A 6.6-kDa protein component of VERY-LOW-DENSITY LIPOPROTEINS; INTERMEDIATE-DENSITY LIPOPROTEINS; and HIGH-DENSITY LIPOPROTEINS. Apo C-I displaces APO E from lipoproteins, modulate their binding to receptors (RECEPTORS, LDL), and thereby decrease their clearance from plasma. Elevated Apo C-I levels are associated with HYPERLIPOPROTEINEMIA and ATHEROSCLEROSIS.
A 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 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 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.
Triglycerides are the most common type of fat in the body, stored in fat cells and used as energy; they are measured in blood tests to assess heart disease risk, with high levels often resulting from dietary habits, obesity, physical inactivity, smoking, and alcohol consumption.
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.
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.
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.
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.
A major and the second most common isoform of apolipoprotein E. In humans, Apo E4 differs from APOLIPOPROTEIN E3 at only one residue 112 (cysteine is replaced by arginine), and exhibits a lower resistance to denaturation and greater propensity to form folded intermediates. Apo E4 is a risk factor for ALZHEIMER DISEASE and CARDIOVASCULAR DISEASES.
A 34-kDa glycosylated protein. A major and most common isoform of apolipoprotein E. Therefore, it is also known as apolipoprotein E (ApoE). In human, Apo E3 is a 299-amino acid protein with a cysteine at the 112 and an arginine at the 158 position. It is involved with the transport of TRIGLYCERIDES; PHOSPHOLIPIDS; CHOLESTEROL; and CHOLESTERYL ESTERS in and out of the cells.
The second most abundant protein component of HIGH DENSITY LIPOPROTEINS or HDL. It has a high lipid affinity and is known to displace APOLIPOPROTEIN A-I from HDL particles and generates a stable HDL complex. ApoA-II can modulate the activation of LECITHIN CHOLESTEROL ACYLTRANSFERASE in the presence of APOLIPOPROTEIN A-I, thus affecting HDL metabolism.
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.
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.
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.
One of three major isoforms of apolipoprotein E. In humans, Apo E2 differs from APOLIPOPROTEIN E3 at one residue 158 where arginine is replaced by cysteine (R158--C). In contrast to Apo E3, Apo E2 displays extremely low binding affinity for LDL receptors (RECEPTORS, LDL) which mediate the internalization and catabolism of lipoprotein particles in liver cells. ApoE2 allelic homozygosity is associated with HYPERLIPOPROTEINEMIA TYPE III.
A 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 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.
A large and highly glycosylated protein constituent of LIPOPROTEIN (A). It has very little affinity for lipids but forms disulfide-linkage to APOLIPOPROTEIN B-100. Apoprotein(a) has SERINE PROTEINASE activity and can be of varying sizes from 400- to 800-kDa. It is homologous to PLASMINOGEN and is known to modulate THROMBOSIS and FIBRINOLYSIS.
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.
The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils.
A lipoprotein that resembles the LOW-DENSITY LIPOPROTEINS but with an extra protein moiety, APOPROTEIN (A) also known as APOLIPOPROTEIN (A), linked to APOLIPOPROTEIN B-100 on the LDL by one or two disulfide bonds. High plasma level of lipoprotein (a) is associated with increased risk of atherosclerotic cardiovascular disease.
A glycoprotein component of HIGH-DENSITY LIPOPROTEINS that transports small hydrophobic ligands including CHOLESTEROL and STEROLS. It occurs in the macromolecular complex with LECITHIN CHOLESTEROL ACYLTRANSFERASE. Apo D is expressed in and secreted from a variety of tissues such as liver, placenta, brain tissue and others.
A class of lipoproteins of small size (18-25 nm) and light (1.019-1.063 g/ml) particles with a core composed mainly of CHOLESTEROL ESTERS and smaller amounts of TRIGLYCERIDES. The surface monolayer consists mostly of PHOSPHOLIPIDS, a single copy of APOLIPOPROTEIN B-100, and free cholesterol molecules. The main LDL function is to transport cholesterol and cholesterol esters to extrahepatic tissues.
A 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)
Receptors on the plasma membrane of nonhepatic cells that specifically bind LDL. The receptors are localized in specialized regions called coated pits. Hypercholesteremia is caused by an allelic genetic defect of three types: 1, receptors do not bind to LDL; 2, there is reduced binding of LDL; and 3, there is normal binding but no internalization of LDL. In consequence, entry of cholesterol esters into the cell is impaired and the intracellular feedback by cholesterol on 3-hydroxy-3-methylglutaryl CoA reductase is lacking.
A thickening and loss of elasticity of the walls of ARTERIES that occurs with formation of ATHEROSCLEROTIC PLAQUES within the ARTERIAL INTIMA.
Cholesterol which is contained in or bound to high-density lipoproteins (HDL), including CHOLESTEROL ESTERS and free cholesterol.
Thickening and loss of elasticity of the walls of ARTERIES of all sizes. There are many forms classified by the types of lesions and arteries involved, such as ATHEROSCLEROSIS with fatty lesions in the ARTERIAL INTIMA of medium and large muscular arteries.
A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.
An autosomal recessively inherited disorder characterized by the accumulation of intermediate-density lipoprotein (IDL or broad-beta-lipoprotein). IDL has a CHOLESTEROL to TRIGLYCERIDES ratio greater than that of VERY-LOW-DENSITY LIPOPROTEINS. This disorder is due to mutation of APOLIPOPROTEINS E, a receptor-binding component of VLDL and CHYLOMICRONS, resulting in their reduced clearance and high plasma levels of both cholesterol and triglycerides.
An enzyme secreted from the liver into the plasma of many mammalian species. It catalyzes the esterification of the hydroxyl group of lipoprotein cholesterol by the transfer of a fatty acid from the C-2 position of lecithin. In familial lecithin:cholesterol acyltransferase deficiency disease, the absence of the enzyme results in an excess of unesterified cholesterol in plasma. EC 2.3.1.43.
Cholesterol which is contained in or bound to low density lipoproteins (LDL), including CHOLESTEROL ESTERS and free cholesterol.

Allele-specific differences in apolipoprotein C-III mRNA expression in human liver. (1/417)

BACKGROUND: Sequence variations at the apolipoprotein (apo)C-III gene locus have been associated with increased plasma triglycerides. In particular, the S2 allele of an SstI polymorphism in the 3' untranslated region has been associated with hypertriglyceridemia in many populations. The aim of this study was to determine whether the variant S2 allele is related to increased mRNA expression in vivo. METHODS: We measured allele-specific apoC-III expression in liver biopsies of five obese subjects, using restriction isotyping and a primer extension method, both based on the SstI polymorphism. RESULTS: The expression of mRNA by the S1 and S2 alleles was similar in two patients, whereas the mRNA encoded by the S2 allele was 14%, 26%, and 29% more abundant than the wild-type mRNA in the remaining three patients. Because other polymorphisms at the apoC-III gene locus have been implicated in the S2-associated hypertriglyceridemia, we determined apoC-III haplotypes comprising promoter polymorphisms at -935, -641, -630, -625, -482, -455, as well as the SstI sites and a BbvI site, both located in the 3' untranslated region. None of these polymorphisms nor any haplotype exhibited a perfect association with allele-specific expression, but variation at the T-482C site correlated in four of five subjects with the relative allele abundance. CONCLUSION: These data provide preliminary evidence for allele-specific differences in apoC-III mRNA expression in vivo and suggest that such differences may contribute to associations of apoC-III gene polymorphisms with hypertriglyceridemia.  (+info)

Vitamin A is linked to the expression of the AI-CIII-AIV gene cluster in familial combined hyperlipidemia. (2/417)

There is growing evidence of the capacity of vitamin A to regulate the expression of the genetic region that encodes apolipoproteins (apo) A-I, C-III, and A-IV. This region in turn has been proposed to modulate the expression of hyperlipidemia in the commonest genetic form of dyslipidemia, familial combined hyperlipidemia (FCHL). The hypothesis tested here was whether vitamin A (retinol), by controlling the expression of the AI-CIII-AIV gene cluster, plays a role in modulating the hyperlipidemic phenotype in FCHL. We approached the subject by studying three genetic variants of this region: a C1100-T transition in exon 3 of the apoC-III gene, a G3206-T transversion in exon 4 of the apoC-III gene, and a G-75-A substitution in the promoter region of the apoA-I gene. The association between plasma vitamin A concentrations and differences in the plasma concentrations of apolipoproteins A-I and C-III based on the different genotypes was assessed in 48 FCHL patients and 74 of their normolipidemic relatives. The results indicated that the subjects carrying genetic variants associated with increased concentrations of apoA-I and C-III (C1100-T and G-75-A) also presented increased plasma concentrations of vitamin A. This was only observed among the FCHL patients, which suggested that certain characteristics of these patients contributed to this association. The G3206-T was not associated with changes in either apolipoprotein concentrations or in vitamin A. In summary, we report a relationship between genetically determined elevations of proteins of the AI-CIII-AIV gene cluster and vitamin A in FCHL patients. More studies will be needed to confirm that vitamin A plays a role in FCHL which might also be important for its potential application to therapeutical approaches.  (+info)

Mass spectral study of polymorphism of the apolipoproteins of very low density lipoprotein. (3/417)

New isoforms of apolipoprotein (apo)C-I and apoC-III have been detected in delipidated fractions from very low density lipoprotein (VLDL) using matrix-assisted laser desorption (MALDI) and electrospray ionization (ESI) mass spectrometry (MS). The cleavage sites of truncated apoC-III isoforms have also been identified. The VLDL fractions were isolated by fixed-angle single-spin ultracentrifugation using a self-generating sucrose density gradient and delipidated using a newly developed C18 solid phase extraction protocol. Fifteen apoC isoforms and apoE were identified in the MALDI spectra and the existence of the more abundant species was verified by ESI-MS. The relative intensities of the apoCs are closely correlated in three normolipidemic subjects. A fourth subject with type V hyperlipidemia exhibited an elevated apoC-III level and a suppressed level of the newly discovered truncated apoC-I isoform. ApoC-II was found to be particularly sensitive to in vitro oxidation. The dynamic range and specificity of the MALDI assay shows that the complete apoC isoform profile and apoE phenotype can be obtained in a single measurement from the delipidated VLDL fraction.  (+info)

Kinetics and mechanism of exchange of apolipoprotein C-III molecules from very low density lipoprotein particles. (4/417)

Transfer of apolipoprotein (apo) molecules between lipoprotein particles is an important factor in modulating the metabolism of the particles. Although the phenomenon is well established, the kinetics and molecular mechanism of passive apo exchange/transfer have not been defined in detail. In this study, the kinetic parameters governing the movement of radiolabeled apoC molecules from human very low density lipoprotein (VLDL) to high density lipoprotein (HDL3) particles were measured using a manganese phosphate precipitation assay to rapidly separate the two types of lipoprotein particles. In the case of VLDL labeled with human [14C]apoCIII1, a large fraction of the apoCIII1 transfers to HDL3 within 1 minute of mixing the two lipoproteins at either 4 degrees or 37 degrees C. As the diameter of the VLDL donor particles is decreased from 42-59 to 23-25 nm, the size of this rapidly transferring apoCIII1 pool increases from about 50% to 85%. There is also a pool of apoCIII1 existing on the donor VLDL particles that transfers more slowly. This slow transfer follows a monoexponential rate equation; for 35-40 nm donor VLDL particles the pool size is approximately 20% and the t1/2 is approximately 3 h. The flux of apoCIII molecules between VLDL and HDL3 is bidirectional and all of the apoCIII seems to be available for exchange so that equilibrium is attained. It is likely that the two kinetic pools of apoCIII are related to conformational variations of individual apo molecules on the surface of VLDL particles. The rate of slow transfer of apoCIII1 from donor VLDL (35-40 nm) to acceptor HDL3 is unaffected by an increase in the acceptor to donor ratio, indicating that the transfer is not dependent on collisions between donor and acceptor particles. Consistent with this, apoCIII1 molecules can transfer from donor VLDL to acceptor HDL3 particles across a 50 kDa molecular mass cutoff semipermeable membrane separating the lipoprotein particles. These results indicate that apoC molecules transfer between VLDL and HDL3 particles by an aqueous diffusion mechanism.  (+info)

CREB-binding protein is a transcriptional coactivator for hepatocyte nuclear factor-4 and enhances apolipoprotein gene expression. (5/417)

Hepatocyte nuclear factor-4 (HNF-4) is a liver-enriched transcription factor that is crucial in the regulation of a large number of genes involved in glucose, cholesterol, and fatty acid metabolism and in determining the hepatic phenotype. We have previously shown that HNF-4 contains transcription activation functions at the N terminus (AF-1) and the C terminus (AF-2) which work synergistically to confer full HNF-4 activity. Here, we show that HNF-4 recruits the CREB-binding protein (CBP) coactivator on promoters of genes that contain functional HNF-4 sites. HNF-4 interacts with the N-terminal region of CBP (amino acids 1-771) and the C-terminal region of CBP (amino acids 1812-2441). The two activating functions of HNF-4, AF-1 and AF-2, interact with the N terminus and the N and C terminus of CBP, respectively. In addition, we show that in contrast to the other nuclear hormone receptors the interaction between HNF-4 and CBP is ligand-independent. Recruitment of CBP by HNF-4 results in an enhancement of the transcriptional activity of the latter. CBP does not activate gene expression in the absence of HNF-4, and dominant negative forms of HNF-4 prevent transcriptional activation by CBP, suggesting that the mere recruitment of CBP by HNF-4 is not sufficient for enhancement of gene expression. These findings demonstrate that CBP acts as a transcriptional coactivator for HNF-4 and provide new insights into the regulatory function of HNF-4.  (+info)

Characterization of remnant-like particles isolated by immunoaffinity gel from the plasma of type III and type IV hyperlipoproteinemic patients. (6/417)

Previous studies have investigated the potential atherogenicity and thrombogenicity of triglyceride-rich lipoprotein (TRL) remnants by isolating them from plasma within a remnant-like particle (RLP) fraction, using an immunoaffinity gel containing specific anti-apoB-100 and anti-apoA-I antibodies. In order to characterize lipoproteins in this RLP fraction and to determine to what extent their composition varies from one individual to another, we have used automated gel filtration chromatography to determine the size heterogeneity of RLP isolated from normolipidemic control subjects (n = 8), and from type III (n = 6) and type IV (n = 9) hyperlipoproteinemic patients, who by selection had similarly elevated levels of plasma triglyceride (406 +/- 43 and 397 +/- 35 mg/dl, respectively). Plasma RLP triglyceride, cholesterol, apoB, apoC-III, and apoE concentrations were elevated 2- to 6-fold (P < 0. 05) in hyperlipoproteinemic patients compared to controls. RLP fractions of type III patients were enriched in cholesterol and apoE compared to those of type IV patients, and RLP of type IV patients were enriched in triglyceride and apoC-III relative to those of normolipidemic subjects. In normolipidemic subjects, the majority of RLP had a size similar to LDL or HDL. The RLP of hyperlipoproteinemic patients were, however, larger and were similar in size to TRL, or were intermediate in size (i.e., ISL) between that of TRL and LDL. Compared to controls, ISL in the RLP fraction of type III patients were enriched in apoE relative to apoC-III, whereas in type IV patients they were enriched in apoC-III relative to apoE. These results demonstrate that: 1) RLP are heterogeneous in size and composition in both normolipidemic and hypertriglyceridemic subjects, and 2) the apoE and apoC-III composition of RLP is different in type III compared to type IV hyperlipoproteinemic patients.  (+info)

ApoCIII gene variants modulate postprandial response to both glucose and fat tolerance tests. (7/417)

BACKGROUND: We investigated the relationship between variation in the apolipoprotein (apo) AI-CIII-AIV gene cluster and response to an oral glucose test (OGTT) and oral fat load test (OFTT) in the EARSII group of young, healthy male offspring whose fathers had had a myocardial infarction before the age of 55 years (cases, n=407) compared with age-matched controls (n=415). The apoCIII variations examined were C3238G (SstI) in the 3'-UTR, C1100T in exon 3, C-482T in the insulin response element (IRE), and T-2854G in the apoCIII-AIV intergenic region. METHODS AND RESULTS: The postprandial response was regulated by variation at the T-2854G and C3238G sites. After the OFTT, carriers of the rare alleles had delayed clearance of triglyceride (Tg) levels; G-2854 carriers showed the largest effect on Tg (AUC, 24% greater, P<0.002; peak, 19% greater, P<0.005), and G3238 carriers showed a smaller response (AUC, 13% greater, P<0.05; peak, 13% greater, P=0.03). However, after adjustment for fasting level of Tg, only the effect with the T-2854G remained significant. Variation at the C-482T (IRE) determined response to the OGTT, with carriers of the rare T-482 having significantly elevated glucose (28.7% AUC, P=0.013) and insulin (20.5% AUC, P<0. 01) concentrations. CONCLUSIONS: These data suggest that specific genetic variants at the apoCIII gene locus differentially affect postprandial and response to OGTT and suggest a novel mechanism for the effects of variation at this locus on risk for atherosclerosis.  (+info)

Apolipoprotein B-containing lipoproteins in renal failure: the relation to mode of dialysis. (8/417)

BACKGROUND: The aim of this study was to establish whether there is a differential effect of mode of dialysis, hemodialysis (HD), or continuous ambulatory peritoneal dialysis (CAPD) on the dyslipidemia of renal failure. METHODS: The lipoprotein profile was determined in 61 non-diabetic patients on chronic HD (N = 30) and CAPD treatment (N = 31), and in a control group of 27 healthy subjects. The analysis included the measurement of individual apolipoprotein (apo) A- and apo B-containing lipoproteins (LPs) separated by sequential immunoaffinity chromatography. Apo A-containing lipoproteins include lipoprotein A-I with apo A-I and lipoprotein A-I:A-II with apo A-I and apo A-II as the main protein constituents, whereas apo B-containing lipoproteins comprise simple cholesterol-rich lipoprotein B (LP-B), with apo B as the only protein moiety and complex triglyceride (TG)-rich lipoprotein B complex (LP-Bc) particles with apo B, apo A-II, apo C, and/or apo E as the protein constituents. RESULTS: CAPD patients had significantly higher concentrations of total cholesterol (6.8 vs. 5.1 mmol/liter), low-density lipoprotein (LDL) cholesterol (4.6 vs. 3.2 mmol/liter), TG (2.3 vs. 1.5 mmol/liter), apo B (155.3 vs. 105.7 mg/dl), LP-B (136.0 vs. 91.9 mg/dl), and LP-Bc (19.3 vs. 13.8 mg/dl) than HD patients. Both HD and CAPD patients had significantly higher TG, VLDL cholesterol, apo C-III, and apo E and significantly lower high-density lipoprotein cholesterol, apo A-II, and lipoprotein A-I:A-II levels than control subjects. The distribution of apo C-III in high-density lipoprotein and VLDL-LDL was altered in CAPD patients in comparison with control subjects. This suggests that the removal of TG-rich lipoproteins is less efficient in patients on CAPD. Normotriglyceridemic (NTG; TG < or = 1.7 mmol/liter, 150 mg/dl) CAPD patients had significantly higher levels of TC, LDL cholesterol, apo B, and LP-B than NTG-HD patients. There was little difference in the LP-Bc levels between NTG-CAPD, NTG-HD, and controls. Similarly, hypertriglyceridemic (HTG) CAPD patients had significantly higher TC, LDL cholesterol, apo B, and LP-B levels than HTG-HD patients. The LP-Bc levels were significantly increased in HTG-HD and HTG-CAPD patients compared with controls, but the slightly higher levels in the CAPD patients did not differ significantly from the HD group. CONCLUSION: CAPD and HD patients have a lipoprotein profile characteristic of renal failure. Patients on long-term CAPD have higher levels of cholesterol-rich apo B-containing lipoproteins unrelated to TG levels. Many patients on CAPD also have a substantial elevation of the plasma concentrations of TG-rich LPs. The clinical significance of increased levels of potentially atherogenic LP-B during CAPD remains to be investigated.  (+info)

Apolipoprotein C-I (apoC-I) is a small protein component of lipoproteins, which are particles that transport all fat molecules (lipids), including cholesterol, in the bloodstream. ApoC-I is primarily produced in the liver and intestines and plays a crucial role in the metabolism of triglyceride-rich lipoproteins, such as very low-density lipoproteins (VLDL) and chylomicrons.

Apolipoprotein C-I has several functions:

1. Inhibition of lipoprotein lipase (LPL): ApoC-I inhibits the activity of LPL, an enzyme responsible for breaking down triglycerides in lipoproteins. This inhibition helps regulate the rate at which fatty acids are released from triglyceride-rich lipoproteins and taken up by cells for energy production or storage.
2. Activation of hepatic lipase (HL): ApoC-I activates HL, an enzyme involved in the catabolism of intermediate-density lipoproteins (IDL) and high-density lipoproteins (HDL). This activation aids in the clearance of these particles from the circulation.
3. Regulation of cholesterol efflux: ApoC-I may also play a role in regulating cholesterol efflux, the process by which excess cholesterol is removed from cells and transported to the liver for excretion.

Genetic variations in the APOC1 gene, which encodes apoC-I, have been associated with alterations in lipid metabolism and an increased risk of cardiovascular disease.

Apolipoprotein C (apoC) is a group of proteins that are associated with lipoproteins, which are complex particles composed of lipids and proteins that play a crucial role in the transport and metabolism of lipids in the body. There are three main types of apoC proteins: apoC-I, apoC-II, and apoC-III.

ApoC-I is involved in the regulation of lipoprotein metabolism and has been shown to inhibit the activity of cholesteryl ester transfer protein (CETP), which is an enzyme that facilitates the transfer of cholesteryl esters from high-density lipoproteins (HDL) to low-density lipoproteins (LDL) and very low-density lipoproteins (VLDL).

ApoC-II is a cofactor for lipoprotein lipase, an enzyme that hydrolyzes triglycerides in chylomicrons and VLDL, leading to the formation of smaller, denser lipoproteins. A deficiency in apoC-II can lead to hypertriglyceridemia, a condition characterized by elevated levels of triglycerides in the blood.

ApoC-III is also involved in the regulation of lipoprotein metabolism and has been shown to inhibit the activity of lipoprotein lipase and CETP. Elevated levels of apoC-III have been associated with an increased risk of cardiovascular disease, possibly due to its effects on lipoprotein metabolism.

In summary, apolipoprotein C is a group of proteins that are involved in the regulation of lipoprotein metabolism and have important roles in the transport and metabolism of lipids in the body.

Apolipoprotein C-III (APOC3) is a protein that is produced in the liver and circulates in the bloodstream. It is a component of certain lipoproteins, including very low-density lipoproteins (VLDL) and chylomicrons, which are responsible for transporting fat molecules, such as triglycerides and cholesterol, throughout the body.

APOC3 plays a role in regulating the metabolism of these lipoproteins. Specifically, it inhibits the activity of an enzyme called lipoprotein lipase, which breaks down triglycerides in VLDL and chylomicrons. As a result, high levels of APOC3 can lead to an increase in triglyceride levels in the blood, which is a risk factor for cardiovascular disease.

Genetic variations in the APOC3 gene have been associated with differences in triglyceride levels and risk of cardiovascular disease. Some studies have suggested that reducing APOC3 levels through genetic editing or other means may be a promising strategy for lowering triglycerides and reducing the risk of heart disease.

VLDL (Very Low-Density Lipoproteins) are a type of lipoprotein that play a crucial role in the transport and metabolism of fat molecules, known as triglycerides, in the body. They are produced by the liver and consist of a core of triglycerides surrounded by a shell of proteins called apolipoproteins, phospholipids, and cholesterol.

VLDL particles are responsible for delivering fat molecules from the liver to peripheral tissues throughout the body, where they can be used as an energy source or stored for later use. During this process, VLDL particles lose triglycerides and acquire more cholesterol, transforming into intermediate-density lipoproteins (IDL) and eventually low-density lipoproteins (LDL), which are also known as "bad" cholesterol.

Elevated levels of VLDL in the blood can contribute to the development of cardiovascular disease due to their association with increased levels of triglycerides and LDL cholesterol, as well as decreased levels of high-density lipoproteins (HDL), which are considered "good" cholesterol.

Triglycerides are the most common type of fat in the body, and they're found in the food we eat. They're carried in the bloodstream to provide energy to the cells in our body. High levels of triglycerides in the blood can increase the risk of heart disease, especially in combination with other risk factors such as high LDL (bad) cholesterol, low HDL (good) cholesterol, and high blood pressure.

It's important to note that while triglycerides are a type of fat, they should not be confused with cholesterol, which is a waxy substance found in the cells of our body. Both triglycerides and cholesterol are important for maintaining good health, but high levels of either can increase the risk of heart disease.

Triglyceride levels are measured through a blood test called a lipid panel or lipid profile. A normal triglyceride level is less than 150 mg/dL. Borderline-high levels range from 150 to 199 mg/dL, high levels range from 200 to 499 mg/dL, and very high levels are 500 mg/dL or higher.

Elevated triglycerides can be caused by various factors such as obesity, physical inactivity, excessive alcohol consumption, smoking, and certain medical conditions like diabetes, hypothyroidism, and kidney disease. Medications such as beta-blockers, steroids, and diuretics can also raise triglyceride levels.

Lifestyle changes such as losing weight, exercising regularly, eating a healthy diet low in saturated and trans fats, avoiding excessive alcohol consumption, and quitting smoking can help lower triglyceride levels. In some cases, medication may be necessary to reduce triglycerides to recommended levels.

Apolipoprotein A-I (ApoA-I) is a major protein component of high-density lipoproteins (HDL) in human plasma. It plays a crucial role in the metabolism and transport of lipids, particularly cholesterol, within the body. ApoA-I facilitates the formation of HDL particles, which are involved in the reverse transport of cholesterol from peripheral tissues to the liver for excretion. This process is known as reverse cholesterol transport and helps maintain appropriate cholesterol levels in the body. Low levels of ApoA-I or dysfunctional ApoA-I have been associated with an increased risk of developing cardiovascular diseases.

Apolipoprotein E (ApoE) is a protein involved in the metabolism of lipids, particularly cholesterol. It is produced primarily by the liver and is a component of several types of lipoproteins, including very low-density lipoproteins (VLDL) and high-density lipoproteins (HDL).

ApoE plays a crucial role in the transport and uptake of lipids in the body. It binds to specific receptors on cell surfaces, facilitating the delivery of lipids to cells for energy metabolism or storage. ApoE also helps to clear cholesterol from the bloodstream and is involved in the repair and maintenance of tissues.

There are three major isoforms of ApoE, designated ApoE2, ApoE3, and ApoE4, which differ from each other by only a few amino acids. These genetic variations can have significant effects on an individual's risk for developing certain diseases, particularly cardiovascular disease and Alzheimer's disease. For example, individuals who inherit the ApoE4 allele have an increased risk of developing Alzheimer's disease, while those with the ApoE2 allele may have a reduced risk.

In summary, Apolipoprotein E is a protein involved in lipid metabolism and transport, and genetic variations in this protein can influence an individual's risk for certain diseases.

Apolipoprotein B-100 (apoB-100) is a large protein component of low-density lipoprotein (LDL), also known as "bad cholesterol." It plays a crucial role in the metabolism and transport of fats and cholesterol in the body. ApoB-100 is responsible for the binding of LDL to specific receptors on cell surfaces, facilitating the uptake of lipoprotein particles by cells. Elevated levels of apoB-100 in the blood are associated with an increased risk of developing cardiovascular diseases, such as atherosclerosis and coronary artery disease.

Apolipoprotein B (ApoB) is a type of protein that plays a crucial role in the metabolism of lipids, particularly low-density lipoprotein (LDL) or "bad" cholesterol. ApoB is a component of LDL particles and serves as a ligand for the LDL receptor, which is responsible for the clearance of LDL from the bloodstream.

There are two main forms of ApoB: ApoB-100 and ApoB-48. ApoB-100 is found in LDL particles, very low-density lipoprotein (VLDL) particles, and chylomicrons, while ApoB-48 is only found in chylomicrons, which are produced in the intestines and responsible for transporting dietary lipids.

Elevated levels of ApoB are associated with an increased risk of cardiovascular disease (CVD), as they indicate a higher concentration of LDL particles in the bloodstream. Therefore, measuring ApoB levels can provide additional information about CVD risk beyond traditional lipid profile tests that only measure total cholesterol, LDL cholesterol, HDL cholesterol, and triglycerides.

Apolipoprotein E (APOE) is a gene that provides instructions for making a protein involved in the metabolism of fats called lipids. One variant of this gene, APOE4, is associated with an increased risk of developing Alzheimer's disease and other forms of dementia.

The APOE4 allele (variant) is less efficient at clearing beta-amyloid protein, a component of the amyloid plaques found in the brains of people with Alzheimer's disease. This can lead to an accumulation of beta-amyloid and an increased risk of developing Alzheimer's disease.

It is important to note that having one or two copies of the APOE4 allele does not mean that a person will definitely develop Alzheimer's disease, but it does increase the risk. Other factors, such as age, family history, and the presence of other genetic variants, also contribute to the development of this complex disorder.

Apolipoprotein E3 (ApoE3) is one of the three major isoforms of apolipoprotein E (ApoE), a protein involved in the metabolism of lipids, particularly cholesterol. ApoE is produced by the APOE gene, which has three common alleles: ε2, ε3, and ε4. These alleles result in three main isoforms of the protein: ApoE2, ApoE3, and ApoE4.

ApoE3 is the most common isoform, found in approximately 77-78% of the population. It has a slightly different amino acid sequence compared to ApoE2 and ApoE4, which can affect its function. ApoE3 is thought to play a neutral or protective role in the risk of developing Alzheimer's disease and cardiovascular diseases, although some studies suggest that it may have a mildly favorable effect on lipid metabolism compared to ApoE4.

Apolipoprotein A-II (ApoA-II) is a protein component of high-density lipoproteins (HDL), often referred to as "good cholesterol." It is one of the major apolipoproteins in HDL and plays a role in the structure, metabolism, and function of HDL particles. ApoA-II is produced primarily in the liver and intestine and helps facilitate the transport of cholesterol from tissues to the liver for excretion. Additionally, ApoA-II has been shown to have anti-inflammatory properties and may play a role in the regulation of the immune response.

Apolipoproteins are a group of proteins that are associated with lipids (fats) in the body and play a crucial role in the metabolism, transportation, and regulation of lipids. They are structural components of lipoprotein particles, which are complexes of lipids and proteins that transport lipids in the bloodstream.

There are several types of apolipoproteins, including ApoA, ApoB, ApoC, ApoD, ApoE, and others. Each type has a specific function in lipid metabolism. For example, ApoA is a major component of high-density lipoprotein (HDL), often referred to as "good cholesterol," and helps remove excess cholesterol from cells and tissues and transport it to the liver for excretion. ApoB, on the other hand, is a major component of low-density lipoprotein (LDL), or "bad cholesterol," and plays a role in the delivery of cholesterol to cells and tissues.

Abnormal levels of apolipoproteins or dysfunctional forms of these proteins have been linked to various diseases, including cardiovascular disease, Alzheimer's disease, and metabolic disorders such as diabetes. Therefore, measuring apolipoprotein levels in the blood can provide valuable information for diagnosing and monitoring these conditions.

Apolipoprotein C-II (ApoC-II) is a type of apolipoprotein, which are proteins that bind to lipids to form lipoprotein complexes. ApoC-II is a component of several lipoproteins, including very low-density lipoproteins (VLDL) and chylomicrons, which are responsible for the transport of fat molecules, such as triglycerides and cholesterol, in the bloodstream.

ApoC-II plays a crucial role in the activation of lipoprotein lipase, an enzyme that breaks down triglycerides in VLDL and chylomicrons into fatty acids, which can then be taken up by cells for energy production or storage. Therefore, ApoC-II deficiency can lead to hypertriglyceridemia, a condition characterized by high levels of triglycerides in the blood.

In addition to its role in lipid metabolism, ApoC-II has been implicated in the development and progression of atherosclerosis, a chronic inflammatory disease that affects the arteries and can lead to serious cardiovascular complications, such as heart attack and stroke.

Apolipoprotein A (apoA) is a type of apolipoprotein that is primarily associated with high-density lipoproteins (HDL), often referred to as "good cholesterol." There are several subtypes of apoA, including apoA-I, apoA-II, and apoA-IV.

ApoA-I is the major protein component of HDL particles and plays a crucial role in reverse cholesterol transport, which is the process by which excess cholesterol is removed from tissues and delivered to the liver for excretion. Low levels of apoA-I have been linked to an increased risk of cardiovascular disease.

ApoA-II is another protein component of HDL particles, although its function is less well understood than that of apoA-I. Some studies suggest that apoA-II may play a role in regulating the metabolism of HDL particles.

ApoA-IV is found in both HDL and chylomicrons, which are lipoprotein particles that transport dietary lipids from the intestine to the liver. The function of apoA-IV is not well understood, but it may play a role in regulating appetite and energy metabolism.

Overall, apolipoproteins A are important components of HDL particles and play a critical role in maintaining healthy lipid metabolism and reducing the risk of cardiovascular disease.

Apolipoprotein E2 (ApoE2) is one of the three major isoforms of the apolipoprotein E (ApoE) protein, which is a component of lipoproteins that are involved in the transport and metabolism of cholesterol and other fats in the body. ApoE is produced by the APOE gene, which has three common alleles: ε2, ε3, and ε4.

The ApoE2 protein is encoded by the ε2 allele of the APOE gene. Compared to the other two isoforms (ApoE3 and ApoE4), ApoE2 has a different amino acid at position 112, where it has a cysteine instead of an arginine. This difference affects the protein's ability to interact with other molecules involved in lipid metabolism, such as the low-density lipoprotein receptor (LDLR).

Individuals who inherit two copies of the ε2 allele (ε2/ε2) have a higher risk of developing type III hyperlipoproteinemia, also known as dysbetalipoproteinemia, which is characterized by elevated levels of cholesterol and triglycerides in the blood due to impaired clearance of remnant lipoproteins. However, not all people with the ε2/ε2 genotype develop type III hyperlipoproteinemia, and other genetic and environmental factors may contribute to the development of this condition.

It's worth noting that having one or two copies of the ε2 allele has been associated with a reduced risk of developing Alzheimer's disease, although the mechanism by which ApoE2 protects against Alzheimer's is not fully understood.

Apolipoprotein B-48 (apoB-48) is a protein component of chylomicrons, which are lipoprotein particles responsible for carrying dietary fat and cholesterol from the intestines to other parts of the body. ApoB-48 is produced in the intestines and is a shorter version of apolipoprotein B-100 (apoB-100), which is a component of low-density lipoproteins (LDL) or "bad cholesterol."

Chylomicrons are assembled and secreted by intestinal cells after a meal, and apoB-48 is essential for the formation and function of these particles. ApoB-48-containing chylomicrons transport dietary lipids to various tissues, including the liver, where they contribute to the maintenance of lipid homeostasis.

Elevated levels of apoB-48 in the blood have been associated with an increased risk of cardiovascular disease, particularly in individuals with familial chylomicronemia syndrome (FCS), a rare genetic disorder characterized by severely elevated triglyceride levels due to impaired clearance of chylomicrons.

High-Density Lipoproteins (HDL) are a type of lipoprotein that play a crucial role in the transportation and metabolism of cholesterol in the body. They are often referred to as "good" cholesterol because they help remove excess cholesterol from cells and carry it back to the liver, where it can be broken down and removed from the body. This process is known as reverse cholesterol transport.

HDLs are composed of a lipid core containing cholesteryl esters and triglycerides, surrounded by a shell of phospholipids, free cholesterol, and apolipoproteins, primarily apoA-I. The size and composition of HDL particles can vary, leading to the classification of different subclasses of HDL with varying functions and metabolic fates.

Elevated levels of HDL have been associated with a lower risk of developing cardiovascular diseases, while low HDL levels increase the risk. However, it is essential to consider that HDL function and quality may be more important than just the quantity in determining cardiovascular risk.

Lipoproteins are complex particles composed of multiple proteins and lipids (fats) that play a crucial role in the transport and metabolism of fat molecules in the body. They consist of an outer shell of phospholipids, free cholesterols, and apolipoproteins, enclosing a core of triglycerides and cholesteryl esters.

There are several types of lipoproteins, including:

1. Chylomicrons: These are the largest lipoproteins and are responsible for transporting dietary lipids from the intestines to other parts of the body.
2. Very-low-density lipoproteins (VLDL): Produced by the liver, VLDL particles carry triglycerides to peripheral tissues for energy storage or use.
3. Low-density lipoproteins (LDL): Often referred to as "bad cholesterol," LDL particles transport cholesterol from the liver to cells throughout the body. High levels of LDL in the blood can lead to plaque buildup in artery walls and increase the risk of heart disease.
4. High-density lipoproteins (HDL): Known as "good cholesterol," HDL particles help remove excess cholesterol from cells and transport it back to the liver for excretion or recycling. Higher levels of HDL are associated with a lower risk of heart disease.

Understanding lipoproteins and their roles in the body is essential for assessing cardiovascular health and managing risks related to heart disease and stroke.

Cholesterol is a type of lipid (fat) molecule that is an essential component of cell membranes and is also used to make certain hormones and vitamins in the body. It is produced by the liver and is also obtained from animal-derived foods such as meat, dairy products, and eggs.

Cholesterol does not mix with blood, so it is transported through the bloodstream by lipoproteins, which are particles made up of both lipids and proteins. There are two main types of lipoproteins that carry cholesterol: low-density lipoproteins (LDL), also known as "bad" cholesterol, and high-density lipoproteins (HDL), also known as "good" cholesterol.

High levels of LDL cholesterol in the blood can lead to a buildup of cholesterol in the walls of the arteries, increasing the risk of heart disease and stroke. On the other hand, high levels of HDL cholesterol are associated with a lower risk of these conditions because HDL helps remove LDL cholesterol from the bloodstream and transport it back to the liver for disposal.

It is important to maintain healthy levels of cholesterol through a balanced diet, regular exercise, and sometimes medication if necessary. Regular screening is also recommended to monitor cholesterol levels and prevent health complications.

Apolipoprotein D (apoD) is a protein that is associated with high-density lipoprotein (HDL) particles in the blood. It is one of several apolipoproteins that are involved in the transport and metabolism of lipids, such as cholesterol and triglycerides, in the body.

ApoD is produced by the APOD gene and is found in various tissues, including the brain, where it is believed to play a role in protecting nerve cells from oxidative stress. It has also been studied for its potential role in Alzheimer's disease and other neurological disorders.

In addition to its role in lipid metabolism and neuroprotection, apoD has been shown to have anti-inflammatory properties and may be involved in the regulation of immune responses. However, more research is needed to fully understand the functions and mechanisms of action of this protein.

Low-density lipoproteins (LDL), also known as "bad cholesterol," are a type of lipoprotein that carry cholesterol and other fats from the liver to cells throughout the body. High levels of LDL in the blood can lead to the buildup of cholesterol in the walls of the arteries, which can increase the risk of heart disease and stroke.

Lipoproteins are complex particles composed of proteins (apolipoproteins) and lipids (cholesterol, triglycerides, and phospholipids) that are responsible for transporting fat molecules around the body in the bloodstream. LDL is one type of lipoprotein, along with high-density lipoproteins (HDL), very low-density lipoproteins (VLDL), and chylomicrons.

LDL particles are smaller than HDL particles and can easily penetrate the artery walls, leading to the formation of plaques that can narrow or block the arteries. Therefore, maintaining healthy levels of LDL in the blood is essential for preventing cardiovascular disease.

Lipids are a broad group of organic compounds that are insoluble in water but soluble in nonpolar organic solvents. They include fats, waxes, sterols, fat-soluble vitamins (such as vitamins A, D, E, and K), monoglycerides, diglycerides, triglycerides, and phospholipids. Lipids serve many important functions in the body, including energy storage, acting as structural components of cell membranes, and serving as signaling molecules. High levels of certain lipids, particularly cholesterol and triglycerides, in the blood are associated with an increased risk of cardiovascular disease.

LDL receptors (Low-Density Lipoprotein Receptors) are cell surface receptors that play a crucial role in the regulation of cholesterol homeostasis within the body. They are responsible for recognizing and binding to LDL particles, also known as "bad cholesterol," which are then internalized by the cell through endocytosis.

Once inside the cell, the LDL particles are broken down, releasing their cholesterol content, which can be used for various cellular processes such as membrane synthesis and hormone production. The LDL receptors themselves are recycled back to the cell surface, allowing for continued uptake of LDL particles.

Mutations in the LDL receptor gene can lead to a condition called familial hypercholesterolemia, which is characterized by high levels of LDL cholesterol in the blood and an increased risk of premature cardiovascular disease.

Atherosclerosis is a medical condition characterized by the buildup of plaques, made up of fat, cholesterol, calcium, and other substances found in the blood, on the inner walls of the arteries. This process gradually narrows and hardens the arteries, reducing the flow of oxygen-rich blood to various parts of the body. Atherosclerosis can affect any artery in the body, including those that supply blood to the heart (coronary arteries), brain, limbs, and other organs. The progressive narrowing and hardening of the arteries can lead to serious complications such as coronary artery disease, carotid artery disease, peripheral artery disease, and aneurysms, which can result in heart attacks, strokes, or even death if left untreated.

The exact cause of atherosclerosis is not fully understood, but it is believed to be associated with several risk factors, including high blood pressure, high cholesterol levels, smoking, diabetes, obesity, physical inactivity, and a family history of the condition. Atherosclerosis can often progress without any symptoms for many years, but as the disease advances, it can lead to various signs and symptoms depending on which arteries are affected. Treatment typically involves lifestyle changes, medications, and, in some cases, surgical procedures to restore blood flow.

HDL (High-Density Lipoprotein) cholesterol is often referred to as "good" cholesterol. It is a type of lipoprotein that helps remove excess cholesterol from cells and carry it back to the liver, where it can be broken down and removed from the body. High levels of HDL cholesterol have been associated with a lower risk of heart disease and stroke.

Arteriosclerosis is a general term that describes the hardening and stiffening of the artery walls. It's a progressive condition that can occur as a result of aging, or it may be associated with certain risk factors such as high blood pressure, high cholesterol, diabetes, smoking, and a sedentary lifestyle.

The process of arteriosclerosis involves the buildup of plaque, made up of fat, cholesterol, calcium, and other substances, in the inner lining of the artery walls. Over time, this buildup can cause the artery walls to thicken and harden, reducing the flow of oxygen-rich blood to the body's organs and tissues.

Arteriosclerosis can affect any of the body's arteries, but it is most commonly found in the coronary arteries that supply blood to the heart, the cerebral arteries that supply blood to the brain, and the peripheral arteries that supply blood to the limbs. When arteriosclerosis affects the coronary arteries, it can lead to heart disease, angina, or heart attack. When it affects the cerebral arteries, it can lead to stroke or transient ischemic attack (TIA). When it affects the peripheral arteries, it can cause pain, numbness, or weakness in the limbs, and in severe cases, gangrene and amputation.

The liver is a large, solid organ located in the upper right portion of the abdomen, beneath the diaphragm and above the stomach. It plays a vital role in several bodily functions, including:

1. Metabolism: The liver helps to metabolize carbohydrates, fats, and proteins from the food we eat into energy and nutrients that our bodies can use.
2. Detoxification: The liver detoxifies harmful substances in the body by breaking them down into less toxic forms or excreting them through bile.
3. Synthesis: The liver synthesizes important proteins, such as albumin and clotting factors, that are necessary for proper bodily function.
4. Storage: The liver stores glucose, vitamins, and minerals that can be released when the body needs them.
5. Bile production: The liver produces bile, a digestive juice that helps to break down fats in the small intestine.
6. Immune function: The liver plays a role in the immune system by filtering out bacteria and other harmful substances from the blood.

Overall, the liver is an essential organ that plays a critical role in maintaining overall health and well-being.

Hyperlipoproteinemia Type III, also known as Broad Beta Disease or Remnant Hyperlipidemia, is a genetic disorder characterized by an increased level of chylomicron remnants and intermediate-density lipoproteins (IDL) in the blood. This results in elevated levels of both low-density lipoprotein (LDL), or "bad" cholesterol, and triglycerides, and decreased levels of high-density lipoprotein (HDL), or "good" cholesterol. The condition can lead to premature atherosclerosis and an increased risk for cardiovascular disease. It is caused by mutations in the APOE gene, which encodes the apolipoprotein E protein, leading to abnormal clearance of lipoproteins from the blood.

Phosphatidylcholine-Sterol O-Acyltransferase (PCOAT, also known as Sterol O-Acyltransferase 1 or SOAT1) is an enzyme that plays a crucial role in the regulation of cholesterol metabolism. It is located in the endoplasmic reticulum and is responsible for the transfer of acyl groups from phosphatidylcholine to cholesterol, forming cholesteryl esters. This enzymatic reaction results in the storage of excess cholesterol in lipid droplets, preventing its accumulation in the cell membrane and potentially contributing to the development of atherosclerosis if not properly regulated.

Defects or mutations in PCOAT can lead to disruptions in cholesterol homeostasis, which may contribute to various diseases such as cardiovascular disorders, metabolic syndrome, and neurodegenerative conditions. Therefore, understanding the function and regulation of this enzyme is essential for developing therapeutic strategies aimed at managing cholesterol-related disorders.

LDL, or low-density lipoprotein, is often referred to as "bad" cholesterol. It is one of the lipoproteins that helps carry cholesterol throughout your body. High levels of LDL cholesterol can lead to a buildup of cholesterol in your arteries, which can increase the risk of heart disease and stroke.

Cholesterol is a type of fat (lipid) that is found in the cells of your body. Your body needs some cholesterol to function properly, but having too much can lead to health problems. LDL cholesterol is one of the two main types of cholesterol; the other is high-density lipoprotein (HDL), or "good" cholesterol.

It's important to keep your LDL cholesterol levels in a healthy range to reduce your risk of developing heart disease and stroke. A healthcare professional can help you determine what your target LDL cholesterol level should be based on your individual health status and risk factors.

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Apolipoprotein B48 on chylomicra and Apolipoprotein B100 on LDL, IDL, and VLDL are important for MTP binding.[citation needed] ... Gordon DA (1997). "Recent advances in elucidating the role of the microsomal triaglyceride transfer protein in apolipoprotein B ... 1999). "A common binding site on the microsomal triaglyceride transfer protein for apolipoprotein B and protein disulfide ... The network of endoplasmic reticulum-resident chaperones (ERp72, GRP94, calreticulin, and BiP) interacts with apolipoprotein b ...
Basu SK, Goldstein JL, Brown MS (Feb 1983). "Independent pathways for secretion of cholesterol and apolipoprotein E by ... 89 (3): 331-40. doi:10.1016/S0092-8674(00)80213-5. PMID 9150132. S2CID 17882616. DeBose-Boyd RA, Brown MS, Li WP, Nohturfft A, ... 65 (3): 429-34. doi:10.1016/0092-8674(91)90460-G. PMID 2018975. S2CID 54388220. Chen WJ, Andres DA, Goldstein JL, Russell DW, ... 102 (3): 315-23. doi:10.1016/S0092-8674(00)00037-4. PMID 10975522. S2CID 18054832. Yang T, Espenshade PJ, Wright ME, et al. ( ...
Apolipoprotein B mRNA editing enzyme, catalytic polypeptide 1 also known as C->U-editing enzyme APOBEC-1 is a protein that in ... The structure of A1 relies on three dimensional folds induced by a zinc complex. These folds allow the enzyme to access the RNA ... "Entrez Gene: APOBEC1 apolipoprotein B mRNA editing enzyme, catalytic polypeptide 1". Rosenberg BR, Hamilton CE, Mwangi MM, ... Lau PP, Zhu HJ, Nakamuta M, Chan L (1997). "Cloning of an Apobec-1-binding protein that also interacts with apolipoprotein B ...
All members of this family are receptors for Apolipoprotein E (ApoE). Therefore, they are often synonymously referred to as ' ... This fragment may serve postnatally to prevent apical dendrites of cortical layer II/III pyramidal neurons from overgrowth, ... Andersen OM, Benhayon D, Curran T, Willnow TE (August 2003). "Differential binding of ligands to the apolipoprotein E receptor ... Herz J, Beffert U (October 2000). "Apolipoprotein E receptors: linking brain development and Alzheimer's disease". Nature ...
Takahashi K, Ikeo K, Gojobori T (1991). "Evolutionary origin of numerous kringles in human and simian apolipoprotein(a)". FEBS ... Kringle domains have been found in plasminogen, hepatocyte growth factors, prothrombin, and apolipoprotein(a). Kringles are ... 212 (3): 541-552. doi:10.1016/0022-2836(90)90330-O. PMID 2157850. Castellino FJ, Beals JM (1987). "The genetic relationships ... Kringle domains are characterised by a triple loop, 3-disulfide bridge structure, whose conformation is defined by a number of ...
... apolipoprotein C is a family of four low molecular weight apolipoproteins, designated as C-I, C-II, C-III, and C-IV that are ... In the fasting state, the C apolipoproteins are mainly associated with HDL. During absorption of dietary fat, the C ... v t e (Articles with short description, Short description matches Wikidata, Apolipoproteins, All stub articles, Protein stubs) ... Mahley RW, Innerarity TL, Rall SC, Weisgraber KH (December 1984). "Plasma lipoproteins: apolipoprotein structure and function ...
A specific isoform of apolipoprotein, APOE4, is a major genetic risk factor for Alzheimer's disease. While apolipoproteins ... The three stages are described as early or mild, middle or moderate, and late or severe. The disease is known to target the ... There are three sets of criteria for the clinical diagnoses of the spectrum of Alzheimer's disease: the 2013 fifth edition of ... Three broad time periods, which can span decades, define the progression of Alzheimer's disease from the preclinical phase, to ...
Katan MB (March 1986). "Apolipoprotein E isoforms, serum cholesterol, and cancer". Lancet. 1 (8479): 507-508. doi:10.1016/s0140 ... Mendelian randomization requires three core instrumental variable assumptions. Namely: The genetic variant(s) being used as an ... in which he advocated a study design using Apolipoprotein E allele as an instrumental variable anchor to study the observed ... 7 (Suppl 3): 9-12. PMID 1855097. Murad, M. Hassan; Asi, Noor; Alsawas, Mouaz; Alahdab, Fares (2016-08-01). "New evidence ...
... and involves apolipoprotein A1. "FAP-IV" is also known as "Finnish-type", and involves gelsolin. Fibrinogen, apolipoprotein A1 ... Senile systemic amyloidosis [abbreviated "SSA"] is also associated with transthyretin aggregation.) "FAP-III" is also known as ... These proteins include: transthyretin (ATTR, the most commonly implicated protein), apolipoprotein A1, and gelsolin. Due to the ... 11 (3): 185-6. doi:10.1038/nrd3675. PMID 22378262. S2CID 256746210. Grogan, Kevin (19 June 2012). "FDA rejects Pfizer rare ...
"Deficiency of glycine N-methyltransferase aggravates atherosclerosis in apolipoprotein E-null mice". Molecular Medicine. 18 (5 ... 87: 132-3. doi:10.1016/j.jprot.2013.01.007. PMID 23340451. Chen CY, Ching LC, Liao YJ, Yu YB, Tsou CY, Shyue SK, Chen YM, Lee ... 235 (3): 296-304. doi:10.1016/j.taap.2008.12.013. PMID 19146867. Chen YM, Shiu JY, Tzeng SJ, Shih LS, Chen YJ, Lui WY, Chen PH ... 18 (3): 412-22. doi:10.2119/molmed.2011.00258. PMC 3356423. PMID 22183894. Chen M, Ho CW, Huang YC, Wu KY, Wu MT, Jeng HA, Chen ...
"Entrez Gene: APOBEC3C apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like 3C". Yu Q, Chen D, König R, Mariani R, ... 457 (3): 295-9. doi:10.1016/j.bbrc.2014.12.103. hdl:2297/44628. PMID 25576866. Yu Q, König R, Pillai S, Chiles K, Kearney M, ... 8 (3): 148-57. PMID 17078485. Madsen P, Anant S, Rasmussen HH, Gromov P, Vorum H, Dumanski JP, Tommerup N, Collins JE, Wright ... 3 (1): 89. doi:10.1038/msb4100134. PMC 1847948. PMID 17353931. Kinomoto M, Kanno T, Shimura M, Ishizaka Y, Kojima A, Kurata T, ...
Ichinose A (1992). "Multiple members of the plasminogen-apolipoprotein(a) gene family associated with thrombosis". Biochemistry ... 4 (3): 449-51. doi:10.1016/0888-7543(89)90356-X. PMID 2714803. Magnaghi P, Citterio E, Malgaretti N, et al. (1994). "Molecular ... 3 (3): 437-42. doi:10.1093/hmg/3.3.437. PMID 8012354. Kida M, Wakabayashi S, Ichinose A (1997). "Characterization of the 5'- ... 259 (3): 618-25. doi:10.1046/j.1432-1327.1999.00055.x. PMID 10092845. Strausberg RL, Feingold EA, Grouse LH, et al. (2003). " ...
"Apolipoprotein C-III(Lys58----Glu). Identification of an apolipoprotein C-III variant in a family with ... Apolipoprotein C-III also known as apo-CIII, and apolipoprotein C3, is a protein that in humans is encoded by the APOC3 gene. ... Apolipoprotein+C-III at the U.S. National Library of Medicine Medical Subject Headings (MeSH) Human APOC3 genome location and ... Zannis VI, Cole FS, Jackson CL, Kurnit DM, Karathanasis SK (Jul 1985). "Distribution of apolipoprotein A-I, C-II, C-III, and E ...
Identification of apolipoprotein D, apolipoprotein A-IV, apolipoprotein E, and apolipoprotein A-I". The Journal of Biological ... Apolipoprotein D (ApoD) is a component of HDL that has no marked similarity to other apolipoprotein sequences. It has a high ... "Entrez Gene: APOD apolipoprotein D". Muffat J, Walker DW (January 2010). "Apolipoprotein D: an overview of its role in aging ... Apolipoproteins+D at the U.S. National Library of Medicine Medical Subject Headings (MeSH) Applied Research on Apolipoproteins ...
Additionally, the fifth protein domain appears to resemble the other four in Apolipoprotein with the exception of three ... Apolipoprotein+H at the U.S. National Library of Medicine Medical Subject Headings (MeSH) Apolipoprotein H and Applied Research ... The first four domains found in Apolipoprotein H resemble each other, however the fifth one appears to be different. This ... PDBe-KB provides an overview of all the structure information available in the PDB for Human Apolipoprotein H (B2G1) (Articles ...
... is a protein that in humans is encoded by the APOA2 gene. It is the second most abundant protein of the ... "Entrez Gene: APOA2 apolipoprotein A-II". Pussinen PJ, Jauhiainen M, Metso J, Pyle LE, Marcel YL, Fidge NH, Ehnholm C (Jan 1998 ... Brewer HB, Lux SE, Ronan R, John KM (May 1972). "Amino acid sequence of human apoLp-Gln-II (apoA-II), an apolipoprotein ... The protein is found in plasma as a monomer, homodimer, or heterodimer with apolipoprotein D. ApoA-II regulates many steps in ...
Sacks FM, Zheng C, Cohn JS (2011). "Complexities of plasma apolipoprotein C-III metabolism". Journal of Lipid Research. 52 (6 ... Its most abundant apolipoproteins are apo A-I and apo A-II. A rare genetic variant, ApoA-1 Milano, has been documented to be ... In the stress response, serum amyloid A, which is one of the acute-phase proteins and an apolipoprotein, is under the ... They are typically composed of 80-100 proteins per particle (organized by one, two or three ApoA). HDL particles enlarge while ...
... peptides such as adrenomedullin and apolipoprotein; and iii) hemin. NRF2 inducers with downstream HO-1 induction include: ... The human genome may encode three isoforms of HMOX. The degradation of heme forms three distinct chromogens as seen in healing ... The reaction comprises three steps, which may be: Heme b3+ + O 2 + NADPH + H+ → α-meso-hydroxyheme3+ + NADP+ + H 2O α-meso- ... 312 (3): C302-C313. doi:10.1152/ajpcell.00360.2016. PMID 28077358. Leung GC, Fung SS, Gallio AE, Blore R, Alibhai D, Raven EL, ...
Definite localization of the APOC2 gene and the polymorphic Hpa I site associated with type III hyperlipoproteinemia". Human ... Myklebost O, Rogne S (August 1986). "The gene for human apolipoprotein CI is located 4.3 kilobases away from the apolipoprotein ... "Two copies of the human apolipoprotein C-I gene are linked closely to the apolipoprotein E gene". The Journal of Biological ... Apolipoprotein C-I is a protein component of lipoproteins that in humans is encoded by the APOC1 gene. The protein encoded by ...
"Apolipoprotein C-III(Lys58----Glu). Identification of an apolipoprotein C-III variant in a family with ... Apolipoprotein C-III also known as apo-CIII, and apolipoprotein C3, is a protein that in humans is encoded by the APOC3 gene. ... Apolipoprotein+C-III at the U.S. National Library of Medicine Medical Subject Headings (MeSH) Human APOC3 genome location and ... Zannis VI, Cole FS, Jackson CL, Kurnit DM, Karathanasis SK (Jul 1985). "Distribution of apolipoprotein A-I, C-II, C-III, and E ...
Probable amyloidogenic proteins are apolipoproteins (Apos), which are vital for the formation and function of lipoproteins. ... A dual apolipoprotein C-II mimetic-apolipoprotein C-III antagonist peptide lowers plasma triglycerides. Wolska A, Lo L, ... Amyloid triangles, squares, and loops of apolipoprotein C-III Michel de Messieres 1 , Rick K Huang, Yi He, Jennifer C Lee ... Amyloid triangles, squares, and loops of apolipoprotein C-III Michel de Messieres et al. Biochemistry. 2014. . ...
All three macaques did not develop significant CD4+ T cell loss over the course of infection, had plasma viral loads that were ... However, the L148A substitution remained stale in the vif amplified from the PBMC and select tissues at necropsy in all three ... Human and monkey A3A amino acid sequences are 81% homologous and can be distinguished by a three amino acid indel located ... To determine if infectious virus was present in the plasma at necropsy, plasma from the three macaques inoculated with ...
Effects of omega-3 fatty acid supplements on serum lipids, apolipoproteins and malondialdehyde in type 2 diabetes patients ... apolipoprotein B-100 (Apo B-100), apolipoprotein A-I (Apo A-I), malondialdehyde (MDA) (as index for lipid peroxidation), and ... Effects of omega-3 fatty acid supplements on serum lipids, apolipoproteins and malondialdehyde in type 2 diabetes patients ... In the omega-3 fatty acid group, fasting TG decreased significantly by 31.2 % (P = 0.01) relative to the placebo group; there ...
Apolipoproteins for Risk Assessment So, LDL-P may play a useful role in patient management by helping judge the adequacy of LDL ... This association and the ability to measure apolipoprotein in nonfasting blood samples had led to recommendations that the apo ... Cite this: HDL Cholesterol, HDL Particle Size and Apolipoprotein A-I: Significance for Cardiovascular Risk - The IDEAL & EPIC- ... HDL Cholesterol, HDL Particle Size and Apolipoprotein A-I: Significance for Cardiovascular Risk - The IDEAL & EPIC-Norfolk ...
We describe a strategy for lowering triglycerides (TGs) with an apolipoprotein C-II (apoC-II) mimetic peptide called D6PV that ... ApoC-III of plasma VLDL on day 5. (D) ApoC-III of plasma LDL on day 5. (E) ApoC-III of plasma HDL on day 5. (F) ApoC-III ... A dual apolipoprotein C-II mimetic-apolipoprotein C-III antagonist peptide lowers plasma triglycerides Anna Wolska 1 , Larry Lo ... A dual apolipoprotein C-II mimetic-apolipoprotein C-III antagonist peptide lowers plasma triglycerides Anna Wolska et al. Sci ...
The ability of sAPP-α to activate microglia was blocked by prior incubation of the protein with apolipoprotein E3 but not ... apolipoprotein E4, a variant associated with an increased risk for Alzheimers6. A product of amyloidogenic β-APP processing ( ... 3,4. Inflammatory events may also contribute to Alzheimers disease5. Here we investigate whether a secreted derivative of β- ... Data are presented as the mean ± s.e.m. for triplicate determinations within one of at least three similar experiments. ...
Familial hypobetalipoproteinemia: analysis of three Spanish cases with two new mutations in the APOB gene. Gene. 2013 Nov 15. ... Beta apolipoproteins. Beta apolipoproteins are the largest of the apolipoproteins. They are critically important for the ... Apolipoprotein B-100 deficiency. Intestinal steatosis despite apolipoprotein B-48 synthesis. J Clin Invest. 1985 Aug. 76(2):403 ... CMs, VLDL, and LDL carry apolipoproteins on their surface; these apolipoproteins have lipid-soluble segments, the beta ...
... mic e at each of the three time points examined. However, at 13 weeks, it appeared that the lesions in the Apoe-/-CCR2-/- m ice ... Human apolipoprotein A-I prevents atherosclerosis associated with apolipoprotein[a] in transgenic mice. J Lipid Res 1994. 35: ... Apolipoprotein A-I transgene corrects apolipoprotein E deficiency-induced atherosclerosis in mice. J Clin Invest 1994. 94:899- ... Expression of human apolipoprotein A-I in transgenic mice results in reduced plasma levels of murine apolipoprotein A-I and the ...
Apolipoprotein CII (apoCII) is a protein found in large fat particles that the gastrointestinal tract absorbs. It is also found ... ApoCII; Apoprotein CII; ApoC2; Lipoprotein lipase deficiency - apolipoprotein CII; Chylomicronemia syndrome - apolipoprotein ... Apolipoprotein measurements may provide more detail about your risk for heart disease, but the added value of this test beyond ... Apolipoprotein CII (apoCII) is a protein found in large fat particles that the gastrointestinal tract absorbs. It is also found ...
Usefulness of apolipoprotein B-depleted serum in cholesterol efflux capacity assays using immobilized liposome-bound gel beads ... apolipoprotein B-depleted serum, cardiovascular disease, cholesterol efflux capacity, high-density lipoprotein ... Enhancing apolipoprotein A-I-dependent cholesterol efflux elevates cholesterol export from macrophages in vivo ... One of the candidates for this purpose is the precipitation method, in which apolipoprotein (apo) B (apoB)-containing ...
Description of APOCIII role and implications in pathologies.
Aged, Aged, 80 and over, Alleles, Alzheimer Disease, Apolipoproteins E, Female, Gene Expression, Genotype, Hippocampus, Humans ... Apolipoprotein E4 (APOE4) allele is a major risk factor for late-onset familial and sporadic Alzheimer disease (AD). The ... Differences in apolipoprotein E3/3 and E4/4 allele-specific gene expression in hippocampus in Alzheimer disease.. ... Differences in apolipoprotein E3/3 and E4/4 allele-specific gene expression in hippocampus in Alzheimer disease.. ...
Apolipoprotein e4 carrier status was associated with an increased risk for early postoperative delirium after controlling for ... Apolipoprotein E e4 allele increases the risk of early postoperative delirium in older patients undergoing noncardiac surgery ... Forty-six patients (24.2%) had at least one copy of the apolipoprotein e4 allele. The presence of one copy of the e4 allele was ... Conclusions: Apolipoprotein e4 carrier status was associated with an increased risk for early postoperative delirium after ...
Inhaled Asbestos Exacerbates Atherosclerosis in Apolipoprotein E-Deficient Mice via CD4+ T Cells. *Naomi K. Fukagawa ... CD4+ T cells infiltrate lesions of apolipoprotein-E-deficient mice. Am J Pathol 149:359-3668701976. Medline, Google Scholar ... The role of interleukin-4 and interleukin-12 in the progression of atherosclerosis in apolipoprotein E-deficient mice. Am J ... MCP-1 deficiency reduces susceptibility to atherosclerosis in mice that overexpress human apolipoprotein B. J Clin Invest 103: ...
Gene dose of apolipoprotein E type 4 allele and the risk of Alzheimers disease in late onset families. Science. 1993 Aug 13; ...
Double-Blind Crossover Study of the Cognitive Effects of Lorazepam in Healthy Apolipoprotein E (APOE)-ε4 Carriers. Cynthia M. ... Physical Exercise and Health, 3: A Guide to Understanding What to Do, How, and Why-Part 1. Dr Andrade gives practical guidance ... Although he cited us,3 he overlooked the evidence we provided indicating that the Bacloville article4 was published without ... cognitive effects of pharmacologically induced somnolence in cognitively normal carriers and noncarriers of the apolipoprotein ...
All the subjects were divided into three groups according to APOE genotypes: (1) E2/2 or E2/3 (APOE E2); (2) E3/3& ... To determine the associations between apolipoprotein E (APOE) genotypes and serum levels of glucose, total cholesterol, and ... Associations between apolipoprotein E genotypes and serum levels of glucose, cholesterol, and triglycerides in a cognitively ... nbsp;(APOE E3); and (3) E2/4, E3/4, or E4/4 (APOE E4). Correlations of serum levels of glucose, total cholesterol, and ...
Deficiency or defects in Apo E are causes of HYPERLIPOPROTEINEMIA TYPE III. ... Apolipoproteins E: A class of protein components which can be found in several lipoproteins including HIGH-DENSITY LIPOPROTEINS ... Apolipoproteins E (ApoE). Subscribe to New Research on Apolipoproteins E A class of protein components which can be found in ... ApoE; Apo E; Apo E Isoproteins; Apolipoprotein E Isoproteins; Apoprotein (E); Apoproteins E; Isoproteins, Apo E; Isoproteins, ...
Among men, factors were age, apolipoprotein A1 level, apolipoprotein B level, and insulin resistance. Seventy-five percent of ... b Defined using Adult Treatment Panel III criteria (13).. c Defined as ,102 cm for men and ,88 cm for women.. d Defined as a ... apolipoprotein A1 (apoA1), total apolipoprotein B (apoB), and homocysteine levels from fasting participants (low-density ... Abbreviations: SE, standard error; OR, odds ratio; CI, confidence interval; apo, apolipoprotein. a Calculated by logistic ...
Creative Biolabs offers high-quality Human apolipoprotein E (APOE), transcript variant 3 (NM_001302689) ORF clone, Untagged to ... Human apolipoprotein E (APOE), transcript variant 3 (NM_001302689) ORF clone, Untagged. [CAT#: NEP-0421-R0264] ... Thank you for your interest in Human apolipoprotein E (APOE), transcript variant 3 (NM_001302689) ORF clone, Untagged. Please ... Human apolipoprotein E (APOE), transcript variant 3 (NM_001302689) ORF clone, Myc-DDK Tagged ...
Apolipoprotein A-I (Apo-A1) is a structural and functional protein that constitutes approximately 70% of the protein in high ... What is the reference range of apolipoprotein A-I (Apo-A1)?. Which conditions are associated with low levels of apolipoprotein ... What are the indications for apolipoprotein A-I (Apo-A1) measurement?. What are considerations for apolipoprotein A-I (Apo-A1) ... encoded search term (Apolipoprotein A-I) and Apolipoprotein A-I What to Read Next on Medscape ...
A Dual Apolipoprotein C-II Mimetic-Apolipoprotein C-III Antagonist Peptide Lowers Plasma Triglycerides. ... entitled "A dual apolipoprotein C-II mimetic-apolipoprotein C-III antagonist peptide lowers plasma triglycerides." published in ...
Change in (A) LDL-C, (B) HDL-C, (C) TC:HDL-C, (D) Apolipoprotein B (apoB), (E) Apolipoprotein A1 (apoA1), (F) ApoB:ApoA1 ratio ... Three participants were withdrawn by the study physician due to failure to attain LDL-C targets on the low-carbohydrate diet ( ... Apolipoproteins versus lipids as indices of coronary risk and as targets for statin treatment. Lancet 2003;361:777-80. ... Apolipoproteins. ApoB and the ApoB:ApoA1 ratio were reduced more on the low-carbohydrate versus the high-carbohydrate diet at ...
Apolipoprotein A5) ELISA Kit from Gentaur Elisa Kits. Cat Number: G-EC-05986. USA, UK & Europe Distribution. ... Rat ApoA5 (Apolipoprotein A5) ELISA Kit , G-EC-05986. Rating * Select Rating. 1 star (worst). 2 stars. 3 stars (average). 4 ... Rat ApoA5 (Apolipoprotein A5) ELISA Kit , G-EC-05986 , Gentaur Elisa Kits ...
Impact of apolipoprotein E4-cerebrospinal fluid β-amyloid interaction on hippocampal volume loss over 1 year in mild cognitive ... Participants were categorised into three groups based on the third of weighted standardised score into low, intermediate, and ... Impact of the apolipoprotein E ε4 allele on the relationship between healthy lifestyle and cognitive decline: a population- ... Apolipoprotein E (APOE) genotype, dementia, and memory performance among Caribbean Hispanic versus US populations. Alzheimers ...
The canonical role of apolipoprotein C-III (apoC-III) is to inhibit the plasma clearance of lipoproteins by low-density ... In liver apoC-III works to increase VLDL secretion, whereas intestinal apoC-III results in the secretion of smaller ... In Aim 1, we identified the role of apoC-III on immune homeostasis. We found that apoC-III overexpression increases Tregs in ... Its likely that apoC-III also plays a tissue-specific role in immune cells which express LDLr. In this dissertation, we aimed ...
  • Apolipoprotein B (ApoB) is a protein that in humans is encoded by the APOB gene. (wikipedia.org)
  • Familial hypobetalipoproteinaemia (FHBL) is a codominant disorder characterised by fatty liver and reduced plasma levels of low-density lipoprotein (LDL) and its protein constituent apolipoprotein B (apoB). (bmj.com)
  • In a group of 59 patients with FHBL genotyped for APOB gene mutations, we found three novel splice-site mutations: c.904+4A→G in intron 8, c.3843−2A→G in intron 24 and c.4217−1G→T in intron 25. (bmj.com)
  • This CETP inhibition, which exchanges a triglyceride molecule for a cholesteryl ester molecule between HDL-C-containing and apolipoprotein B (ApoB)-containing particles, also this particular therapeutic has been shown in prior studies to decrease ApoB significantly and, actually, to even decrease Lp(a), which is interesting. (medscape.com)
  • Novel biomarkers of risk, such as apolipoprotein (Apo) A1 and ApoB (2), and the inflammatory markers C-reactive protein (CRP), fibrinogen, and homocysteine (3-5), have been proposed. (cdc.gov)
  • Previously published data have shown an allele-specific variation in the in vitro binding of apolipoprotein E (apoE) to tau, which prompted the hypothesis that apoE binding may protect tau from phosphorylation, apoE3 being more efficient than apoE4. (ox.ac.uk)
  • We have, therefore, investigated the effects of apoE on tau phosphorylation in vitro by the proline-directed kinase, glycogen synthase kinase (GSK)-3 beta. (ox.ac.uk)
  • The aim of this study was to evaluate a microsurgical technique of syngeneic heterotopic transplantation of the thoracic aorta of young apolipoprotein E-deficient (ApoE-/-) mice to the abdominal aorta of wild-type recipients. (degruyter.com)
  • The APOE gene provides instructions for making a protein called apolipoprotein E. This protein combines with fats (lipids) in the body to form molecules called lipoproteins. (medlineplus.gov)
  • There are at least three slightly different versions (alleles) of the APOE gene. (medlineplus.gov)
  • It is thought that the apolipoprotein E produced from the e4 allele of the APOE gene may disrupt the transport of a protein called alpha-synuclein into and out of cells. (medlineplus.gov)
  • The APOE e2 allele has been shown to greatly increase the risk of a rare condition called hyperlipoproteinemia type III. (medlineplus.gov)
  • Methods: Aortic plaque deposition was assessed in streptozotocin-induced diabetic apolipoprotein E (Apoe) knockout (KO) and At 2 r (also known as Agtr2)/Apoe double-KO (DKO) mice. (monash.edu)
  • Currently, it includes the three genes associated with autosomal-dominant AD ( APP , PSEN1 , PSEN2 ) plus four genes associated with AD through association studies or pathology ( APOE , MAPT , SORL1 , and TREM2 ). (alzforum.org)
  • APOE encodes a secreted apolipoprotein involved in lipid metabolism. (alzforum.org)
  • The impact of common variants in the apolipoprotein gene cluster (APOC3-A4-A5) on prospective coronary heart disease (CHD) risk was examined in healthy UK men. (nih.gov)
  • Apolipoprotein C-III, also known as apo-CIII, is a protein that in humans is encoded by the APOC3 gene. (nsjbio.com)
  • The apolipoprotein A-I gene is actively expressed in the rapidly myelinating avian peripheral nerve. (rupress.org)
  • The expression of the apolipoprotein A-I (apo A-I) gene was investigated in the myelinating sciatic nerve. (rupress.org)
  • Apoliprotein (apo) A-IV gene contains 3 exons separated by two introns. (joplink.net)
  • The protein encoded by this gene is a component of high-density lipoprotein (HDL), but is unique in that it shares greater structural similarity to lipocalin than to other members of the apolipoprotein family, and has a wider tissue expression pattern. (genscript.com)
  • Title: Identification of apolipoprotein D as a cardioprotective gene using a mouse model of lethal atherosclerotic coronary artery disease. (genscript.com)
  • One gene abnormality affects apolipoprotein E (apo E)-the protein part of certain lipoproteins, which transport cholesterol through the bloodstream. (msdmanuals.com)
  • The Ratio of High-Density Lipoprotein Cholesterol to Apolipoprotein A-I Predicts Myocardial Injury Following Elective Percutaneous Coronary Intervention. (medscape.com)
  • In advanced stages of the condition, a protein called apolipoprotein A-1 (apoA-1) can form amyloid deposits, which are similar in structure to those associated with Alzheimer's disease. (sciencedaily.com)
  • Apolipoprotein B is the primary apolipoprotein of chylomicrons, VLDL, Lp(a), IDL, and LDL particles (LDL-commonly known as "bad cholesterol" when in reference to both heart disease and vascular disease in general), which is responsible for carrying fat molecules (lipids), including cholesterol, around the body to all cells within all tissues. (wikipedia.org)
  • These particles consist of a core of cholesterol esters and triglycerides surrounded by a monolayer of free cholesterol, phospholipids, and proteins (apolipoproteins). (medscape.com)
  • Simvastatin is one of nine known statins, specific inhibitors of hepatic enzyme 3-hydroxy-3-methylglutaryl-coenzyme A reductase, the rate-limiting step of cholesterol biosynthesis, and is believed to reduce plasma cholesterol levels by decreasing the activity of this enzyme. (degruyter.com)
  • Biomedical consequences of elevated cholesterol-containing lipoproteins and apolipoproteins on cardiovascular and non-cardiovascular outcomes. (ucl.ac.uk)
  • Subjects with hyperhomocysteinaemia had significantly elevated total cholesterol, LDL cholesterol, apolipoprotein A and apolipoprotein B and lower vitamin B levels compared with subjects with 12 normohomocysteinaemia. (who.int)
  • Hcy levels correlated with total cholesterol ( r = 0.09), apolipoprotein A ( r = 0.012), and B ( r = 0.013) levels and total/HDL cholesterol ratio ( r = -0.085). (who.int)
  • APOA4 on prebeta and prebeta-b particles efflux cholesterol from peripheral tissues via ATP-binding cassette transporter A1 (ABCA1) (step 3). (jci.org)
  • Researchers found that epigallocatechin-3-gallate (EGCG), most commonly associated with green tea, binds to the amyloid fibres of apoA-1. (sciencedaily.com)
  • Title: Apolipoprotein D modulates amyloid pathology in APP/PS1 Alzheimer's disease mice. (genscript.com)
  • Title: Amyloid-?25-35 induces apolipoprotein D Synthesis and growth arrest in HT22 hippocampal cells. (genscript.com)
  • ApoC-III impairs the lipolysis of TRLs [triacylglycerol (triglyceride)-rich lipoproteins] by inhibiting lipoprotein lipase and the hepatic uptake of TRLs by remnant receptors. (portlandpress.com)
  • Other apolipoproteins (A, C, D, E, and their subtypes) are soluble and are exchanged between lipoproteins during metabolism. (medscape.com)
  • It showed a 13% reduction in four-point major adverse cardiovascular events (MACEs) and a 15% reduction in three-point MACEs, including a 22% reduction in myocardial infarction over about a 5-year follow-up. (medscape.com)
  • Definition of human apolipoprotein A-I epitopes recognized by autoantibodies present in patients with cardiovascular diseases. (medscape.com)
  • Established clinical cardiovascular disease in patients with diabetes, chronic kidney disease (CKD) stages 3/4, or heterozygous familial hypercholesterolemia (HeFH). (medscape.com)
  • Overproduction of apolipoprotein B can result in lipid-induced endoplasmic reticulum stress and insulin resistance in the liver. (wikipedia.org)
  • Each lipoprotein is characterized by its lipid composition and by the type and number of apolipoproteins it possesses. (medscape.com)
  • these apolipoproteins have lipid-soluble segments, the beta apolipoproteins, which remain part of the lipoprotein throughout its metabolism. (medscape.com)
  • In the metabolic syndrome, increased apoC-III concentration, resulting from hepatic overproduction of VLDL (very-LDL) apoC-III, is strongly associated with delayed catabolism of triacylglycerols and TRLs. (portlandpress.com)
  • A unique feature of APOA4 is that it is an intestinal apolipoprotein secreted on HDL and chylomicrons. (jci.org)
  • The chylomicrons with APOA4 then enter circulation (step 2), where APOA4 is exchanged for APOC2 on liver-derived large HDL (step 3), generating APOA4-containing large HDL (step 4). (jci.org)
  • Western blot testing of 1) rat liver, 2) rat RH35, 3) mouse liver and 4) mouse HEPA1-6 cell lysate with APOC3 antibody at 0.5ug/ml. (nsjbio.com)
  • PVDF membrane was probed with 0.25 µg/mL of Sheep Anti-Mouse/Rat Apolipoprotein H/ApoH Antigen Affinity-purified Polyclonal Antibody (Catalog # AF6575) followed by HRP-conjugated Anti-Sheep IgG Secondary Antibody (Catalog # HAF016 ). (rndsystems.com)
  • Variants of apolipoprotein E have been studied extensively as risk factors for many different conditions. (medlineplus.gov)
  • ApoC-III (apolipoprotein C-III), an important regulator of lipoprotein metabolism, is strongly associated with hypertriglyceridaemia and the progression of CVD. (portlandpress.com)
  • Regulating apoC-III metabolism may be an important new therapeutic approach to managing dyslipidaemia and CVD risk in the metabolic syndrome. (portlandpress.com)
  • Apolipoprotein H (ApoH), also known as beta 2‑Glycoprotein I/ beta 2-GPI, is a variably glycosylated member of the complement control superfamily of proteins with a molecular weight of aproximately 50 kDa (1, 2). (rndsystems.com)
  • It is best known for its three major alleles-APOE2, APOE3, and APOE4 -with APOE4 increasing the risk for Alzheimer's disease and APOE2 reducing it. (alzforum.org)
  • An increase in apoC-III levels induces the development of hypertriglyceridemia. (nsjbio.com)
  • Data from family studies confirmed familial clustering [3-5]. (springer.com)
  • In addition, experimental evidence shows that apoC-III may also have a direct role in atherosclerosis. (portlandpress.com)
  • Distribution of apolipoprotein(a) in the plasma from patients with lipoprotein lipase deficiency and with type III hyperlipoproteinemia. (jci.org)
  • We have determined the phenotype, concentration, and distribution of apo(a) in plasma from patients with lipoprotein lipase (LPL) deficiency (type I hyperlipoproteinemia, n = 14), in apo E 2/2 homozygotes with type III hyperlipoproteinemia (n = 12) and in controls (n = 16). (jci.org)
  • Considering apo(a) type, the plasma concentration of apo(a) was normal in type III patients but significantly reduced in LPL deficiency. (jci.org)
  • Genetic deficiency of apolipoprotein D in the mouse is associated with nonfasting hypertriglyceridemia and hyperinsulinemia. (genscript.com)
  • This paper reports three cases of severe scombroid poisoning in previously healthy patients, which presented diffuse macular erythema, hypotension, palpitations, and abnormal electrocardiogram (ECG). (degruyter.com)
  • Apolipoprotein A-I Increases Insulin Secretion and Production From Pancreatic ß-Cells via a G-Protein-cAMP-PKA-FoxO1-Dependent Mechanism. (medscape.com)
  • Apolipoprotein A1 serum levels were significantly lower in acne twins [10]. (springer.com)
  • It was observed that there was no difference in the plasma clearance of [125 I]Aβ and that of the 3 H-cholesteryl ester, a marker of the emulsion particles, demonstrating that Aβ remains associated with these particles throughout both their lipolysis and tissue uptake. (iospress.com)
  • Intervention1: Pegozafermin: In Double blind randomized period, patients with diagnosis of Severe Hypertriglyceridemia will be randomized 3 3 2, pegozafermin 30 mg, pegozafermin 20 mg, placebo, n equal to 135 in each pegozafermin arm and n equal to 90 in the placebo arm. (who.int)
  • Control Intervention1: Placebo (Tris buffer solution (containing Arginine hydrochloride, and polysorbate 80)): In Double blind randomized period, patients with diagnosis of Severe Hypertriglyceridemia, subjects will be randomized 3 3 2, pegozafermin 30 mg, pegozafermin 20 mg, placebo, n equal to 135 in each pegozafermin arm and n equal to 90 in the placebo arm. (who.int)
  • Survey (NHANES III), conducted from 1988 through 1994, was the seventh in a series of these surveys based on a complex, multi-stage sample plan. (cdc.gov)
  • The following table summarizes the NHANES III data which are currently available on CD-ROM, including this release. (cdc.gov)
  • For the laboratory component, some previously release variables have been augmented with NHANES III Phase 2 data. (cdc.gov)
  • Mus musculus apolipoprotein D (Apod), transcript variant 3, mRNA. (genscript.com)
  • Effect of Leptin Administration on Circulating Apolipoprotein CIII levels in Patients With Lipodystrophy. (umassmed.edu)
  • AR/the polyol pathway have been demonstrated to play important roles in the development and progression of diabetic complications in a number of tissues including kidney, retina, lens, and peripheral neuron tissues [ 3 - 5 ]. (hindawi.com)
  • Title: Cerebral Apolipoprotein-D Is Hypoglycosylated Compared to Peripheral Tissues and Is Variably Expressed in Mouse and Human Brain Regions. (genscript.com)
  • Another small molecule that's in development now is obicetrapib in two phase 3 studies. (medscape.com)
  • In direct ELISAs, approximately 40% cross-reactivity with recombinant human Apolipoprotein H/ApoH is observed. (rndsystems.com)
  • Temperature‐Responsive Nanoparticles Enable Specific Binding of Apolipoproteins from Human Plasma. (mpg.de)
  • [3] Since that time, the number of Americans age 85 and older has increased more than tenfold, [4] and as age is the biggest risk factor for dementia, many in the health care community now refer to the rising numbers of elderly as ominously portending an "epidemic" of dementia. (citizen.org)
  • Further analysis found that in addition to the above three risk factors, hypertension (OR=2.98, 95% CI: 1.16- 7.64), lacunar infarction (OR=2.39, 95% CI: 1.19- 4.81) also increased the risk of deep/mixed CMBs. (dovepress.com)
  • Lysophosphatidic acid and apolipoprotein A1 predict increased risk of developing World Trade Center-lung injury: a nested case-control study. (cdc.gov)
  • Diabetes or CKD stages 3/4 with one or more risk factors. (medscape.com)
  • Diabetes or CKD stages 3/4 with no other risk factors. (medscape.com)
  • The A-I and A-IV genes are transcribed from the same strand, while the A-1 and C-III genes are convergently transcribed. (nsjbio.com)
  • 3] In fact a quick BLAST search of Propionibacterium acnes genes for 16S ribosomal RNA (GenBank: AB097215.1) against M. tuberculosis shows an 88% identity within the first 100 hits. (j-alz.com)
  • Total RNA from tumors the expression of thousands of genes (3) to address complex questions was isolated using two successive rounds of Trizol. (lu.se)
  • Epsilon-3: People with the epsilon-3 type are neither protected nor more likely to develop the disease. (msdmanuals.com)
  • 2. Uncontrolled or newly diagnosed (=3 months since diagnosis) Type 2 diabetes mellitus as determined by the Principal Investigator. (who.int)
  • [ 3 ] (Jervis 1948) Further research has confirmed premature aging and clinical deterioration, and the presence of neuropathological changes in AD. (medscape.com)
  • Differential effects of apolipoprotein E isoforms on phosphorylation at specific sites on tau by glycogen synthase kinase-3 beta identified by nano-electrospray mass spectrometry. (ox.ac.uk)
  • Methods: Two hundred sixty-three cognitively normal participants with a family history of sporadic AD who underwent. (lu.se)
  • Methods: Two hundred sixty-three cognitively normal participants with a family history of sporadic AD who underwent resting-state and task-based functional MRI using encoding and retrieval tasks were included from the PREVENT-AD cohort. (lu.se)
  • Apolipoprotein A4's (APOA4's) functions on HDL in humans are not well understood. (jci.org)
  • Several therapies pertinent to the metabolic syndrome, such as PPAR (peroxisome-proliferator-activated receptor) agonists and statins, can regulate apoC-III transport in the metabolic syndrome. (portlandpress.com)