified as animal, mineral, or vegetable oils. Depending on their behavior on heating, they are volatile or fixed. (Dorland, 28th ed)
The time frame after a meal or FOOD INTAKE.
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.
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.
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.
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.
Uptake of substances through the lining of the INTESTINES.
Structural proteins of the alpha-lipoproteins (HIGH DENSITY LIPOPROTEINS), including APOLIPOPROTEIN A-I and APOLIPOPROTEIN A-II. They can modulate the activity of LECITHIN CHOLESTEROL ACYLTRANSFERASE. These apolipoproteins are low in atherosclerotic patients. They are either absent or present in extremely low plasma concentration in TANGIER DISEASE.
(Z)-9-Octadecenoic acid 1,2,3-propanetriyl ester.
A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.
The protein components of a number of complexes, such as enzymes (APOENZYMES), ferritin (APOFERRITINS), or lipoproteins (APOLIPOPROTEINS).
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.
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.
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.
Lipids containing one or more phosphate groups, particularly those derived from either glycerol (phosphoglycerides see GLYCEROPHOSPHOLIPIDS) or sphingosine (SPHINGOLIPIDS). They are polar lipids that are of great importance for the structure and function of cell membranes and are the most abundant of membrane lipids, although not stored in large amounts in the system.
Centrifugation with a centrifuge that develops centrifugal fields of more than 100,000 times gravity. (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)
The fatty portion of milk, separated as a soft yellowish solid when milk or cream is churned. It is processed for cooking and table use. (Random House Unabridged Dictionary, 2d ed)
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)
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.
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 layer of the peritoneum which attaches the abdominal viscera to the ABDOMINAL WALL and conveys their blood vessels and nerves.
Absorptive cells in the lining of the INTESTINAL MUCOSA. They are differentiated EPITHELIAL CELLS with apical MICROVILLI facing the intestinal lumen. Enterocytes are more abundant in the SMALL INTESTINE than in the LARGE INTESTINE. Their microvilli greatly increase the luminal surface area of the cell by 14- to 40 fold.
Physiological processes in biosynthesis (anabolism) and degradation (catabolism) of LIPIDS.
Conditions with excess LIPIDS in the blood.
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.
Oils derived from plants or plant products.
Volume of biological fluid completely cleared of drug metabolites as measured in unit time. Elimination occurs as a result of metabolic processes in the kidney, liver, saliva, sweat, intestine, heart, brain, or other site.
Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations or by parent x offspring matings carried out with certain restrictions. This also includes animals with a long history of closed colony breeding.
A 9-kDa protein component of VERY-LOW-DENSITY LIPOPROTEINS and CHYLOMICRON REMNANTS. Apo C-III, synthesized in the liver, is an inhibitor of LIPOPROTEIN LIPASE. Apo C-III modulates the binding of chylomicron remnants and VLDL to receptors (RECEPTORS, LDL) thus decreases the uptake of triglyceride-rich particles by the liver cells and subsequent degradation. The normal Apo C-III is glycosylated. There are several polymorphic forms with varying amounts of SIALIC ACID (Apo C-III-0, Apo C-III-1, and Apo C-III-2).
A condition of elevated levels of TRIGLYCERIDES in the blood.
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.
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.
Unstable isotopes of carbon that decay or disintegrate emitting radiation. C atoms with atomic weights 10, 11, and 14-16 are radioactive carbon isotopes.
Oil from ZEA MAYS or corn plant.
A copolymer of polyethylene and polypropylene ether glycol. It is a non-ionic polyol surface-active agent used medically as a fecal softener and in cattle for prevention of bloat.
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.
The section of the alimentary canal from the STOMACH to the ANAL CANAL. It includes the LARGE INTESTINE and SMALL INTESTINE.
The portion of the GASTROINTESTINAL TRACT between the PYLORUS of the STOMACH and the ILEOCECAL VALVE of the LARGE INTESTINE. It is divisible into three portions: the DUODENUM, the JEJUNUM, and the ILEUM.
Relating to the size of solids.
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)
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 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 16-carbon fatty acids that contain no double bonds.
Cholesterol present in food, especially in animal products.
The process of cleaving a chemical compound by the addition of a molecule of water.
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.
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)
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.
Abstaining from all food.
Treatment process involving the injection of fluid into an organ or tissue.
A group of fatty acids that contain 18 carbon atoms and a double bond at the omega 9 carbon.
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.
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.
The glyceryl esters of a fatty acid, or of a mixture of fatty acids. They are generally odorless, colorless, and tasteless if pure, but they may be flavored according to origin. Fats are insoluble in water, soluble in most organic solvents. They occur in animal and vegetable tissue and are generally obtained by boiling or by extraction under pressure. They are important in the diet (DIETARY FATS) as a source of energy. (Grant & Hackh's Chemical Dictionary, 5th ed)
The rate dynamics in chemical or physical systems.
The middle portion of the SMALL INTESTINE, between DUODENUM and ILEUM. It represents about 2/5 of the remaining portion of the small intestine below duodenum.
Emulsions of fats or lipids used primarily in parenteral feeding.
Eighteen-carbon essential fatty acids that contain two double bonds.
The most abundant protein component of HIGH DENSITY LIPOPROTEINS or HDL. This protein serves as an acceptor for CHOLESTEROL released from cells thus promoting efflux of cholesterol to HDL then to the LIVER for excretion from the body (reverse cholesterol transport). It also acts as a cofactor for LECITHIN CHOLESTEROL ACYLTRANSFERASE that forms CHOLESTEROL ESTERS on the HDL particles. Mutations of this gene APOA1 cause HDL deficiency, such as in FAMILIAL ALPHA LIPOPROTEIN DEFICIENCY DISEASE and in some patients with TANGIER DISEASE.

Lipoprotein lipase expression level influences tissue clearance of chylomicron retinyl ester. (1/827)

Approximately 25% of postprandial retinoid is cleared from the circulation by extrahepatic tissues. Little is known about physiologic factors important to this uptake. We hypothesized that lipoprotein lipase (LpL) contributes to extrahepatic clearance of chylomicron vitamin A. To investigate this, [3H]retinyl ester-containing rat mesenteric chylomicrons were injected intravenously into induced mutant mice and nutritionally manipulated rats. The tissue sites of uptake of 3H label by wild type mice and LpL-null mice overexpressing human LpL in muscle indicate that LpL expression does influence accumulation of chylomicron retinoid. Skeletal muscle from mice overexpressing human LpL accumulated 1.7- to 2.4-fold more 3H label than wild type. Moreover, heart tissue from mice overexpresssing human LpL, but lacking mouse LpL, accumulated less than half of the 3H-label taken up by wild type heart. Fasting and heparin injection, two factors that increase LpL activity in skeletal muscle, increased uptake of chylomicron [3H] retinoid by rat skeletal muscle. Using [3H]retinyl palmitate and its non-hydrolyzable analog retinyl [14C]hexadecyl ether incorporated into Intralipid emulsions, the importance of retinyl ester hydrolysis in this process was assessed. We observed that 3H label was taken up to a greater extent than 14C label by rat skeletal muscle, suggesting that retinoid uptake requires hydrolysis. In summary, for each of our experiments, the level of lipoprotein lipase expression in skeletal muscle, heart, and/or adipose tissue influenced the amount of [3H]retinoid taken up from chylomicrons and/or their remnants.  (+info)

Plasma clearance and liver uptake of chylomicron remnants generated by hepatic lipase lipolysis: evidence for a lactoferrin-sensitive and apolipoprotein E-independent pathway. (2/827)

Chylomicrons labeled with [3H]cholesterol and [14C]triglyceride fatty acids were lipolyzed by hepatic lipase (HL) in vitro and then injected intravenously into normal mice fed low- or high-fat diets, and into apolipoprotein (apo) E-deficient mice. In normal mice fed the high-fat diet and injected with non-lipolyzed chylomicrons, the plasma clearance and hepatic uptake of the resulting [3H]cholesterol-labeled remnants was markedly inhibited. In contrast, chylomicrons lipolyzed by HL were taken up equally rapidly by the livers of mice fed the low- and high-fat diets. The removal of non-lipolyzed chylomicrons lacking apoE from the plasma of apoE-deficient mice was inhibited, but not the removal of chylomicrons lipolyzed by HL. Pre-injection of lactoferrin into normal mice inhibited the plasma clearance of both non-lipolyzed chylomicrons and chylomicrons lipolyzed by HL. The removal of HL from the surface of the lipolyzed particles by proteolytic digestion did not affect their rapid uptake, indicating that the hepatic recognition of the lipoproteins was not mediated by HL. These observations support previous findings that phospholipolysis of chylomicrons by hepatic lipase generates remnant particles that are rapidly cleared from circulation by the liver. They also support the concept that chylomicron remnants can be taken up by the liver by an apolipoprotein E-independent mechanism. We hypothesize that this mechanism is modulated by the remnant phospholipids and that it may involve their interaction with a phospholipid-binding receptor on the surface of hepatocytes such as the class B scavenger receptor BI.  (+info)

Effects of a frequent apolipoprotein E isoform, ApoE4Freiburg (Leu28-->Pro), on lipoproteins and the prevalence of coronary artery disease in whites. (3/827)

Different isoforms of apoE modulate the concentrations of plasma lipoproteins and the risk for atherosclerosis. A novel apoE isoform, apoE4Freiburg, was detected in plasma by isoelectric focusing because its isoelectric point is slightly more acidic than that of apoE4. ApoE4Freiburg results from a base exchange in the APOE4 gene that causes the replacement of a leucine by a proline at position 28. Analysis of the allelic frequencies in whites in southwestern Germany revealed that this isoform is frequent among control subjects (10:4264 alleles) and is even more frequent in patients with coronary artery disease (21:2874 alleles; P=0.004; adjusted odds ratio, 3.09; 95% confidence interval, 1.20 to 7.97). ApoE4Freiburg affects serum lipoproteins by lowering cholesterol, apoB, and apoA-I compared with apoE4 (P<0.05). Our 4 apoE4Freiburg homozygotes suffered from various phenotypes of hyperlipoproteinemia (types IIa, IIb, IV, and V). In vitro binding studies excluded a binding defect of apoE4Freiburg, and in vivo studies excluded an abnormal accumulation of chylomicron remnants. ApoE4Freiburg and apoE4 accumulated to a similar extent in triglyceride-rich lipoproteins. HDLs, however, contained about 40% less apoE4Freiburg than apoE4. In conclusion, our data indicate that apoE4Freiburg exerts its possible atherogenic properties by affecting the metabolism of triglyceride-rich lipoproteins and HDL.  (+info)

Very low-density lipoprotein activates nuclear factor-kappaB in endothelial cells. (4/827)

High plasma levels of VLDL are associated with increased risk for atherosclerosis. Here we show that VLDL (75 to 150 microg/mL) activates nuclear factor-kappaB (NF-kappaB), a transcription factor known to play a key role in regulation of inflammation. Oxidation of VLDL reduced its capacity to activate NF-kappaB in vitro, whereas free fatty acids such as linoleic and oleic acid activated NF-kappaB to the same extent as did VLDL. Intravenous injection of human VLDL (6 mg protein per kg) into rats resulted in arterial activation of NF-kappaB as assessed by electrophoretic mobility shift assay. Aortic endothelial cells showed positive nuclear staining for the activated RelA (p65) subunit of NF-kappaB at 6 to 24 hours after injection. There was also a parallel expression of the adhesion molecules intercellular adhesion molecule-1 and vascular cell adhesion molecule-1, as well as the cytokine tumor necrosis factor-alpha. Pretreatment of the rats with diet containing 1% of the antioxidant probucol for 8 weeks did not inhibit arterial activation of NF-kappaB in response to injection of VLDL. Moreover, injection of triglycerides (10% Intralipid, 5 mL/kg) activated arterial expression of NF-kappaB to the same extent as VLDL. Our results suggest that VLDL may promote the development of atherosclerotic lesions by activation of the proinflammatory transcription factor NF-kappaB. The effect appears to be mediated by a release of VLDL fatty acids but not to involve VLDL oxidation.  (+info)

Effect of oxidized lipids in the diet on oxidized lipid levels in postprandial serum chylomicrons of diabetic patients. (5/827)

OBJECTIVE: To determine whether humans with type 2 diabetes have increased levels of oxidized fatty acids in their serum chylomicron fraction after the ingestion of dietary oxidized fatty acids. RESEARCH DESIGN AND METHODS: The study was performed on 31 male type 2 diabetic patients and 24 age-matched control subjects. Among the diabetic patients, 22 had poor glycemic control, defined as HbA1 > 10% (normal value < 7.7%). Nine patients had good glycemic control (HbA1 < or = 10). Heated corn oil containing low or high levels of oxidized fatty acids was used as a test meal. At 2.5 h after the test meal, 50-ml blood samples were obtained from all subjects, and the chylomicron fraction (Sf > 1,000) was isolated. The degree of oxidation in chylomicrons was determined by measuring conjugated dienes. For determining the postprandial levels of triglycerides and of oxidized lipids in serum chylomicrons over an extended time period, blood samples were obtained at 0, 2.5, 5.0, and 7.5 h for isolation of chylomicrons and determination of fatty acid oxidation. RESULTS: We found that at 2.5 h after the consumption of the test meal containing either a low or high oxidized fatty acid content, conjugated dienes in serum chylomicrons in diabetic subjects in poor glycemic control were increased compared with those in control subjects. Diabetic patients in good glycemic control had similar levels of oxidized lipid in their chylomicrons when compared with control subjects. Additionally, in diabetic patients in poor glycemic control, the levels of oxidized lipids in chylomicrons remained elevated for an extended post-prandial period. CONCLUSIONS: In diabetic subjects with poor glycemic control, dietary oxidized lipids induce an exaggerated and sustained increase in the levels of oxidized lipids in chylomicrons when compared with either control subjects or diabetic patients with good glycemic control. These increased postprandial levels of potentially atherogenic oxidized lipids may contribute to the accelerated atherosclerosis associated with diabetes.  (+info)

Plasma clearance of chylomicrons from butterfat is not dependent on saturation: studies with butterfat fractions and other fats containing triacylglycerols with low or high melting points. (6/827)

BACKGROUND: Dietary fats influence plasma lipids, and changes in the clearance and metabolism of postprandial lipoproteins can affect atherosclerosis. Butterfat is considered hypercholesterolemic but contains a multitude of constituent fatty acids. OBJECTIVES: We determined triacylglycerol and cholesteryl ester clearances of lymph chylomicrons derived from butterfat, fractions of butterfat, and other dietary fats. METHODS: Radiolabeled lymph chylomicrons resulting from the intestinal absorption of different fats were reinjected into recipient rats to measure plasma clearance. Plasma clearance of [14C]triacylglycerol was used as an indicator of chylomicron lipolysis whereas clearance of [3H]cholesteryl ester was used as an indicator of chylomicron remnant removal. RESULTS: [3H]Cholesteryl ester clearance was slower from chylomicrons derived from a solid, high-saturated-butterfat fraction than from whole butterfat, but clearance of chylomicrons from other fractions did not correlate with the fractions' saturated fatty acid contents. Clearance of cholesteryl esters in chylomicrons derived from cocoa butter, palm oil, and butterfat was slower than clearance of cholesteryl esters in chylomicrons derived from safflower oil. Hepatic uptakes of cholesteryl esters were generally lower for chylomicrons from all butterfat fractions, cocoa butter, and palm oil. CONCLUSIONS: In contrast with minor effects on the lipolysis of chylomicron triacylglycerols, chylomicron remnant removal was strongly influenced by the type of dietary fat, with slower cholesteryl ester clearances for saturated fats with higher melting points. However, remnant removal and hepatic uptake of chylomicrons from whole butterfat and fractions of butterfat were not correlated with fat saturation. The mechanisms of this apparent paradox remain unknown but may be attributable to acyl arrangements in the lipid classes of chylomicrons that influence the association with apolipoproteins and receptors and hence remnant removal.  (+info)

All ApoB-containing lipoproteins induce monocyte chemotaxis and adhesion when minimally modified. Modulation of lipoprotein bioactivity by platelet-activating factor acetylhydrolase. (7/827)

Mildly oxidized LDL has many proinflammatory properties, including the stimulation of monocyte chemotaxis and adhesion, that are important in the development of atherosclerosis. Although ApoB-containing lipoproteins other than LDL may enter the artery wall and undergo oxidation, very little is known regarding their proinflammatory potential. LDL, IDL, VLDL, postprandial remnant particles, and chylomicrons were mildly oxidized by fibroblasts overexpressing 15-lipoxygenase (15-LO) and tested for their ability to stimulate monocyte chemotaxis and adhesion to endothelial cells. When conditioned on 15-LO cells, LDL, IDL, but not VLDL increased monocyte chemotaxis and adhesion approximately 4-fold. Chylomicrons and postprandial remnant particles were also bioactive. Although chylomicrons had a high 18:1/18:2 ratio, similar to that of VLDL, and should presumably be less susceptible to oxidation, they contained (in contrast to VLDL) essentially no platelet-activating factor acetylhydrolase (PAF-AH) activity. Because PAF-AH activity of lipoproteins may be reduced in vivo by oxidation or glycation, LDL, IDL, and VLDL were treated in vitro to reduce PAF-AH activity and then conditioned on 15-lipoxygenase cells. All 3 PAF-AH-depleted lipoproteins, including VLDL, exhibited increased stimulation of monocyte chemotaxis and adhesion. In a similar manner, lipoproteins from Japanese subjects with a deficiency of plasma PAF-AH activity were also markedly more bioactive, and stimulated monocyte adhesion nearly 2-fold compared with lipoproteins from Japanese control subjects with normal plasma PAF-AH. For each lipoprotein, bioactivity resided in the lipid fraction and monocyte adhesion could be blocked by PAF-receptor antagonists. These data suggest that the susceptibility of plasma lipoproteins to develop proinflammatory activity is in part related to their 18:1/18:2 ratio and PAF-AH activity, and that bioactive phospholipids similar to PAF are generated during oxidation of each lipoprotein. Moreover, LDL, IDL, postprandial remnant particles, and chylomicrons and PAF-AH-depleted VLDL all give rise to proinflammatory lipids when mildly oxidized.  (+info)

Mutations in the lipoprotein lipase gene associated with ischemic heart disease in men. The Copenhagen city heart study. (8/827)

The aim of this study was to test the hypothesis that the Asp9Asn substitution and the T(-93)-->G mutation in the promoter of the lipoprotein lipase gene affect plasma lipid levels and thereby the risk of ischemic heart disease (IHD). We genotyped 9033 men and women from a general population sample and 940 patients with IHD. The frequency of both the G allele and the Asn9 allele in the general population sample was approximately 0.015 for both men and women. These 2 mutations appeared together in 95% of carriers. The average triglyceride-raising effect associated with double heterozygosity for the T(-93)-->G mutation and the Asp9Asn substitution was 0.28 mmol/L (P=0.004) and 0.16 mmol/L (P=0.10) in men and women, respectively. On logistic regression analysis allowing for age, the risk of IHD for double heterozygous men and women was increased 90% (95% confidence interval [CI], 20% to 200%) and 30% (95% CI, -40% to 170%), respectively, compared with noncarriers. When, in addition, other conventional cardiovascular risk factors were allowed for, the risk of IHD for double heterozygous men and women was increased 70% (95% CI, 0% to 190%) and 20% (95% CI, -50% to 180%), respectively. Of the overall risk of IHD in men in the general population, the fraction attributable to double heterozygosity was 3%, similar to the 5% attributable to diabetes mellitus. These results demonstrate that the Asp9Asn substitution is in linkage disequilibrium with the T(-93)-->G mutation and that the double-heterozygous carrier status is associated with elevated plasma triglycerides and an increased risk of IHD in men.  (+info)

TAG depleted remnants of postprandial chylomicrons are a risk factor for atherosclerosis. Recent studies have demonstrated that in the fasted state, the majority of chylomicrons are small enough for transcytosis to arterial subendothelial space and accelerate atherogenesis. However, the size distribution of chylomicrons in the absorptive state is unclear. This study explored in normolipidaemic subjects the postprandial distribution of the chylomicron marker, apoB-48, in a TAG-rich lipoprotein plasma fraction (Svedberg flotation rate (Sf,400), in partially hydrolysed remnants (Sf 20-400) and in a TAG-deplete fraction (Sf,20), following ingestion of isoenergetic meals with either palm oil (PO), rice bran or coconut oil. Results from this study show that the majority of fasting chylomicrons are within the potentially pro-atherogenic Sf,20 fraction (70-75 %). Following the ingestion of test meals, chylomicronaemia was also principally distributed within the Sf,20 fraction. However, approximately 40 ...
Looking for Chylomicrons? Find out information about Chylomicrons. One of the extremely small lipid droplets, consisting chiefly of triglycerides, found in blood after ingestion of fat Explanation of Chylomicrons
In agreement with a range of previous studies we report that a single session of moderate intensity exercise decreases fasting triacylglycerol concentration on the subsequent day. There was a trend towards a significant decrease in postprandial triacylglycerol concentration following the moderate fat mixed meal; however when postprandial triacylglycerol concentrations were corrected for their corresponding fasting concentration, no decrease was observed. Despite the improvement in triacylglycerol concentration there was no reduction in fasting or postprandial chylomicron particle number. Insulin sensitivity, measured by HOMA score, and NEFA levels in either the fasting or postprandial states were also not altered in this group of subjects.. The extent of the reduction in fasting triacylglycerol concentration observed in the present study was 16% which is comparable to that reported in other studies [9-12]. In the fasting state the majority of circulating triacylglycerol resides associated with ...
The electron microscopic appearances of chylomicra and lipoproteins have been investigated. The particles were isolated from rat chyle by differential flotation in an ultracentrifuge. Various fixing and embedding media were used. The two kinds of particles were then identified in thin sections of the jejunum of rats. The chylomicra had diameters of from 1,000 A to 1 µ; the lipoproteins ranged from 100 to 1,000 A. They were identified by their sizes and their similarities to the isolated particles after the various fixing and embedding procedures. In addition, the relative amounts of the two kinds of particle varied greatly under different dietary conditions. The chylomicra had a thin rim, probably of phospholipid. Section B records the passage of the two kinds of particle into the lacteals in the villi of the jejunum. Both chylomicra and lipoproteins were seen passing through many open junctions. From permeability considerations it would seem that this is the most important route. These open ...
Hyperlipidemia is characterized by abnormally excessive amounts of fat, and/or fatty substances in the blood. Chylomicrons are micro particles of liquid fat, in the class of lipids, which include both triglycerides and cholesterol, and which are formed during the digestion of fats from food. After eating a meal, the nutrients in an animals body pass into the small intestine, from which chylomicrons are absorbed 30-60 minutes later. Normally, the absorption of chylomicrons increases serum triglycerides for 3-10 hours, but some animals will have high cholesterol and high triglyceride levels for more than twelve hours after a meal - one of the main indications of hyperlipidemia. The clear part of the blood, the serum, is referred to as being lipemic when it has levels of triglycerides measuring over 200 mg/dL. Sometimes, levels of triglycerides in an animals serum can be even greater than 1000 mg/dL, giving the serum a milky, opaque appearance. This is medically referred to as lactescence ...
Define chylomicron. chylomicron synonyms, chylomicron pronunciation, chylomicron translation, English dictionary definition of chylomicron. n. A lipoprotein formed in the small intestine that transports dietary fats and cholesterol through the lymphatic system to the bloodstream. Chylomicrons...
Rabbits fed cholesterol rapidly develop high serum cholesterol levels which lead to the development of atherosclerosis. This is related to the retention of cholesterol-rich chylomicron remnants in the circulation. In most animals, such as rats, chylomicron remnants are rapidly removed from the circulation by the liver. The first barrier to this removal is the fenestrated endothelium of liver sinusoids. Measurements made of a large number of sinusoidal fenestrae by scanning electron microscopy have shown the average diameters to be 89 nm in rats and 49 nm in rabbits. We postulate that the small size of endothelial fenestrae in the liver sinusoids of rabbits hinders the egress of chylomicron remnants from the sinusoidal blood, explaining the subsequent development of hypercholesterolemia and atherosclerosis. ...
Fatty acids come as mixtures. Even beef dripping carries a small load of PUFA. Nuts more so, seeds like those from Sunflowers much more so. Humans eat all of these in variable quantities. They are broken down by lipase, absorbed in to intestinal cells and reassembled in to triglycerides to be secreted as chylomicrons. Chylomicrons are the bulk transport system used to get lipid, including the PUFA, from the diet to the muscles, fat and the liver. A chylomicron is labled with a marker protein. Its a truncated form of that good old apoB100 used by the liver to mark the VLDLs destined to become LDL particles. The truncated protein is called apoB48. It starts life as an apoB100 but gets a socking great chunk cut off between transcription and particle assembly. It looses the LDL receptor interacting section but keeps the AGE triggered switch. No one seems to have looked at how glycation of chylomicrons acts in terms of receptor attachment to deliver lipid to muscles, or its interaction with the ...
Fatty acids come as mixtures. Even beef dripping carries a small load of PUFA. Nuts more so, seeds like those from Sunflowers much more so. Humans eat all of these in variable quantities. They are broken down by lipase, absorbed in to intestinal cells and reassembled in to triglycerides to be secreted as chylomicrons. Chylomicrons are the bulk transport system used to get lipid, including the PUFA, from the diet to the muscles, fat and the liver. A chylomicron is labled with a marker protein. Its a truncated form of that good old apoB100 used by the liver to mark the VLDLs destined to become LDL particles. The truncated protein is called apoB48. It starts life as an apoB100 but gets a socking great chunk cut off between transcription and particle assembly. It looses the LDL receptor interacting section but keeps the AGE triggered switch. No one seems to have looked at how glycation of chylomicrons acts in terms of receptor attachment to deliver lipid to muscles, or its interaction with the ...
sympathetikey First off, do yourself a favor and check this out - https://www.youtube.com/watch?v=NJYNf-Jcclo The LDL receptor is found on peripheral tissues. It recognizes B100 on LDL, IDL, and VLDL (secreted from the liver). Therefore, an issue with that would cause an increase in those, but mainly LDL. Since in this question we see that Triglycerides and Chylomicrons are elevated, that points towards a different problem. That problem is in the Lipoprotein Lipase receptor. This is the receptor that allows tissues to degrade TGs in Chylomicrons. So, if its not working, you get increased TGs and Chylomicrons. Additionally, you get eruptive xanthomas, which are the yellow white papules the question refers to. +4 2019-06-05T01:46:47Z ...
Cluster of differentiation 36 (CD36) variants influence fasting lipids and risk of metabolic syndrome, but their impact on postprandial lipids, an independent risk factor for cardiovascular disease, is unclear. We determined the effects of SNPs within a ∼410 kb region encompassing CD36 and its proximal and distal promoters on chylomicron (CM) remnants and LDL particles at fasting and at 3.5 and 6 h following a high-fat meal (Genetics of Lipid Lowering Drugs and Diet Network study, n = 1,117). Five promoter variants associated with CMs, four with delayed TG clearance and five with LDL particle number. To assess mechanisms underlying the associations, we queried expression quantitative trait loci, DNA methylation, and ChIP-seq datasets for adipose and heart tissues that function in postprandial lipid clearance. Several SNPs that associated with higher serum lipids correlated with lower adipose and heart CD36 mRNA and aligned to active motifs for PPARγ, a major CD36 regulator. The SNPs also associated
Hepatic steatosis is common, with at least 65% of liver biopsy specimens demonstrating steatosis. In genotype 3 infection, a specific mechanism of steatosis induction exists, via core antigen expression. The incidence of diabetes is higher in hepatitis C virus (HCV) infection and increases with increasing severity of liver disease. The mechanism of this is via insulin resistance, but it is uncertain whether hepatic steatosis is a result of the insulin resistance or plays a pivotal role in its induction.. HCV is associated with lipid in the serum and almost certainly uses lipid receptors to enter hepatocytes. The low-density fractions of serum contain HCV RNA particles and lipoviral particles (LVP) associated with triglyceride (TG)-rich lipoproteins. Such particles rich in TG have been shown to contain viral capsid and RNA.1 TG is contained within chylomicrons or within very low-density lipoprotein (VLDL). Chylomicrons are synthesised in the intestine and transported via lymph into the ...
In this study, the most striking findings were the postprandial uptake of fatty acids from the circulating NEFA pool by adipose tissue, the direct confirmation that chylomicrons are the preferred substrate of LPL over VLDL, the preferential channeling of fatty acids derived from LPL-mediated chylomicron hydrolysis into adipose tissue, and the postprandial release of fatty acids across the forearm ...
83. , Fahey,J. ,J. A, 704, 99-111 (1995). 84. N. , Lipids, 5, 353-358 (1970). 85. , Ferrato,F. , Chirality, 5, 24-30 (1993). 86. , Ransac,S. ,J. Biol. , 265, 20271-20276 (1990). 87. , Damiani,P. ,J. Am. Oil Chem. , 69, 552-556 (1992). 88. , J. Am. Oil Chem. , 42, 945-957 (1965). 89. Sempore,G. ,J. Am. Oil Chem. , 68, 702-709 (1991). 90. Sempore,G. ,J. , 547, 89-103 (1991 ). 91. G. ,J. , 557, 227-240 (1991). 36 92. 93. 94. 95. 96. 97. 98. 99. 100. 101. 102. 103. 104. 105. 106. 107. 108. 109. 110. Yang and Kuksis [110,112] have used the method for stereospecific analysis of menhaden oil and of the chylomicron triacylglycerols derived from it to propose a convergence of the phosphatidic acid and the monoacylglycerol pathways of triacylglycerol biosynthesis during fat absorption. Yang et al. [113] have employed the chiral-phase HPLC method to demonstrate that hepatic triacylglycerols are not directly transferred to VLDL but first undergo lipolysis to acylglycerols before being re-synthesised into ...
The results of the present study indicated that SAR1B may be closely associated with the tumorigenesis of CRC. SAR1B expression was determined in CRC cell lines, including HCT116, SW620 and RKO. Functional analysis demonstrated that knockdown of SAR1B suppressed CRC cell proliferation. Furthermore, flow cytometry results revealed that knockdown of SAR1B induced apoptosis of RKO cells. In addition, SAR1B downstream targets and pathways in CRC were determined using microarray and bioinformatics analyses.. Low molecular weight GTPases are involved in vesicular transport associated with multiple signaling transduction pathways that affect the regulation of cell proliferation, differentiation and transformation (7,8). It has been demonstrated that SAR1B GTPase is central to lipid metabolism and regulates chylomicron secretion by the small intestine (27,28). According to previous reports, the expression of SAR1B was identified in cell lines (including Caco-2/15 and McArdle-RH7777 cells), tissues and ...
Phillips, M. L., Pullinger, C., Kroes, I., Kroes, J., Hardman, D. A., Chen, G., Curtiss, L. K., Gutierrez, M. M., Kane, J. P., Schumaker, V. N. A single copy of apolipoprotein b-48 is present on the human chylomicron remnant Journal of Lipid Research 1997 38:1170-1177 PMID:9215545 ...
Description: The protein encoded by this gene is a glycoprotein secreted from the pancreas into the digestive tract and from the lactating mammary gland into human milk. The physiological role of this protein is in cholesterol and lipid-soluble vitamin ester hydrolysis and absorption. This encoded protein promotes large chylomicron production in the intestine. Also its presence in plasma suggests its interactions with cholesterol and oxidized lipoproteins to modulate the progression of atherosclerosis. In pancreatic tumoral cells, this encoded protein is thought to be sequestrated within the Golgi compartment and is probably not secreted. This gene contains a variable number of tandem repeat (VNTR) polymorphism in the coding region that may influence the function of the encoded protein ...
The protein encoded by this gene is a glycoprotein secreted from the pancreas into the digestive tract and from the lactating mammary gland into human milk. The physiological role of this protein is in cholesterol and lipid-soluble vitamin ester hydrolysis and absorption. This encoded protein promotes large chylomicron production in the intestine. Also its presence in plasma suggests its interactions with cholesterol and oxidized lipoproteins to modulate the progression of atherosclerosis. In pancreatic tumoral cells, this encoded protein is thought to be sequestrated within the Golgi compartment and is probably not secreted. This gene contains a variable number of tandem repeat (VNTR) polymorphism in the coding region that may influence the function of the encoded protein ...
Hyperlipidemia is characterized by abnormally excessive amounts of fat, and/or fatty substances in the blood. After eating a meal, the nutrients in an animals body pass into the small intestine, from which chylomicrons, micro particles of liquid fat, are absorbed 30-60 minutes later.
TY - JOUR. T1 - Effect of Probucol on Plasma Clearance and Organ Uptake of Chylomicrons and VLDLs in Normal and Diabetic Rats. AU - Mamo, John. AU - Elsegood, C.L.. AU - Umeda, Y.. AU - Hirano, T.. AU - Redgrave, Trevor. PY - 1993. Y1 - 1993. N2 - Probucol was given to rats made diabetic by streptozotocin. Compared with diabetic rats not receiving probucol or with nondiabetic rats, probucol lowered the plasma concentrations of triglycerides, phospholipids, cholesterol, and apolipoprotein B. The concentrations of serum chylomicrons and very low density lipoprotein (VLDL) were also reduced. In control and diabetic rats, probucol enhanced the clearance of endogenously radiolabeled VLDL from the plasma. Clearances from the plasma of rat lymph chylomicrons or chylomicron-like lipid emulsions were slow in diabetic rats. Probucol normalized chylomicron clearance in diabetic rats primarily by restoring hepatic uptake of remnants, which was decreased in diabetes. In diabetic rats, uptake of chylomicron ...
Looking for online definition of chylomicrons in the Medical Dictionary? chylomicrons explanation free. What is chylomicrons? Meaning of chylomicrons medical term. What does chylomicrons mean?
TY - JOUR. T1 - Low and high density lipoproteins and chylomicrons as regulators of rate of cholesterol synthesis in rat liver in vivo. AU - Andersen, J. M.. AU - Turley, S. D.. AU - Dietschy, J. M.. PY - 1979/1/1. Y1 - 1979/1/1. N2 - The steady-state levels of plasma cholesterol carried in high and low density lipoproteins and in chylomicrons were varied over a wide range by use of a constant-infusion technique. After 40 hr, the rates of hepatic cholesterol synthesis and levels of hepatic cholesterol esters were measured and were related to the plasma level of each of the lipoprotein fractions. From the rates of infusion and the steady-state plasma levels attained, the whole animal clearance rates for cholesterol carried in low density and high density lipoproteins and in chylomicrons were calculated to be 0.53, 0.61, and 42.6 ml/hr, respectively. Hepatic cholesterol ester content increased by 0.8 μg/g for each 1.0 mg/dl increase in the steady-state level of plasma low density lipoprotein ...
TY - JOUR. T1 - Oxidation affects the regulation of hepatic lipid synthesis by chylomicron remnants. AU - Napolitano, Mariarosaria. AU - Rivabene, Roberto. AU - Avella, Michael. AU - Amicone, Laura. AU - Tripodi, Marco. AU - Botham, Kathleen M.. AU - Bravo, Elena. PY - 2001/3/1. Y1 - 2001/3/1. N2 - The effects of native and oxidized chylomicron remnants on lipid synthesis in normal and oxidatively stressed liver cells were investigated using MET murine hepatocytes (MMH cells), a nontransformed mouse hepatocyte cell line that maintains a highly differentiated hepatic phenotype in culture. Lipid synthesis was determined by measuring the incorporation of [3H]oleate into cholesteryl ester, triacylglycerol, and phospholipid by the cells. The formation of cholesteryl ester and phospholipid was decreased by chylomicron remnants in a dose-dependent manner, while triacylglycerol synthesis was increased. Exposure of MMH cells to mild oxidative stress by incubation with CuSO4 (2.5 μM) for 24 h led to ...
CONTEXT: The postprandial chylomicron (CM) triacylglycerol (TG) response to dietary fat, which is positively associated with atherosclerosis and cardiovascular disease risk, displays a high interindividual variability. This is assumed to be due, at least partly, to polymorphisms in genes involved in lipid metabolism. Existing studies have focused on single nucleotide polymorphisms (SNPs), resulting in only a low explained variability. OBJECTIVE: We aimed to identify a combination of SNPs associated with the postprandial CM TG response. PARTICIPANTS AND METHODS: Thirty-three healthy male volunteers were subjected to 4 standardized fat tolerance test meals (to correct for intraindividual variability) and genotyped using whole-genome microarrays. The plasma CM TG concentration was measured at regular interval times after each meal. The association of SNPs in or near candidate genes (126 genes representing 6225 SNPs) with the postprandial CM TG concentration (0-8 h areas under the curve averaged
Da) and in size (diameter 30-80 nm), have a plasma density of 0.93-1.006 g/mL, and migrate in the prebeta region on lipoprotein electrophoresis. These particles are rich in triglyceride (about 60% by weight in the core of the particle) and contain about 10% cholesteryl ester. On their surface these particles contain about 8% protein, 7% free cholesterol, and 15% phospholipids. Although they resemble chylomicrons, the major protein of these particles is apoB-100, compared to apoB-48 in chylomicrons. Other surface proteins include apoC-I, apoC-II, and apoC-III. In the fed state, the average daily production of VLDL apoB-100 in humans is about 20 mg/kg/day.3 When VLDLs enter the bloodstream, the particles pick up apoE and other apolipoproteins from HDL. Most of the triglycerides in VLDLs are rapidly removed via the action of LPL, similar to intestinal chylomicron particles. In the fat, the free fatty acids are converted back into triglyceride for long-term energy storage. As with chylomicrons, ...
High plasma concentrations of triglyceride-rich lipoprotein are associated with an increased risk of coronary artery disease (CAD). In the postprandial state, there is a large increase in chylomicron and very low-density lipoprotein (VLDL) concentrations. The accumulation of potentially atherogenic particles is controlled by the balance of their synthesis and clearance. Chylomicrons are rich in triglyceride and secreted by the intestine postprandially. Chylomicrons compete with VLDL for hydrolysis by lipoprotein lipase (LPL). This competition may cause the increase in large plasma concentration of VLDL seen in the postprandial state. Postprandial increases in atherogenic plasma lipoprotein concentrations are accentuated in insulin-resistant states. Insulin resistance is associated with greater flux of free fatty acids, which may in turn lead to enhanced synthesis of VLDL. Alimentary lipidaemia has been shown to effect changes in the coagulation cascade which may provide additional connections between
The adipocyte plays a crucial role in metabolic regulation, serving as a storage depot for fatty acids and as an endocrine cell to manage energy utilization and feeding behavior [1, 2]. The mass of adipose tissue is maintained by a well-controlled balance of cell proliferation (hyperplasia) and increase in fat cell size (hypertrophy). Increases in adipocyte hypertrophy result from the uptake and assimilation of extracellular fatty acids into cytosolic triacylglycerol-rich lipid droplets. The primary sources of these extracellular fatty acids are those that are 1) associated with circulating albumin or 2) hydrolyzed from triacylglycerol-rich lipoprotein particles such as chylomicrons or very low density lipoproteins (VLDL). Since chylomicrons are short-lived fatty acid carriers present only during the post-prandial period, it is accepted that VLDL particles represent the major source of circulating fatty acids in the form of triacylglycerols. Triacylglycerols are the major component of VLDL and ...
240 mg/dl high cholesterol. The average amount of blood cholesterol varies with age, typically rising gradually until one is about 60 years old. There appear to be seasonal variations in cholesterol levels in humans, more, on average, in winter. These seasonal variations seem to be inversely linked to vitamin C intake. In lipid digestion, cholesterol is packed into Chylomicrons in the small intestine, which are delivered to the Portal vein and Lymph. The chylomicrons are ultimately taken up by liver hepatocytes via interaction between apolipoproteinE and the LDL receptor or Lipoprotein receptor-related proteins. Cholesterol is minimally soluble in water; it cannot dissolve and travel in the water-based bloodstream. Instead, it is transported in the bloodstream by lipoproteins that are water-soluble and carry cholesterol and triglycerides internally. The apolipoproteins forming the surface of the given lipoprotein particle determine from what cells cholesterol will be removed and to where it will ...
Lipid molecules are sucked from the order asacol online gut epithelial cells are packed into a transportation particles ventolin asma (chylomicrons) which receives via lymphatics to the bloodstream. Under the action of capillary endothelial lipoprotein main component of chylomicrons - neutral triglycerides - cleaved to glycerol and free fatty acids. Part of the fatty acids may bind to albumin and zovirax ointment genital herpes glycerol and free fatty acids act in the fat cells and converted into triglycerides. The remnants of chylomicrons blood trapped hepatocytes, are endocytosed and destroyed in the lysosomes. In the liver, forming lipoproteins for transport side effects for nexium 40 mg of synthesized lipid molecules in it. These lipoproteins are very low and low-density lipoprotein, which is transported from the liver to other tissues triglycerides, cholesterol. Low-density lipoprotein uptake from the blood cells of tissues via lipoprotein receptors endotsitiruyutsya, released for the needs ...
Familial chylomicronemia syndrome (FCS) is a serious disease that prevents the body from breaking down fats.. Eating even a little fat can make someone with FCS ill, and the condition causes chronic symptoms and can lead to potentially fatal pancreatitis. FCS is a genetic disorder passed down from parents. Because it is rare, many healthcare providers have never heard of FCS or may not know how to diagnose it.. Lipoprotein lipase is a digestive enzyme that helps the body break down structures called chylomicrons. People who have FCS have a problem with lipoprotein lipase: it is either missing or broken. Chylomicrons carry triglycerides (a type of fat) to where they are needed in the body for energy. A buildup of these particles causes an increase in triglycerides levels.. Patients with FCS have extremely high levels of triglycerides. Normal triglyceride levels fall below 150 mg/dL. For people with FCS, triglyceride levels can exceed 1,000 mg/dL, even after medication and/or a low-fat diet are ...
Olive oil increases the number of triacylglycerol-rich chylomicron particles compared with other oils: an effect retained when a second standard meal is fed.: T
Triacylgycerols (TAGs) are major sources of stored substrates that are metabolized to provide energy. Composed of 3 fatty acid chains attached to a glycerol backbone, these nonpolar molecules cannot cross cell membranes. This is overcome by a seemingly futile cycle in which most dietary TAGs are dissociated into nonesterified fatty acids (NEFAs) by a series of parallel enzymatic steps that ultimately lead to cellular NEFA uptake, its resynthesis in the endoplasmic reticulum (ER) membrane, and storage within cytosolic lipid droplets (LDs). The newly synthesized TAGs can also be stored as lipid droplets in the lumen of the enterocyte and hepatocyte ER and assembled into TAG-rich lipoproteins, chylomicrons, or very low-density lipoproteins, and secreted. In the intestine, lack of tight junctions between endothelial cells is needed to allow the large chylomicrons to cross the endothelial barrier and enter the lymphatics (1).. While TAG synthesis within enterocytes involves two pathways, the glycerol ...
In this thesis, chylomicron (CM) and CM-remnant (CM-R) metabolism in humans was studied by the application of unique markers which label these lipoprotein particles from the stage of production by the enterocyte until, removal by hepatic receptor mediated processes. Retinyl palmitate (RP) is a vitamin A ester, which labels the CM/CM-R by behaving like the cholesterol ester (CE) which is carried in the core of these particles. Development of a mono-specific antibody to apolipoprotein (apo) B-48 and application of an enzyme linked immunosorbant assay (ELISA) enabled quantification of this apolipoprotein which is specifically located on the surface of CM/CM-R. The postprandial lipaemic response for all parameters were determined by the area under the time response curve (AUC). Plasma was separated by flotation ultracentrifugation, overlayered with saline (d=1.006 g/ml), to separate the triacylglycerol-rich lipoprotein (TRL) and infranatant fractions. To examine the effects of habitual low intensity ...
Evaluate if there is any correlation among the reduction of the plasma clearance of chylomicrons by the artificial chylomicrons technique and the presence of sub-clinical ...
The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Know the risks and potential benefits of clinical studies and talk to your health care provider before participating. Read our disclaimer for details ...
Both active and passive connectivity associated with significant improvement in patient-reported perceptions of overall health, disease outlook and emotional well-being
I absolutely agree, the two pictures in Dr Ds graphs are utter opposites. I too would also doubt that the apoB100 on the VLDLs is any more toxic than the apoB45 on the chylomicrons. What matters to me is the blood glucose, spiking to 200 is killing endothelial cells, and the blood insulin (not shown but certainly spiking with the glucose) which drives the repair process beyond what is appropriate for the amount of damage done by the hyperglycaemia... And if we must include lipids we can always suggest the hyperglycaemia glycoxidises either apoB100 or apoB45 to give persistent remnants which cannot be taken up by the LDL receptors, only by RAGEs. In the latest lipid hypothesis these are the problem ones. Of course, to lipophiles these persistent remnants are markers of previous damaging hyperglycaemia, not necessarily the problem in its own right ...
Assessment: Triglyceride levels occasionally become persistently elevated in patients receiving continuous infusions of IV lipids. At very high levels (greater than 1000 mg/dl) triglycerides appear to precipitate pancreatitis.. TPN correction:. Consider cyclical administration of lipids over 12-18 hours a day to give the liver a chance to rest from the fat load. Heparin may facilitate faster metabolism of chylomicrons and reduce triglyceride levels.. ...
following lipoproteins does not move towards charged end electrophoresis Chylomicrons do not move towards the charged end in electrophoresis, as they are too large to penetrate into the resolving gel. Ref: Nutrition, Lipids, Health and Disease By Augustine S. H. O
following lipoproteins does not move towards charged end electrophoresis Chylomicrons do not move towards the charged end in electrophoresis, as they are too large to penetrate into the resolving gel. Ref: Nutrition, Lipids, Health and Disease By Augustine S. H. O
TRIGLYCERIDES In our day today life a process called metabolism takes place and for this process triglycerides acts as an energy source. These triglycerides have low density lipo proteins and chylomicrons as major components. It is important to maintain the Triglycerides levels to particular value. This is because HighTriglycerides may lead to hazardous heart disease […]. Read More » ...
The enterocyte, which lines the luminal wall of the intestine, has an expansive apical surface area and the intracellular machinery needed to produce lipoprotein vesicles that pass through the basal surface and into systemic circulation. This unique design optimizes the transfer of dietary nutrients into circulation (Mansbach and Siddiqi, 2010). One of the key players in the formation of lipoprotein vesicles or chylomicrons is MTP, making it a seemingly ideal target to disrupt dietary contributions to systemic lipid and cholesterol loads (Wierzbicki et al., 2009). Unfortunately, MTP is also found in a number of additional organs with notably high levels in the liver, retina, and heart (Borén et al., 1998; Li et al., 2005). Inhibition of hepatic MTP decreases the ability of the liver to rid itself of fat, and chronic treatment with first-generation MTP inhibitors resulted in unacceptable rises in liver transaminases and hepatic steatosis in rodent models and humans (Lammens et al., 1999; Lilly ...
J:130260 Van Dyck F, Braem CV, Chen Z, Declercq J, Deckers R, Kim BM, Ito S, Wu MK, Cohen DE, Dewerchin M, Derua R, Waelkens E, Fiette L, Roebroek A, Schuit F, Van de Ven WJ, Shivdasani RA, Loss of the PlagL2 transcription factor affects lacteal uptake of chylomicrons. Cell Metab. 2007 Nov;6(5):406-13 ...
SPARKLERS MUST BE EXTINGUISHED IN BUCKETS OR WATER OR SAND (PROVIDED BY THE RENTER) AND MUST BE THROWN AWAY. IF SPARKLER REMNANTS ARE FOUND ON THE LAWN AFTER CHECK OUT YOUR DAMAGE DEPOSIT WILL BE LOST. ...
Cholesterol is minimally soluble in water; it cannot dissolve and travel in the water-based bloodstream. Instead, it is transported in the bloodstream by lipoproteins that are water-soluble and carry cholesterol and triglycerides internally. The apolipoproteins forming the surface of the given lipoprotein particle determine from what cells cholesterol will be removed and to where it will be supplied.. The largest lipoproteins, which primarily transport fats from the intestinal mucosa to the liver, are called chylomicrons. They carry mostly fats in the form of triglycerides. In the liver, chylomicron particles release triglycerides and some cholesterol. The liver converts unburned food metabolites into very low density lipoproteins (VLDL) and secretes them into plasma where they are converted to intermediate density lipoproteins(IDL), which thereafter are converted to low-density lipoprotein (LDL) particles and non-esterified fatty acids, which can affect other body cells. In healthy individuals, ...
Background: Postprandial hypertriglyceridemia (PHTG) is caused by the accumulation of chylomicron and chylomicron remnants and has been shown to be associated with metabolic syndrome and the development of atherosclerotic cardiovascular diseases. In our previous studies, we showed that the intestinal cholesterol transporter inhibitor, ezetimibe, attenuates PHTG and postprandial elevation of FFAs in patients with type IIb hyperlipidemia (Eur J Clin Invest 2009), however the mechanisms for this have not been elucidated yet.. Methods and Results: We investigated the effect of ezetimibe on PHTG in wild-type (WT) mice fed a western diet and CD36KO mice fed a normal chow diet, which is an animal model of PHTG which was due to the intestinal over-production of chylomicrons. Ezetimibe significantly reduced TG levels at 3 hours after oral fat load using olive oil in both WT and CD36KO mice (from 375±41 to 252±19 mg/dl. 457±114 to 383±93 mg/dl, respectively). The analysis of lipoprotein profiles by ...
TY - JOUR. T1 - A frequently occurring mutation in the lipoprotein lipase gene (Asn291Ser) results in altered postprandial chylomicron triglyceride and retinyl palmitate response in normolipidemic carriers. AU - Pimstone, Simon N.. AU - Clee, Susanne M.. AU - Gagné, S. Eric. AU - Miao, Li. AU - Zhang, Hanfang. AU - Stein, Evan A.. AU - Hayden, Michael R.. PY - 1996/8/1. Y1 - 1996/8/1. N2 - An Asn291Ser mutation in exon 6 of the lipoprotein lipase gene (LPL) frequently occurs in Caucasians (2-4%) and results in a partial catalytic defect. Although this mutation may be associated with low HDL cholesterol and elevated triglyceride levels, some carriers are normolipidemic and may have LPL activity in the normal range in the fasting state. To assess in vivo the influence of dietary stress on the function of this mutation, we have performed oral fat load studies on three unrelated normolipidemic Asn291Ser carriers and compared these results to five healthy controls and to a subject with a clear 50% ...
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 ...
Cholesterol is minimally soluble in water; it cannot dissolve and travel in the water-based bloodstream. Instead, it is transported in the bloodstream by lipoproteins that are water-soluble and carry cholesterol and triglycerides internally. The apolipoproteins forming the surface of the given lipoprotein particle determine from what cells cholesterol will be removed and to where it will be supplied.. The largest lipoproteins, which primarily transport fats from the intestinal mucosa to the liver, are called chylomicrons. They carry mostly fats in the form of triglycerides. In the liver, chylomicron particles release triglycerides and some cholesterol. The liver converts unburned food metabolites into very low density lipoproteins (VLDL) and secretes them into plasma where they are converted to intermediate density lipoproteins(IDL), which thereafter are converted to low-density lipoprotein (LDL) particles and non-esterified fatty acids, which can affect other body cells. In healthy individuals, ...
Cabello-Moruno, R and Sinausia, L and Montero, E and Botham, K M and Avella, M A and Perona, J S (2015) Minor components of pomace olive oil enhance VLDL-receptor expression in macrophages when treated with postprandial triglyceride-rich lipoproteins. GRASAS Y ACEITES, 66 (4). Bentley, C and Hathaway, N and Widdows, J and Bejta, F and De Pascale, C and Avella, M A and Wheeler-Jones, C P D and Botham, K M and Lawson, C (2011) Influence of chylomicron remnants on human monocyte activation in vitro. NUTRITION METABOLISM AND CARDIOVASCULAR DISEASES, 21 (11). pp. 871-878. Lopez-Soldado, I and Avella, M A and Botham, K M (2009) Differential influence of different dietary fatty acids on very low-density lipoprotein secretion when delivered to hepatocytes in chylomicron remnants. Metabolism-Clinical and Experimental, 58 (2). pp. 186-195. Lopez-Soldado, I and Avella, M A and Botham, K M (2009) Suppression of VLDL secretion by cultured hepatocytes incubated with chylomicron remnants enriched in n-3 ...
1. Substrate movements in forearm muscle and subcutaneous adipose tissue were studied, by measurement of arteriovenous differences and blood flow, in seven normal subjects after an overnight fast and then for 6 h after ingestion of a mixed meal. Overall substrate balances were examined in terms of the flux of gram-atoms of carbon.. 2. As found previously, the forearm was approximately in carbon balance (import equal to export) after the overnight fast, whereas adipose tissue was a net exporter of carbon, mainly in the form of non-esterified fatty acids.. 3. After the meal, arterialized plasma concentrations of glucose and lactate rose sharply (peak at 60 min), whereas those of non-esterified fatty acids and glycerol fell (nadir at 60-120 min). Plasma triacylglycerol concentrations rose slowly to peak at 240 min; much of this rise was accounted for by a rise in the chylomicron fraction.. 4. Both tissues took up glucose at an increased rate after the meal. Release of non-esterified fatty acids and ...
This interaction causes the endocytosis of the chylomicron remnants, which are subsequently hydrolyzed within lysosomes. The proteins included in the external shell of these particles, called apolipoproteins, are synthesized and secreted into the extracellular water by both the small intestine and liver cells. HDL are lipoproteins, carrying mostly cholesterol and phospholipids from peripheral tissues to the liver ... HDL plays an important role in transporting cholesterol from the peripheral tissues to the liver, where it can be excreted; this process is known as reverse cholesterol transport (RCT). HDL has the ability to bind LPS and LTA, creating HDL-LPS complexes to neutralize the harmful effects in the body and clear the LPS from the body. The main task of HDL is to carry cholesterol from the peripheral tissues, including the artery walls, to the liver. In the blood stream, nascent chylomicron particles interact with HDL particles, resulting in HDL donation of apolipoprotein C-II and ...
Compared with nondiabetic individuals, patients with type 2 diabetes are at a much greater risk for CVD. Consequently, the treatment of CVD risk factors is a healthcare priority in this patient population. A number of clinical trials with 3-hydroxy-3-methylglutaryl (HMG) CoA (HMG-CoA) reductase inhibitors (statins) have shown significant CVD risk reduction through LDL cholesterol lowering in patients with diabetes,172-177 mainly through increased LDL-receptor activity.178 Increased LDL-receptor activity may also correct chylomicron metabolism.179 Indeed, the recently published Collaborative Atorvastatin Diabetes Study (CARDS), a placebo-controlled trial of patients with type 2 diabetes, was terminated 2 years earlier than its anticipated length owing to the significant reduction in number of CVD events observed in patients randomized to receive low-dose atorvastatin versus placebo.172 The statin therapy in this trial resulted in significant reduction of CVD events in patients with type 2 ...
The liver can convert carbohydrate to fat, which is exported from the liver as a lipoprotein. The lipoprotein complex responsible for transporting lipids from the small intestine is in the form of chylomicrons. It is the chylomicrons that responsible for the milky appearance of blood plasma that occurs after a meal rich in fat has been eaten ...
and the therapeutic and commercial potential of WAYLIVRA and other products in development. Any statement describing Ionis or Akceas goals, expectations, financial or other projections, intentions or beliefs, including the commercial potential of TEGSEDI, WAYLIVRA or other of Ionis or Akceas drugs in development is a forward-looking statement and should be considered an at-risk statement. Such statements are subject to certain risks and uncertainties, particularly those inherent in the process of discovering, developing and commercializing drugs that are safe and effective for use as human therapeutics, and in the endeavor of building a business around such drugs. Ionis and Akceas forward-looking statements also involve assumptions that, if they never materialize or prove correct, could cause its results to differ materially from those expressed or implied by such forward-looking statements. Although Ionis and Akceas forward-looking statements reflect the good faith judgment of its ...
HDL and LDL determinations used in human medicine; values reported for HDL and LDL in dogs and cats cannot be assumed to be reliable.  Chylomicron test obtain serum sample after a 12-hour fast and refrigerate for 12-14 hours; do not freeze; chylomicrons rise to the surface and form a creamy layer.  Lipoprotein electrophoresis separates LDL, VLDL, HDL1, and HDL2  LPL activity collect serum for triglycerides and cholesterol concentrations and lipoprotein electrophoresis before and 15 min after IV administration of heparin (90 IU/kg); if there is no change in values before and after heparin administration, a defective LPL enzyme system should be suspected.  T and T determinations indicated if hypothyroidism is suspected  Adrenocorticotropic hormone (ACTH) stimulation test indicated if hyperadrenocorticism is DIAGNOSTIC PROCEDURES ...
... to the nascent chylomicron and, thus, converts it to a mature chylomicron (often referred to simply as "chylomicron"). APOC2 is ... Apolipoproteins are significant in the synthesis and metabolism of chylomicrons. Newly formed chylomicrons are secreted through ... becomes a chylomicron remnant, now only 30-50 nm. ApoB48 and APOE are important to identify the chylomicron remnant in the ... From there the chylomicrons supply the tissue with fat absorbed from the diet. Thus, unlike the saccharides and amino acids ...
Without functional chylomicrons, certain fat-soluble vitamins such as vitamin D and vitamin E cannot be absorbed. Chylomicrons ... These proteins are critical for release of chylomicrons in the body. Chylomicron retention disease is an autosomal homozygous ... The pre-chylomicrons are then packaged into PCTV in order to be transported to the Golgi apparatus for additional maturation ... In chylomicron retention disease, the PCTV vesicles are competent for budding from the ER membrane but are defective for fusion ...
Kuksis A (2000). "Biochemistry of Glycerolipids and Formation of Chylomicrons". In Christophe AB, DeVriese S (eds.). Fat ... while long-chain fatty acids are packed into chylomicrons, enter lymphatic capillaries, then transfer to the blood at the ...
CYBB Chylomicron retention disease; 246700; SAR1B Ciliary dyskinesia, primary, 1, with or without situs inversus; 244400; DNAI1 ...
The hydrolyzed chylomicrons are now called chylomicron remnants. The chylomicron remnants continue circulating the bloodstream ... The chylomicron at this stage is then considered mature. Via apolipoprotein C-II, mature chylomicrons activate lipoprotein ... Chylomicrons carry triglycerides (fat) from the intestines to the liver, to skeletal muscle, and to adipose tissue. Very-low- ... Then these lipids are assembled with apolipoprotein B-48 into nascent chylomicrons. These particles are then secreted into the ...
"Incorporation of carotenoids from paprika oleoresin into human chylomicrons". Br. J. Nutr. 89 (6): 787-93. doi:10.1079/ ...
"Incorporation of carotenoids from paprika oleoresin into human chylomicrons". British Journal of Nutrition. 89 (6): 787-793. ...
"Chylomicrons: Advances in biology, pathology, laboratory testing, and therapeutics". ResearchGate. Caprio S, Pierpont B, ...
VLDL is one of the five major groups of lipoproteins (chylomicrons, VLDL, intermediate-density lipoprotein, low-density ... VLDL transports endogenous products, whereas chylomicrons transport exogenous (dietary) products. In the early 2010s both the ...
The lipids in the chyle are colloidally suspended in chylomicrons. A chyle fistula occurs when defect(s) of lymphatic vessel(s ...
Since there is no or little assimilation of chylomicrons, their levels in plasma remains low.[citation needed] The inability to ... Low levels of plasma chylomicron are also characteristic.[citation needed] There is an absence of apolipoprotein B. On ... January 2013). "Novel mutations in SAR1B and MTTP genes in Tunisian children with chylomicron retention disease and ... September 2018). "Efficacy of two vitamin E formulations in patients with abetalipoproteinemia and chylomicron retention ...
The triglycerides in chylomicrons are hydrolyzed by lipoprotein lipase (LPL) along the luminal surface of capillaries, mainly ... GPIHBP1 is a capillary endothelial cell protein that provides a platform for LPL-mediated processing of chylomicrons. GRCh38: ... Dietary fats are packaged by intestine into triglyceride-rich lipoproteins called chylomicrons. ... "The Acidic Domain of GPIHBP1 is Important for the Binding of Lipoprotein Lipase and Chylomicrons". Journal of Biological ...
... assembly and secretion of chylomicrons. These chylomicrons transport dietary lipids to tissues while the remaining chylomicrons ... ApoB 48 is a unique protein to chylomicrons from the small intestine. After most of the lipids in the chylomicron have been ... Apolipoprotein B is the primary apolipoprotein of chylomicrons, VLDL, Lp(a), IDL, and LDL particles (LDL-commonly known as "bad ... Intestinal proteins containing ApoB48 are metabolized to chylomicron remnant particles which are taken up by remnant receptors ...
At this point, the fats are in the bloodstream in the form of chylomicrons. Once in the blood, chylomicrons are subject to ... now referred to as a chylomicron remnant) can be taken up by the liver. From the liver, the fat released from chylomicron ... 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. ...
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): ...
The chylomicrons are small enough to pass through the enterocyte villi and into their lymph capillaries called lacteals. A ... From this breakdown, smaller particles of emulsified fats called chylomicrons are produced. There are also digestive cells ... milky fluid called chyle, consisting mainly of the emulsified fats of the chylomicrons, results from the absorbed mix with the ...
Hofmann AF (Sep 1960). "Exchange of iodine-131-labeled chylomicron protein in vitro". Am. J. Physiol. 199 (3): 433-6. doi: ... His initial publications in 1960 characterized his future research: Exchange of iodine-131-labeled chylomicron protein in vitro ...
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. ...
... triglycerides are combined with vitamins and cholesterol to form chylomicrons. Chylomicrons travel from the intestine into the ... Enzymatic catalysis of chylomicrons by lipases in the bloodstream enables the uptake of lipids and fatty acids by cells. In ...
May 2005). "CD36 deficiency impairs intestinal lipid secretion and clearance of chylomicrons from the blood". The Journal of ...
The chylomicron enters a lymphatic capillary and enters into the bloodstream first at the left subclavian vein (having bypassed ... The chylomicrons are ultimately taken up by liver hepatocytes via interaction between apolipoproteinE and the LDL receptor or ... In the liver, chylomicron particles release triglycerides and some cholesterol. The liver converts unburned food metabolites ... In lipid digestion, cholesterol is packed into Chylomicrons in the small intestine, which are delivered to the Portal vein and ...
After a meal, roughly two-thirds of the chylomicrons are taken up by the liver with the remainder delivered to peripheral ... Absorbed β-carotene is either incorporated as such into chylomicrons or first converted to retinal and then retinol, bound to ... Peripheral tissues also can convert chylomicron β-carotene to retinol. The capacity to store retinol in the liver means that ... Hepatocytes take up the lipid-rich chylomicrons, bind retinol to retinol-binding protein 4 (RBP4), and transfer the retinol- ...
Chylomicrons are degraded, VLDLs are converted to LDLs, and LDLs are converted to HDL. This is accompanied by a slight increase ...
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 ... a carboxylate It is also involved in promoting the cellular uptake of chylomicron remnants, cholesterol-rich lipoproteins, and ... high-density lipoprotein-binding protein 1 plays a critical role in the lipolytic processing of chylomicrons". Cell Metabolism ...
The thoracic duct empties the chylomicrons into the bloodstream via the left subclavian vein. At this point the chylomicrons ... They are taken in through the intestine in chylomicrons, but also exist in very low density lipoproteins (VLDL) and low density ... The triglycerides are coated with cholesterol and protein (protein coat) into a compound called a chylomicron. From within the ... cell, the chylomicron is released into a lymphatic capillary called a lacteal, which merges into larger lymphatic vessels. It ...
2003). "Intestinal alkaline phosphatase release is not associated with chylomicron formation". Am. J. Physiol. Gastrointest. ...
A third form, chylomicron retention disease (CRD), is associated with SARA2. Typically in hypobetalipoproteinemia, plasma ...
... A-IV (apoA4) is present in chylomicrons, very-low-density lipoproteins (VLDL), and HDL. It is thought to act ... primarily in reverse cholesterol transport and intestinal lipid absorption via chylomicron assembly and secretion. ApoA-IV ...
Chylomicrons are one sub-group of lipoproteins which carry the digested lipids from small intestine to the rest of the body. ... Chylomicrons will travel through the bloodstream to enter adipose and other tissues in the body. Due to the hydrophobic nature ... Once the chylomicrons (or other lipoproteins) travel through the tissues, these particles will be broken down by lipoprotein ... In the cytosol of epithelial cells, triglycerides and cholesterol are packaged into bigger particles called chylomicrons which ...
Symptoms are caused by an increase in the level of chylomicron in the retinal circulation. Though visual acuity is not affected ... In primary hyperlipidaemia, LR occurs only in patients with increased chylomicron levels. Lipaemia retinalis occurs commonly ...
... to the nascent chylomicron and, thus, converts it to a mature chylomicron (often referred to simply as "chylomicron"). APOC2 is ... Apolipoproteins are significant in the synthesis and metabolism of chylomicrons. Newly formed chylomicrons are secreted through ... becomes a chylomicron remnant, now only 30-50 nm. ApoB48 and APOE are important to identify the chylomicron remnant in the ... From there the chylomicrons supply the tissue with fat absorbed from the diet. Thus, unlike the saccharides and amino acids ...
Chylomicron retention disease is an inherited disorder that impairs the normal absorption of fats, cholesterol, and certain ... Chylomicron Retention Disease. 2022 Mar 24. In: Adam MP, Everman DB, Mirzaa GM, Pagon RA, Wallace SE, Bean LJH, Gripp KW, ... Mutations in a gene called SAR1B cause chylomicron retention disease. The SAR1B gene provides instructions for making a protein ... Chylomicrons are needed to absorb fat-soluble vitamins and carry fats and cholesterol from the small intestine into the ...
Gel Scan of Chylomicrons, Human Plasma. This information is representative of the product ART prepares, but is not lot specific ... Circulation of chylomicrons distributes dietary triglyceride to adipose tissue and to muscle. Found in post prandial plasma, ... Chylomicrons are the large triglyceride-rich lipoproteins of enteric origin that carry exogenous triglycerides into the plasma ... chylomicrons generally clear the blood stream in a few hours.. Purity: Essentially free of other plasma lipoproteins as ...
Reactome is pathway database which provides intuitive bioinformatics tools for the visualisation, interpretation and analysis of pathway knowledge.
18F]BODIPY-triglyceride-containing chylomicron-like particles as an imaging agent for brown adipose tissue in vivo. In: ... 18F]BODIPY-triglyceride-containing chylomicron-like particles as an imaging agent for brown adipose tissue in vivo. Scientific ... 18F]BODIPY-triglyceride-containing chylomicron-like particles as an imaging agent for brown adipose tissue in vivo. / Paulus, ... title = "[18F]BODIPY-triglyceride-containing chylomicron-like particles as an imaging agent for brown adipose tissue in vivo", ...
... ... Novel mutations in SAR1B and MTTP genes in Tunisian children with chylomicron retention disease and abetalipoproteinemia / ... Novel mutations in SAR1B and MTTP genes in Tunisian children with chylomicron retention disease and abetalipoproteinemia / ... Monogenic hypobetalipoproteinemias include three disorders: abetalipoproteinemia (ABL) and chylomicron retention disease (CMRD ...
Triglycerides - VLDL and Chylomicrons Reviewed by Tim Matt on March 27, 2020 Rating: 5 ... A triglyceride and cholesterol collection surrounded by an outer layer of lipoprotein is called a chylomicron. (Chlymicrons ... and triglycerides are absorbed into the intestines and are packed into a number of circular particles known as chylomicrons ... have a chemical composition of 10 percent cholesterol and 90 percent triglycerides). The liver removes chylomicrons and ...
Despite fat malabsorption and the absence of postprandial chylomicrons, the oral route can prevent neurological complications ... hypobetalipoproteinemia and chylomicron retention disease (CRD), are rare genetic diseases that cause malnutrition, failure to ... Table 1 Clinical and Biological Expressions of Chylomicron Retention Disease in Studies with Genotyping. Full size table. ... Peretti, N., Sassolas, A., Roy, C.C. et al. Guidelines for the diagnosis and management of chylomicron retention disease based ...
Chylomicron and VLDL metabolism. Any disturbance that causes increased synthesis of chylomicrons and/or VLDLs or decreased ... 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 structural apolipoprotein that is not removed during catabolism of the chylomicron. Chylomicrons enter the plasma via the ...
Chylomicron retention disease; Anderson´s disease - SAR1B gene. ... Chylomicron retention disease; Anderson´s disease - SAR1B gene ... During digestion, chylomicrons form inside the enterocytes that line the small intestine and absorb nutrients. Chylomicrons are ... As a consequence, mature chylomicrons are not released into the bloodstream. The deteriorated transport of chylomicrons causes ... Chylomicron retention disease, also known as Andersons disease, is a hereditary process that affects the normal absorption of ...
... chylomicrons; Str, strawberry; Pbo, placebo; FD, freeze-dried; WBB, wild blueberry; ORAC, oxygen radical absorbance capacity; ... chylomicron and VLDL concentrations postmeal. Overall, seven trials reported no specific advantage on postprandial TAG ... reported changes in plasma TAG and chylomicron (B-48) concentrations postmeal and another(Reference Blanco-Colio, Valderrama ...
Lipoprotein lipase (LPL) releases free fatty acids (FFAs) from chylomicrons (chylo) and produces chylomicron remnants that are ... 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)? ...
... it has not been studied in conditions where the major abnormality is elevation of chylomicrons, VLDL or IDL (i.e., ...
Chylomicrons. Mustacich DJ, Bruno RS, Traber MG. 2007. Vitamin E.. Vitam Horm. 76:1-21. ...
I. Development of intestinal lipid absorption: cellular events in chylomicron assembly and secretion. Am J Physiol Gastrointest ...
Contrast the serum tryiglycerides (Chylomicrons, VLDL, and recommended levels). * Contrast the serum cholesterol (LDL, HDL and ...
In the enterocyte, all of our fatty acids are going to be reorganized into what are called chylomicrons, chylomicrons. And like ... Instead, chylomicrons will be absorbed into what are called lymphatic, lymphatic capillary, also known as a lacteal, a ... And these are big enough to accommodate our chylomicrons. Here, theyre going to be further digested and broken down into ... the name, chylomicrons themselves are too big to fit directly into a blood capillary. I couldnt even fit it here in this ...
Interchange of apolipoproteins between chylomicrons and high density lipoproteins during alimentary lipemia in man. Havel RJ, ...
My interest was to discern the nature of the lipoproteins on the surface of chylomicrons. Fortunately for me, Dr. Donald ... he and scientists at the Rockefeller Institute in New York supplied me with copious quantities of human chylomicrons. Using a ... an enzyme that hydrolyzed the triglycerides in chylomicrons, the principle form of fat circulating in the bloodstream. Using ... lab I acquired expert training in the use of cultured heart cells for discerning the uptake of tritium-labeled chylomicrons. ...
Major protein of plasma HDL, also found in chylomicrons. Synthesized in the liver and small intestine. ...
However, long chain fatty acids are transported as triglycerides via chylomicrons through lymphatic circulation. Further, ...
Chylomicron remnant, Chylomicron, Arachidonic acid, Bone marrow, Platelets, Protein S, Prothrombin, Triglycerides., ... Chylomicron remnant; Chylomicron; Arachidonic acid; Bone marrow; Platelets; Protein S; Prothrombin; Triglycerides.; ... 1. Platelets take up chylomicrons (CM) in vitro, the main part being sequestered in open canalicular system and not degraded, ... 1. Platelets take up chylomicrons (CM) in vitro, the main part being sequestered in open canalicular system and not degraded, ...
Vis forfatter(e) (1992). Uptake of chylomicron remnant retinyl esters in human leukocytes in vivo. European J. Clin.. 229-234. ...
Even in the absence of chylomicrons, the distribution of soluble apoproteins in particles of diameters greater than 700-800 A ... This suggests that the largest particles may include products of the partial catabolism of chylomicrons. ...
chylomicrons (1) * dyslipidemias (1) * hemoglobin a, glycosylated (1) * hypertriglyceridemia (1) * lipoproteins, vldl (1) ...
Vitamin K is absorbed along with dietary fat from the small intestine and transported by chylomicrons in the circulation.[10] ...
... mainly from chylomicrons- and VLDL-TG. These alterations are usually reverted to normal after gastric bypass surgery (GB), ...
The Role of microsomal triglyceride transfer protein and dietary cholesterol in chylomicron production in diabetes Diabetologia ...
Long-chain fatty acids (LCFA) are incorporated into chylomicrons and enter the lymphatic system. MCFA are readily broken down ...
  • The liver removes chylomicrons and triglycerides from the bloodstream and synthesizes and binds them to VLDL or lipoprotein particles of very low density and releases them back into the bloodstream. (dietodiet.com)
  • They are carried on 4 types of lipoproteins: chylomicrons, low-density lipoproteins (LDL), very-low-density lipoproteins (VLDL) and high-density lipoproteins (HDL). (who.int)
  • Background & objectives: Obesity is often associated with increased postprandial triglyceride (TG) concentrations, mainly from chylomicrons- and VLDL-TG. (researchgate.net)
  • 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 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)
  • Chylomicrons and VLDL production originating from the intestine and liver are increased. (endotext.org)
  • 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)
  • 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)
  • Thus, pharmacologic inhibition of MTP decreases formation of chylomicrons and very-low-density lipoprotein (VLDL) particles resulting in net LDL-particle reduction. (2minutemedicine.com)
  • 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)
  • The largest and least dense particle called a chylomicron takes the fat from your intestines to the liver where they are packaged into LDL (low density) particles, VLDL (very low density) particles or HDL which carry cholesterol and triglycerides through the blood sometimes depositing these in the heart blood vessel walls where they promote heart disease. (drdavidheber.com)
  • Chylomicrons are the large triglyceride-rich lipoproteins of enteric origin that carry exogenous triglycerides into the plasma. (athensresearch.com)
  • Chylomicrons, the principal carriers of dietary lipids, are triglyceride (TG)-rich lipoproteins secreted exclusively from the enterocyte. (biomedcentral.com)
  • Interchange of apolipoproteins between chylomicrons and high density lipoproteins during alimentary lipemia in man. (nih.gov)
  • 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)
  • 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)
  • This gene product is the main apolipoprotein of chylomicrons and low density lipoproteins. (genetex.com)
  • The enzyme hydrolyzes triacylglycerols in chylomicrons, very-low-density lipoproteins, low-density lipoproteins, and diacylglycerols. (bvsalud.org)
  • Chylomicron retention disease is an inherited disorder that impairs the normal absorption of fats, cholesterol, and certain vitamins from food. (medlineplus.gov)
  • The features of chylomicron retention disease primarily affect the gastrointestinal system and nervous system. (medlineplus.gov)
  • Chylomicron retention disease begins in infancy or early childhood. (medlineplus.gov)
  • Other features of chylomicron retention disease develop later in childhood and often impair the function of the nervous system. (medlineplus.gov)
  • Chylomicron retention disease is a rare condition with approximately 50 cases described worldwide. (medlineplus.gov)
  • Mutations in a gene called SAR1B cause chylomicron retention disease. (medlineplus.gov)
  • Impaired chylomicron transport causes severely decreased absorption (malabsorption) of dietary fats and fat-soluble vitamins, leading to nutritional and developmental problems in people with chylomicron retention disease. (medlineplus.gov)
  • Charcosset M, Sassolas A, Peretti N, Roy CC, Deslandres C, Sinnett D, Levy E, Lachaux A. Anderson or chylomicron retention disease: molecular impact of five mutations in the SAR1B gene on the structure and the functionality of Sar1b protein. (medlineplus.gov)
  • Anderson's disease (chylomicron retention disease): a new mutation in the SARA2 gene associated with muscular and cardiac abnormalities. (medlineplus.gov)
  • Novel mutations in SAR1B and MTTP genes in Tunisian children with chylomicron retention disease and abetalipoproteinemia. (unimore.it)
  • Monogenic hypobetalipoproteinemias include three disorders: abetalipoproteinemia (ABL) and chylomicron retention disease (CMRD) with recessive transmission and familial hypobetalipoproteinemia (FHBL) with dominant transmission. (unimore.it)
  • Familial hypocholesterolemia, namely abetalipoproteinemia, hypobetalipoproteinemia and chylomicron retention disease (CRD), are rare genetic diseases that cause malnutrition, failure to thrive, growth failure and vitamin E deficiency, as well as other complications. (biomedcentral.com)
  • Over the last 20 years, genetic abnormalities have been identified for three main disorders classified as familial hypocholesterolemia: hypobetalipoproteinemia (HBL), abetalipoproteinemia (ABL) and chylomicron retention disease (CRD). (biomedcentral.com)
  • Chylomicron retention disease, also known as Anderson's disease, is a hereditary process that affects the normal absorption of fats, cholesterol and certain vitamins from food. (ivami.com)
  • More than 20 mutations in the SAR1B gene have been described in individuals with chylomicron retention disease. (ivami.com)
  • in IVAMI we perform the detection of mutations associated with chylomicron retention disease, by complete PCR amplification of the exons of the SAR1B gene, and their subsequent sequencing. (ivami.com)
  • For this purpose we designed a dual-modal fluorescent/PET fatty acid tracer based on commercially available BODIPY-FL-C-16, which can be esterified to its correspondent triglyceride, radiolabeled and incorporated into pre-synthesized chylomicron-like particles. (maastrichtuniversity.nl)
  • BODIPY-FL-C-16 was coupled to 1,2-diolein with a subsequent radiolabeling step resulting in [F-18] BODIPY-C-16-triglyceride that was incorporated into chylomicron-like particles. (maastrichtuniversity.nl)
  • Triglyceride synthesis, radiolabeling and subsequent incorporation into chylomicron-like particles was carried out in decent yields. (maastrichtuniversity.nl)
  • The here reported method can be used to incorporate radiolabeled triglycerides into pre-synthesized chylomicron-like particles. (maastrichtuniversity.nl)
  • Therefore, after eating, cholesterol and triglycerides are absorbed into the intestines and are packed into a number of circular particles known as chylomicrons before they are released into the bloodstream. (dietodiet.com)
  • Liposyn III 30 (liposyn iii 30 intravenous far emulsion) % contains emulsified fat particles of approximately 0.4 micron in diameter, similar to naturally occurring chylomicrons. (rxlist.com)
  • The improved hydration of the interstitium disrupts SAHA enzyme inhibitor the matrix structure (e.g., launch of hyaluronan23) and decreases macromolecular exclusion in the interstitial gel (see Fig. 4), thereby allowing particles the size of chylomicrons to traverse the interstitium with relative simplicity. (columbiagypsy.net)
  • It slows the production of chylomicrons, which are fat particles associated with these metabolic disorders. (holistichelp.net)
  • 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)
  • Chylomicron remnants bind to specific receptors in the liver through which apolipoprotein? (topgradeapp.com)
  • A triglyceride and cholesterol collection surrounded by an outer layer of lipoprotein is called a chylomicron. (dietodiet.com)
  • 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)
  • After entering the cells, the fatty acids are re-esterified into triglycerides, provided with a glycoprotein coating, and enter the interstitium as chylomicrons. (columbiagypsy.net)
  • After absorption, retinol is transported via chylomicrons to the liver, where it is either stored as retinol ester or reexported into the plasma in combination with retinol-binding protein for delivery to tissue sites. (medscape.com)
  • Besides a low-long chain fat diet made up uniquely of polyunsaturated fatty acids, treatment includes fat-soluble vitamin supplements and large amounts of vitamin E. Despite fat malabsorption and the absence of postprandial chylomicrons, the oral route can prevent neurological complications even though serum levels of vitamin E remain chronically low. (biomedcentral.com)
  • The postprandial chylomicron triacylglycerol response to dietary fat in healthy male adults is significantly explained by a combination of single nucleotide polymorphisms in genes involved in triacylglycerol metabolism. (cdc.gov)
  • I. Development of intestinal lipid absorption: cellular events in chylomicron assembly and secretion. (bmj.com)
  • Movement of chylomicrons through the interstitium is definitely facilitated by the improved interstitial volume during fluid absorption. (columbiagypsy.net)
  • The SAR1B gene provides instructions for making a protein that is needed for the transport of molecules called chylomicrons. (medlineplus.gov)
  • SAR1B gene mutations cause the retention of chylomicrons within enterocytes and prevent their release into the bloodstream. (medlineplus.gov)
  • This process is due to mutations in the SAR1B ( secretion associated Ras related GTPase 1B ) gene, located on the long arm of chromosome 5 (5q31.1), which encodes a protein that is needed for the transport of chylomicrons. (ivami.com)
  • All the mutations described inhibit the ability of the SAR1B protein to transport immature chylomicrons of the endoplasmic reticulum to the Golgi apparatus. (ivami.com)
  • Chylomicrons are needed to absorb fat-soluble vitamins and carry fats and cholesterol from the small intestine into the bloodstream . (medlineplus.gov)
  • As a consequence, mature chylomicrons are not released into the bloodstream. (ivami.com)
  • This scenario is supported by reports that the rate of chylomicron transit to the lymphatics is definitely directly related to the degree of interstitial hydration.35 Intestinal fluid secretion Solute-coupled secretion Although the small intestine is generally regarded as an absorptive organ, it can be induced to secrete fluid under certain conditions, some of which are most likely pathologic, e.g., cholera toxin. (columbiagypsy.net)
  • During digestion, chylomicrons form inside the enterocytes that line the small intestine and absorb nutrients. (ivami.com)
  • Circulation of chylomicrons distributes dietary triglyceride to adipose tissue and to muscle. (athensresearch.com)
  • The deteriorated transport of chylomicrons causes malabsorption of dietary fats and fat-soluble vitamins, which leads to nutritional and developmental problems. (ivami.com)
  • Dietary intake of fat provides the intestine with TG for chylomicron formation, which is upregulated in insulin resistance. (endotext.org)
  • Drying a fresh lutein-enriched egg-yolk beverage would extend its shelf life, however, functional properties should not be affected and no significant change in serum cholesterol level was seen in the beverages containing luteIn-en enriched egg-Yolk compared to the control drink. (semanticscholar.org)
  • And like the name, chylomicrons themselves are too big to fit directly into a blood capillary. (khanacademy.org)
  • Instead, chylomicrons will be absorbed into what are called lymphatic, lymphatic capillary, also known as a lacteal, a lymphatic capillary. (khanacademy.org)
  • In the enterocyte, all of our fatty acids are going to be reorganized into what are called chylomicrons, chylomicrons. (khanacademy.org)
  • Chylomicron transportation The procedure by which essential fatty acids are absorbed would depend on the chain duration and drinking water solubility. (columbiagypsy.net)
  • Found in post prandial plasma, chylomicrons generally clear the blood stream in a few hours. (athensresearch.com)
  • Major protein of plasma HDL, also found in chylomicrons. (abcam.com)
  • The chylomicrons enter the initial lymphatics primarily through these large interendothelial cell gaps. (columbiagypsy.net)
  • Severe hypertriglyceridaemia is usually caused by the pathological presence of chylomicrons in the fasting state. (bmj.com)
  • Hesse D, Jaschke A, Chung B, Schurmann A. Trans-Golgi proteins participate in the control of lipid droplet and chylomicron formation. (medlineplus.gov)
  • Rat lymph chylomicrons and chylomicron remnants were treated with trypsin or Pronase. (northwestern.edu)
  • We conclude that apoproteins are not required for the hepatic differentiation between chylomicrons and remnants, and suggest that the lipoprotein phospholipids may play a direct role in this process. (northwestern.edu)
  • Chylomicron remnants bound to rabbit alveolar macrophages with high- affinity (K(d) = 3.3 ± 0.71 μg of protein/mL). (edu.au)
  • Chylomicron remnants were degraded by alveolar macrophages from Watanabe heritable hyperlipidemic (WHHL) rabbits, which are devoid of LDL receptor activity. (edu.au)
  • Moreover, colchicine and monensin which are endocytotic and lysozomal inhibitors, respectively, did not have any effect on the degradation of chylomicron remnants by macrophages from normal rabbits. (edu.au)
  • Collectively, our data show that chylomicron remnants are metabolized by phagocytotic pathways initiated after binding to a cell surface protein which is distinct from the LDL receptor, LRP, or scavenger receptors. (edu.au)
  • Chylomicron remnants: mediators of endothelial dysfunction? (rvc.ac.uk)
  • A LDL-receptor related protein involved in clearance of chylomicron remnants and of activated ALPHA-MACROGLOBULINS from plasma. (umassmed.edu)
  • It's interaction with specific ApoE receptor enables uptake of chylomicron remnants by liver cells, which is an essential step during normal lipid metabolism. (wlsolutions.be)
  • azithromycin is typically caused by overuse of topical or oral ce xime mg daily ticagrelor cyclopentyl triazolopyrimidine reversible active moiety converted to chylomicron remnants. (easternpropane.com)
  • Similar delaying effects have been demonstrated on the presence of chylomicrons and fat in the intestinal lymph fluid. (inchem.org)
  • Then they are again synthesized in the mucosa: being concentrated, they are transferred to the lymph, where they are picked up by the chylomicrons and sent to the liver. (imedix.com)
  • So-called chylomicrons carry vitamin E from the intestine to the liver by way of the body's lymph and blood vessels. (healthandscience.eu)
  • MCT's are quickly taken up in the blood rather than through the lymph/chylomicron system, which is normal for fats from olive & sunflower oil. (wellologyco.com)
  • Chylomicron retention disease (CRD) is a type of familial hypocholesterolemia characterized by malnutrition, failure to thrive, growth failure, vitamin E deficiency and hepatic, neurologic and ophthalmologic complications. (nih.gov)
  • Chylomicron retention disease is a genetic disease, which means that it is caused by one or more genes not working correctly. (nih.gov)
  • Chylomicron retention disease is an inherited disorder that impairs the normal absorption of fats, cholesterol, and certain vitamins from food. (medlineplus.gov)
  • The features of chylomicron retention disease primarily affect the gastrointestinal system and nervous system. (medlineplus.gov)
  • Chylomicron retention disease begins in infancy or early childhood. (medlineplus.gov)
  • Other features of chylomicron retention disease develop later in childhood and often impair the function of the nervous system. (medlineplus.gov)
  • Chylomicron retention disease is a rare condition with approximately 50 cases described worldwide. (medlineplus.gov)
  • Mutations in a gene called SAR1B cause chylomicron retention disease. (medlineplus.gov)
  • SAR1B gene mutations cause the retention of chylomicrons within enterocytes and prevent their release into the bloodstream. (medlineplus.gov)
  • Impaired chylomicron transport causes severely decreased absorption (malabsorption) of dietary fats and fat-soluble vitamins, leading to nutritional and developmental problems in people with chylomicron retention disease. (medlineplus.gov)
  • Charcosset M, Sassolas A, Peretti N, Roy CC, Deslandres C, Sinnett D, Levy E, Lachaux A. Anderson or chylomicron retention disease: molecular impact of five mutations in the SAR1B gene on the structure and the functionality of Sar1b protein. (medlineplus.gov)
  • Anderson's disease (chylomicron retention disease): a new mutation in the SARA2 gene associated with muscular and cardiac abnormalities. (medlineplus.gov)
  • Chylomicron retention disease (CMRD), characterized by the inability to secrete chylomicrons from the enterocytes following the ingestion of fat, typically presents in infancy with failure to thrive, diarrhea, vomiting, abdominal distention, and malabsorption of fat. (nih.gov)
  • In chylomicron retention disease, a hereditary disorder, the body cannot make chylomicrons. (medicine.com)
  • For example, only about 25 percent of all people who suffer from cancer, diabetes, cardiovascular diseases or chylomicron retention disease (CRD) currently die. (worlddata.info)
  • Adipose, which is fat tissue, takes triglyceride from the chylomicrons. (healthline.com)
  • Assessing your risk for cardiovascular disease is based on your 'baseline' blood lipid levels-that is, your blood lipid levels at a time when circulating chylomicrons are not temporarily increasing your triglyceride and cholesterol counts. (verywellhealth.com)
  • Muscle and adipose tissue remove some of the triglyceride from the chylomicron and the chylomicron remnant is taken up by the liver and metabolized into a cholesterol rich lipoprotein. (jabfm.org)
  • The SAR1B gene provides instructions for making a protein that is needed for the transport of molecules called chylomicrons. (medlineplus.gov)
  • Activated 0.2-macroglobulin and lactoferrin had no effect on chylomicron remnant degradation, indicating that the low- density lipoprotein receptor-related protein was not involved. (edu.au)
  • This protein is a major protein of plasma HDL and is also found in chylomicrons. (nih.gov)
  • No differences in postprandial energy metabolism, serum lipids, lipoprotein, or chylomicron concentrations are observed between drinks. (wur.nl)
  • Normally, vitamin E derived from food is absorbed in the intestine and then transported into the liver on molecules called chylomicrons. (medlineplus.gov)
  • Chylomicrons - carry triacylglycerol (fat) from the intestines to the liver and to adipose tissue . (medindia.net)
  • The postprandial chylomicron triacylglycerol response to dietary fat in healthy male adults is significantly explained by a combination of single nucleotide polymorphisms in genes involved in triacylglycerol metabolism. (cdc.gov)
  • We have identified that apolipoprotein B48 (APOB48), the structural component of chylomicron synthesis and secretion, is dramatically downregulated following iAs exposure. (nih.gov)
  • Since the synthesis and secretion of Apo B-containing chylomicrons in the intestine is also impaired, malabsorption of fat-soluble vitamins occurs. (medicover-genetics.com)
  • In addition, the scavenger receptor inhibitors polyinosinic acid and fucoidan increased degradation of chylomicron remnant-ruling out uptake as a consequence of lipoprotein modification. (edu.au)
  • These studies further substantiate the lymphatic uptake of SMEDDS through chylomicron flow blocking approach. (eurekaselect.com)
  • Intermediate density lipoprotein (IDL) Low density lipoprotein (LDL) High density lipoprotein (HDL) Chylomicron composition. (hofc.org)
  • From the lymphatic system , the chylomicrons are then transported to the circulatory system. (jackwestin.com)
  • the emulsion was used as a surrogate for the study of chylomicron metabolism. (elsevier.com)
  • The apolipoprotein contained in chylomicron emulsified by bile acid can improve the activity of lipoprotein lipase therby greatly increase the hydrolysis metabolism of fat. (rengty.com)
  • Our results show that dietary zinc influences both the amount of chylomicrons in blood plasma and the concentrations of retinol and arachidonic acid in chylomicrons. (ac.rs)
  • Excess chylomicrons result in recurrent and severe acute inflammation of the pancreas, called pancreatitis, the most debilitating and life-threatening clinical complication of LPLD. (prnewswire.com)
  • Hesse D, Jaschke A, Chung B, Schurmann A. Trans-Golgi proteins participate in the control of lipid droplet and chylomicron formation. (medlineplus.gov)
  • The initial chylomicrons should also alter shown with the solvent or a ethylenediamine enlargement electrode in patients from a equal sehen of enzymes before and after romance to avoid that exchangers are the bias proteins simultaneously. (democo.de)
  • The chylomicrons are raised only after eating a fat-containing meal. (who.int)
  • Specifically chylomicrons: absorbed/bundled dietary fat in transit. (blogspot.com)
  • However, the results demonstrated an increase in the blood plasma retinol concentration in the LZ group compared to the SZ group when calculated per milligram of plasma chylomicrons (p lt 0.01). (ac.rs)
  • The rationale behind fasting is to eliminate chylomicrons in the blood. (medscape.com)
  • Chylomicrons are unable to directly enter our blood like monosaccharides because they are simply too large to squeeze into capillaries that supply the portal vein. (thenutritiondr.com)
  • As chylomicrons move through our lymphatic vessels, they eventually dump into our blood and circulate. (thenutritiondr.com)
  • Chylomicrons appear to bind perhaps once before being irreversibly removed from circulation. (blogspot.com)
  • Chylomicrons are ejected from those cells and enter our circulation indirectly through lymphatic vessels. (thenutritiondr.com)