Proteins that bind to and transfer CHOLESTEROL ESTERS between LIPOPROTEINS such as LOW-DENSITY LIPOPROTEINS and HIGH-DENSITY LIPOPROTEINS.
Fatty acid esters of cholesterol which constitute about two-thirds of the cholesterol in the plasma. The accumulation of cholesterol esters in the arterial intima is a characteristic feature of atherosclerosis.
Conjugated protein-carbohydrate compounds including mucins, mucoid, and amyloid glycoproteins.
Cholesterol which is contained in or bound to high-density lipoproteins (HDL), including CHOLESTEROL ESTERS and free cholesterol.
Transport proteins that carry specific substances in the blood or across cell membranes.
Lipid-protein complexes involved in the transportation and metabolism of lipids in the body. They are spherical particles consisting of a hydrophobic core of TRIGLYCERIDES and CHOLESTEROL ESTERS surrounded by a layer of hydrophilic free CHOLESTEROL; PHOSPHOLIPIDS; and APOLIPOPROTEINS. Lipoproteins are classified by their varying buoyant density and sizes.
A ubiquitous family of proteins that transport PHOSPHOLIPIDS such as PHOSPHATIDYLINOSITOL and PHOSPHATIDYLCHOLINE between membranes. They play an important role in phospholipid metabolism during vesicular transport and SIGNAL TRANSDUCTION.
The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils.
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.
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.
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.
Cholesterol present in food, especially in animal products.
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 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)
Conditions with abnormally elevated levels of LIPOPROTEINS in the blood. They may be inherited, acquired, primary, or secondary. Hyperlipoproteinemias are classified according to the pattern of lipoproteins on electrophoresis or ultracentrifugation.
Substances used to lower plasma CHOLESTEROL levels.
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.
Cholesterol which is contained in or bound to very low density lipoproteins (VLDL). High circulating levels of VLDL cholesterol are found in HYPERLIPOPROTEINEMIA TYPE IIB. The cholesterol on the VLDL is eventually delivered by LOW-DENSITY LIPOPROTEINS to the tissues after the catabolism of VLDL to INTERMEDIATE-DENSITY LIPOPROTEINS, then to LDL.
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.
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 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.
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.
An enzyme that catalyzes the formation of cholesterol esters by the direct transfer of the fatty acid group from a fatty acyl CoA derivative. This enzyme has been found in the adrenal gland, gonads, liver, intestinal mucosa, and aorta of many mammalian species. EC 2.3.1.26.
An enzyme that catalyzes the hydrolysis of CHOLESTEROL ESTERS and some other sterol esters, to liberate cholesterol plus a fatty acid anion.
Physiological processes in biosynthesis (anabolism) and degradation (catabolism) of LIPIDS.
A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.
Lipids containing one or more phosphate groups, particularly those derived from either glycerol (phosphoglycerides see GLYCEROPHOSPHOLIPIDS) or sphingosine (SPHINGOLIPIDS). They are polar lipids that are of great importance for the structure and function of cell membranes and are the most abundant of membrane lipids, although not stored in large amounts in the system.
A condition with abnormally high levels of CHOLESTEROL in the blood. It is defined as a cholesterol value exceeding the 95th percentile for the population.
A highly dense subclass of the high-density lipoproteins, with particle sizes below 7 nm. They are also known as nascent HDL, composed of a few APOLIPOPROTEIN A-I molecules which are complexed with PHOSPHOLIPIDS. The lipid-poor pre-beta-HDL particles serve as progenitors of HDL3 and then HDL2 after absorption of free cholesterol from cell membranes, cholesterol esterification, and acquisition of apolipoproteins A-II, Cs, and E. Pre-beta-HDL initiate the reverse cholesterol transport process from cells to liver.
An enzyme of the hydrolase class that catalyzes the reaction of triacylglycerol and water to yield diacylglycerol and a fatty acid anion. It is produced by glands on the tongue and by the pancreas and initiates the digestion of dietary fats. (From Dorland, 27th ed) EC 3.1.1.3.
The movement of materials (including biochemical substances and drugs) through a biological system at the cellular level. The transport can be across cell membranes and epithelial layers. It also can occur within intracellular compartments and extracellular compartments.
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.
An enzyme of the hydrolase class that catalyzes the reaction of triacylglycerol and water to yield diacylglycerol and a fatty acid anion. The enzyme hydrolyzes triacylglycerols in chylomicrons, very-low-density lipoproteins, low-density lipoproteins, and diacylglycerols. It occurs on capillary endothelial surfaces, especially in mammary, muscle, and adipose tissue. Genetic deficiency of the enzyme causes familial hyperlipoproteinemia Type I. (Dorland, 27th ed) EC 3.1.1.34.
Conditions with excess LIPIDS in the blood.
A class of protein components which can be found in several lipoproteins including HIGH-DENSITY LIPOPROTEINS; VERY-LOW-DENSITY LIPOPROTEINS; and CHYLOMICRONS. Synthesized in most organs, Apo E is important in the global transport of lipids and cholesterol throughout the body. Apo E is also a ligand for LDL receptors (RECEPTORS, LDL) that mediates the binding, internalization, and catabolism of lipoprotein particles in cells. There are several allelic isoforms (such as E2, E3, and E4). Deficiency or defects in Apo E are causes of HYPERLIPOPROTEINEMIA TYPE III.
Derivatives of oxazolidin-2-one. They represent an important class of synthetic antibiotic agents.
Intermediate-density subclass of the high-density lipoproteins, with particle sizes between 7 to 8 nm. As the larger lighter HDL2 lipoprotein, HDL3 lipoprotein is lipid-rich.
An enzyme that catalyzes the oxidation of cholesterol in the presence of molecular oxygen to 4-cholesten-3-one and hydrogen peroxide. The enzyme is not specific for cholesterol, but will also oxidize other 3-hydroxysteroids. EC 1.1.3.6.
A condition of elevated levels of TRIGLYCERIDES in the blood.
The rate dynamics in chemical or physical systems.
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.
Substances that lower the levels of certain LIPIDS in the BLOOD. They are used to treat HYPERLIPIDEMIAS.
The process of converting an acid into an alkyl or aryl derivative. Most frequently the process consists of the reaction of an acid with an alcohol in the presence of a trace of mineral acid as catalyst or the reaction of an acyl chloride with an alcohol. Esterification can also be accomplished by enzymatic processes.
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.
Fats present in food, especially in animal products such as meat, meat products, butter, ghee. They are present in lower amounts in nuts, seeds, and avocados.
Errors in the metabolism of LIPIDS resulting from inborn genetic MUTATIONS that are heritable.
Abnormalities in the serum levels of LIPIDS, including overproduction or deficiency. Abnormal serum lipid profiles may include high total CHOLESTEROL, high TRIGLYCERIDES, low HIGH DENSITY LIPOPROTEIN CHOLESTEROL, and elevated LOW DENSITY LIPOPROTEIN CHOLESTEROL.
7-carbon saturated monocarboxylic acids.
A family of scavenger receptors that are predominately localized to CAVEOLAE of the PLASMA MEMBRANE and bind HIGH DENSITY LIPOPROTEINS.
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
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.
Organic, monobasic acids derived from hydrocarbons by the equivalent of oxidation of a methyl group to an alcohol, aldehyde, and then acid. Fatty acids are saturated and unsaturated (FATTY ACIDS, UNSATURATED). (Grant & Hackh's Chemical Dictionary, 5th ed)
A superfamily of large integral ATP-binding cassette membrane proteins whose expression pattern is consistent with a role in lipid (cholesterol) efflux. It is implicated in TANGIER DISEASE characterized by accumulation of cholesteryl ester in various tissues.
Relating to the size of solids.
Compounds containing the -SH radical.

Lipid transfer inhibitor protein defines the participation of lipoproteins in lipid transfer reactions: CETP has no preference for cholesteryl esters in HDL versus LDL. (1/740)

Cholesteryl ester transfer protein (CETP) catalyzes the net transfer of cholesteryl ester (CE) between lipoproteins in exchange for triglyceride (heteroexchange). It is generally held that CETP primarily associates with HDL and preferentially transfers lipids from this lipoprotein fraction. This is illustrated in normal plasma where HDL is the primary donor of the CE transferred to VLDL by CETP. However, in plasma deficient in lipid transfer inhibitor protein (LTIP) activity, HDL and LDL are equivalent donors of CE to VLDL (Arterioscler Thromb Vasc Biol. 1997;17:1716-1724). Thus, we have hypothesized that the preferential transfer of CE from HDL in normal plasma is a consequence of LTIP activity and not caused by a preferential CETP-HDL interaction. We have tested this hypothesis in lipid mass transfer assays with partially purified CETP and LTIP, and isolated lipoproteins. With a physiological mixture of lipoproteins, the preference ratio (PR, ratio of CE mass transferred from a lipoprotein to VLDL versus its CE content) for HDL and LDL in the presence of CETP alone was approximately 1 (ie, no preference). Fourfold variations in the LDL/HDL ratio or in the levels of HDL in the assay did not result in significant preferential transfer from any lipoprotein. On addition of LTIP, the PR for HDL was increased up to 2-fold and that for LDL decreased in a concentration-dependent manner. Under all conditions where LDL and HDL levels were varied, LTIP consistently resulted in a PR >1 for CE transfer from HDL. Short-term experiments with radiolabeled lipoproteins and either partially purified or homogenous CETP confirmed these observations and further demonstrated that CETP has a strong predilection to mediate homoexchange (bidirectional transfer of the same lipid) rather than heteroexchange (CE for TG); LTIP had no effect on the selection of CE or TG by CETP or its mechanism of action. We conclude, in contrast to current opinion, that CETP has no preference for CE in HDL versus LDL, suggesting that the previously reported stable binding of CETP to HDL does not result in selective transfer from this lipoprotein. These data suggest that LTIP is responsible for the preferential transfer of CE from HDL that occurs in plasma. CETP and LTIP cooperatively determine the extent of CETP-mediated remodeling of individual lipoprotein fractions.  (+info)

Increased atherosclerosis in ApoE and LDL receptor gene knock-out mice as a result of human cholesteryl ester transfer protein transgene expression. (2/740)

The plasma cholesteryl ester transfer protein (CETP) plays a major role in the catabolism of HDL cholesteryl ester (CE). CETP transgenic mice have decreased HDL cholesterol levels and have been reported to have either increased or decreased early atherosclerotic lesions. To evaluate the impact of CETP expression on more advanced forms of atherosclerosis, we have cross-bred the human CETP transgene into the apoE knock-out (apoE0) background with and without concomitant expression of the human apo A-I transgene. In this model the CETP transgene is induced to produce plasma CETP levels 5 to 10 times normal human levels. CETP expression resulted in moderately reduced HDL cholesterol (34%) in apoE0 mice and markedly reduced HDL cholesterol (76%) in apoE0/apoA1 transgenic mice. After injection of radiolabeled HDL CE, the CETP transgene significantly delayed the clearance of CE radioactivity from plasma in apoE0 mice, but accelerated the clearance in apoE0/apoA1 transgenic mice. ApoE0/CETP mice displayed an increase in mean atherosclerotic lesion area on the chow diet (approximately 2-fold after 2 to 4 months, and 1.4- to 1.6-fold after 7 months) compared with apoE0 mice (P<0.02). At 7 months apoA1 transgene expression resulted in a 3-fold reduction in mean lesion area in apoE0 mice (P<0.001). In the apoE0/apoA1 background, CETP produced an insignificant 1.3- to 1.7-fold increase in lesion area. In further studies the CETP transgene was bred onto the LDL receptor knock-out background (LDLR0). After 3 months on the Western diet, the mean lesion area was increased 1.8-fold (P<0.01) in LDLR0/CETP mice, compared with LDLR0 mice. These studies indicate that CETP expression leads to a moderate increase in atherosclerosis in apoE0 and LDLR0 mice, and suggest a proatherogenic effect of CETP activity in metabolic settings in which clearance of remnants or LDL is severely impaired. However, apoA1 overexpression has more dramatic protective effects on atherosclerosis in apoE0 mice, which are not significantly reversed by concomitant expression of CETP.  (+info)

A cholesteryl ester transfer protein gene mutation and vascular disease in dialysis patients. (3/740)

Among patients undergoing maintenance hemodialysis, a decreased high-density lipoprotein cholesterol (HDL-C) concentration is among the most common abnormalities of lipid metabolism and apparently is an independent risk factor for vascular disease. A common missense mutation of cholesteryl ester transfer protein gene, D442G (Asp 442 to Gly), increases HDL-C levels through the reduced activity of cholesteryl ester transfer from HDL to VLDL, but the mutation also may lead to reduced activity of reverse cholesterol transport. To investigate the effect of the D442G polymorphism on atherosclerotic complications in dialysis patients, the genotype and allele frequency of the polymorphism were determined in 414 unselected dialysis patients and 220 control subjects, and postprandial serum lipid levels were measured in the dialysis patients. A similar genotype distribution was found between hemodialysis patients and healthy control subjects, and in dialysis patients with and without vascular disease. Serum levels of total cholesterol and HDL-C did not differ between patients with and without the mutation and in patients with and without vascular disease. However, patients with sub-median HDL-C levels (<45 mg/dl) had an independent odds ratio of 1.8 for vascular disease (95% confidence interval, 1.04 to 3.2; P < 0.05). In this low-HDL-C subgroup, patients with the D442G mutation had a significantly higher prevalence of vascular disease than those with no mutation (54.5% versus 24.4%; P < 0.05), and an independent odds ratio of 4.9 (95% confidence interval, 1.05 to 22.65; P < 0.05). In conclusion, the D442G mutation is an independent risk factor for atherosclerotic complications in dialysis patients with HDL-C levels below 45 mg/dl.  (+info)

Structure-specific inhibition of cholesteryl ester transfer protein by azaphilones. (4/740)

The effect of thirteen different fungal azaphilones, which have a common 6-iso-chromane-like ring, was tested on cholesteryl ester transfer protein (CETP) activity in vitro. Chaetoviridin B showed the most potent inhibitory activity with an IC50 value of < 6.2 microM, followed by sclerotiorin with an IC50 value of 19.4 microM. Rotiorin, chaetoviridin A and rubrorotiorin had moderate inhibitory activity (IC50 ; 30 approximately 40 microM), but others showed very weak or no inhibitory activity. The relationship between the structures and their inhibitory activity indicated that the presence of an electrophilic ketone(s) and/or enone(s) at both C-6 and C-8 positions in the isochromane-like ring is essential for eliciting CETP inhibitory activity. The transfer activity of both CE and TG was inhibited by sclerotiorin to approximately the same extent (IC50: 14.4 and 10.3 microM, respectively). A model of the reaction suggested that sclerotiorin reacts with a primary amine of amino acids such as lysine in the protein to form a covalent bond.  (+info)

Estrogen-mediated increases in LDL cholesterol and foam cell-containing lesions in human ApoB100xCETP transgenic mice. (5/740)

The murine double transgenic mouse expressing both human apoB100 and cholesteryl ester transfer protein (CETP), has been used as a model to understand the effects mediated by various therapeutic modalities on serum lipoproteins and on atherosclerotic lesion progression. In the present study the effects of estrogen therapy on serum lipoproteins were investigated after mice were placed on an atherosclerotic diet. The daily oral administration of 20 or 100 microg/kg of 17 alpha-ethinyl estradiol resulted in a significant, dose-dependent increase in LDL cholesterol over a 20-week regimen. These differences were apparent by 6 weeks and further increases were observed through the 20-week period. Although CETP did result in a reduction in total HDL, estrogen did not have any impact on the amount of CETP activity associated with the HDL particles. The significant increase in LDL cholesterol was associated with increases in the amount of apoB100 and B48 and apoE-containing particles. Hepatic apoB message levels, however, were not different between the experimental groups. Although the extent of atherosclerotic lesions was modest, <0.5% of the aortic surface area in the vehicle group, the high-dose estrogen group, showed an increase in lesion area consistent with the elevation in LDL cholesterol. These lesions, primarily restricted to the aortic root and aortic semilunar valves, were more intensely stained with Oil Red O in the high-dose estrogen group when compared with the vehicle controls.  (+info)

Wiedendiol-A inhibits cholesteryl ester binding to its transfer protein. (6/740)

AIM: To study the wiedendiol-A (W-A) inhibition mechanism of plasma cholesteryl ester (CE) transfer protein (CETP) on the transfer of CE. METHODS: Using gel filtration method. RESULTS: W-A at 30 mumol.L-1 inhibited association of CE with CETP by 76% and CETP transfer activity by 81%. In addition, W-A enhanced binding of TP2, a monoclonal antibody with a CETP C-terminal epitope which is involved in CE binding, to CETP, suggesting a W-A-induced conformational change at the epitope for increased TP2 binding. When CETP activity was measured by varying high-density lipoproteins (HDL) concentration, the apparent Vmax of CE transfer was inhibited by 74% and 83% in the presence of W-A at 14 and 25 mumol.L-1, respectively, while the apparent K(m) of HDL for CETP did not change. CONCLUSION: W-A action is mediated through interaction between W-A and CETP, but not through those between W-A and lipoproteins.  (+info)

Remodeling of HDL by CETP in vivo and by CETP and hepatic lipase in vitro results in enhanced uptake of HDL CE by cells expressing scavenger receptor B-I. (7/740)

The transport of HDL cholesteryl esters (CE) from plasma to the liver involves a direct uptake pathway, mediated by hepatic scavenger receptor B-I (SR-BI), and an indirect pathway, involving the exchange of HDL CE for triglycerides (TG) of TG-rich lipoproteins by cholesteryl ester transfer protein (CETP). We carried out HDL CE turnover studies in mice expressing human CETP and/or human lecithin:cholesterol acyltransferase (LCAT) transgenes on a background of human apoA-I expression. The fractional clearance of HDL CE by the liver was delayed by LCAT transgene, while the CETP transgene increased it. However, there was no incremental transfer of HDL CE radioactivity to the TG-rich lipoprotein fraction in mice expressing CETP, suggesting increased direct removal of HDL CE in the liver. To evaluate the possibility that this might be mediated by SR-BI, HDL isolated from plasma of the different groups of transgenic mice was incubated with SR-BI transfected or control CHO cells. HDL isolated from mice expressing CETP showed a 2- to 4-fold increase in SR-BI-mediated HDL CE uptake, compared to HDL from mice lacking CETP. The addition of pure CETP to HDL in cell culture did not lead to increased selective uptake of HDL CE by cells. However, when human HDL was enriched with TG by incubation with TG-rich lipoproteins in the presence of CETP, then treated with hepatic lipase, there was a significant enhancement of HDL CE uptake. Thus, the remodeling of human HDL by CETP, involving CE;-TG interchange, followed by the action of hepatic lipase (HL), leads to the enhanced uptake of HDL CE by cellular SR-BI. These observations suggest that in animals such as humans in which both the selective uptake and CETP pathways are active, the two pathways could operate in a synergistic fashion to enhance reverse cholesterol transport.  (+info)

Characterization of a cholesterol response element (CRE) in the promoter of the cholesteryl ester transfer protein gene: functional role of the transcription factors SREBP-1a, -2, and YY1. (8/740)

Cholesteryl ester transfer protein (CETP) is expressed in human adipocytes, where it acts to promote selective uptake of HDL-CE (Benoist, F., M. McDonnell, P. Lau, R. Milne, and R. McPherson. 1997. J. Biol. Chem. 272: 23572;-23577). In contrast to other major sterol-responsive genes such as 3-hydroxy-3-methylglutaryl coenzyme A reductase CETP expression is up-regulated rather than down-regulated in response to cholesterol. To define elements involved in cholesterol-mediated up-regulation of CETP gene expression, deletion derivatives of the CETP promoter were cloned into a luciferase reporter construct and transfected into the human liposarcoma cell line SW872, cultured in the presence or absence of lipoproteins. A fragment associated with a positive cholesterol response was identified between nucleotides -361 and -138 (relative to the initiation site of transcription) of the promoter. This region contains a tandem repeat of a sequence known to mediate sterol dependent regulation of the hamster HMG-CoA reductase gene. We have putatively denoted this region, the cholesterol response element (CRE). Using gel mobility shift assays we demonstrate that both YY1 and SREBP-1 interact with the CRE of CETP. Furthermore, in transient co-transfection experiments, both YY1 and SREBP-1a were found to trans-activate, in a dose-dependent manner, the luciferase activity of constructs harboring the CRE. We also demonstrate that SREBP-2, is able to trans-activate a luciferase construct harboring the CRE although much less effectively as compared to SREBP-1. Finally, functional analysis of the CRE confirms its regulatory role in modulating CETP gene expression through its interaction with YY1 and SREBP-1a.  (+info)

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

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

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

There are several types of hypercholesterolemia, including:

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

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

There are several types of hyperlipidemia, including:

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

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

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

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

There are several causes of hypertriglyceridemia, including:

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

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

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

There are several types of arteriosclerosis, including:

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

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

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

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

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

There are several types of dyslipidemias, including:

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

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

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

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

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

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

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

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

Cholesterol+ester+transfer+proteins at the US National Library of Medicine Medical Subject Headings (MeSH) (Articles with short ... Cholesteryl ester transfer protein (CETP), also called plasma lipid transfer protein, is a plasma protein that facilitates the ... "Concerted actions of cholesteryl ester transfer protein and phospholipid transfer protein in type 2 diabetes: effects of ... "Effects of an inhibitor of cholesteryl ester transfer protein on HDL cholesterol". The New England Journal of Medicine. 350 (15 ...
The cholesterol ester transfer protein(CETP) helps the transfer of cholesterol esters from lipoproteins to other lipoproteins ... There is a very common pattern of two different cholesterol ester transfer protein gene mutations (D442G, 5.1%; intron 14G:A, ... there is increased coronary heart disease in Japanese-American men with a mutation in the cholesterol ester transfer protein ... It plays a fundamental role in the reverse transport of cholesterol to the liver, which is why a mutation in this can lead to ...
... a novel cholesteryl ester transfer protein inhibitor, in individuals with below-average high-density lipoprotein cholesterol ... by inhibiting cholesterylester transfer protein (CETP), which normally transfers cholesterol from HDL cholesterol to very low ... a novel cholesteryl ester transfer protein inhibitor, in individuals with below-average high-density lipoprotein cholesterol ... "Effects of an inhibitor of cholesteryl ester transfer protein on HDL cholesterol". New England Journal of Medicine. 350 (15): ...
"Cholesterol ester transfer protein inhibition by TA-8995 in patients with mild dyslipidaemia (TULIP): A randomised, double- ... CETP inhibitors inhibit cholesterylester transfer protein (CETP), which normally transfers cholesterol from HDL cholesterol to ... Drugs in this class substantially increase HDL cholesterol, lower LDL cholesterol, and enhance reverse cholesterol transport. ... A CETP inhibitor is a member of a class of drugs that inhibit cholesterylester transfer protein (CETP). They are intended to ...
... and selective inhibitor of cholesteryl ester transfer protein that elevates HDL cholesterol without inducing aldosterone or ... "Assessment of Clinical Effects of Cholesteryl Ester Transfer Protein Inhibition With Evacetrapib in Patients at a High Risk for ... that inhibits cholesterylester transfer protein (CETP inhibitor). CETP collects triglycerides from very low-density ... "Study of Evacetrapib (LY2484595) in Participants With High Cholesterol (ACCENTUATE)". Kolata, Gina (3 April 2016). "Dashing ...
... transfer protein Cholesteryl ester storage disease Acyl CoA cholesteryl acyltransferase (ACAT) Lecithin- ... Cholesteryl ester, a dietary lipid, is an ester of cholesterol. The ester bond is formed between the carboxylate group of a ... Cholesteryl ester is found in human brains as lipid droplets which store and transport cholesterol. Increased levels of ... Cholesterol+Esters at the US National Library of Medicine Medical Subject Headings (MeSH) Phillips, Gabrielle R.; Hancock, ...
Anacetrapib is a cholesteryl ester transfer protein inhibitor that raises high-density lipoprotein (HDL) cholesterol and ... February 2009). "Efficacy and safety of the cholesteryl ester transfer protein inhibitor anacetrapib as monotherapy and ... One reason for this is that elastin, the principal load-bearing protein present in the wall of the aorta, is reduced in the ... In short, raising HDL cholesterol is beneficial because it induces programmed cell death. The walls of a failing aorta are ...
... of high density lipoprotein subfractions in lipid transfer reactions mediated by cholesterol ester transfer protein (CETP)". J ... This protein forms complexes with lipoproteins and may be involved in transport and/or esterification of cholesterol. GRCh38: ... 2008). "Lipid transfer inhibitor protein (apolipoprotein F) concentration in normolipidemic and hyperlipidemic subjects". J. ... Wang X, Driscoll DM, Morton RE (1999). "Molecular cloning and expression of lipid transfer inhibitor protein reveals its ...
StAR-related lipid transfer protein 4 (STARD4) is a soluble protein involved in cholesterol transport. It can transfer up to 7 ... "Intracellular cholesterol transporter StarD4 binds free cholesterol and increases cholesteryl ester formation". Journal of ... "The cholesterol-regulated StarD4 gene encodes a StAR-related lipid transfer protein with two closely related homologues, StarD5 ... "Differential gene regulation of StarD4 and StarD5 cholesterol transfer proteins. Activation of StarD4 by sterol regulatory ...
The cholesteryl esters can be transferred, with the help of CETP (cholesterylester transfer protein) in exchange for ... The cholesterol is converted to cholesteryl esters by the enzyme LCAT (lecithin-cholesterol acyltransferase). ... Cholesterol from non-hepatic peripheral tissues is transferred to HDL by the ABCA1 (ATP-binding cassette transporter). ... Reverse cholesterol transport is a multi-step process resulting in the net movement of cholesterol from peripheral tissues back ...
... cholesterol acyltransferase and cholesteryl ester transfer protein in abnormal high density lipoprotein metabolism in insulin ... that converts free cholesterol into cholesteryl ester (a more hydrophobic form of cholesterol), which is then sequestered into ... Lecithin-cholesterol acyltransferase (Thr123----Ile) and lecithin-cholesterol acyltransferase (Thr347----Met)". J. Clin. Invest ... 1992). "Interaction of rat lecithin-cholesterol acyltransferase with rat apolipoprotein A-I and with lecithin-cholesterol ...
Ezetimibe is a selective inhibitor of dietary cholesterol absorption. Lomitapide is a microsomal triglyceride transfer protein ... Flaxseed oil Investigational classes of hypolipidemic agents: CETP inhibitors (cholesteryl ester transfer protein), 1 candidate ... Similar to ezetimibe, phytosterols reduce the absorption of cholesterol in the gut, so they are most effective when consumed ... Lecithin has been shown to effectively decrease cholesterol concentration by 33%, lower LDL by 38% and increase HDL by 46%. ...
HPS3/TIMI 55 REVEAL assessed the effect of cholesterol ester transfer protein (CETP) inhibition with anacetrapib 100 mg versus ... PROMPT-TIMI 35 evaluated novel protein markers of ischemia using proteomic testing in a prospective cohort of patients with ... VESALIUS-CV will assess the effect of lowering low-density lipoprotein cholesterol (LDL-C) with evolocumab on major ... FOURIER (TIMI 59)/EBBINGHAUS - FOURIER assessed the Impact of additional LDL-cholesterol reduction on major cardiovascular ...
Its main function is inhibition of cholesteryl ester transfer protein (CETP), probably by altering the electric charge of HDL ... cholesterol with an important role in the exchange of esterified cholesterol between lipoproteins and in removal of cholesterol ... When proteins rich in triglycerides like chylomicrons and VLDL are broken down, this apoprotein is transferred again to HDL. It ... C-I accounts for the ability of plasma high density lipoproteins to inhibit the cholesteryl ester transfer protein activity". ...
Other medications that are in various stages of development include thyromimetics, cholesterol-ester-transfer protein (CETP ... This size variation at the gene level is expressed on the protein level as well, resulting in apo(a) proteins with 10 to more ... Apo(a) proteins vary in size due to a size polymorphism [KIV-2 VNTR], which is caused by a variable number of kringle IV ... Lp(a) is not fully synthesised until the precursor protein is released from the cell, so the slower rate of production for the ...
... which is mediated by cholesteryl ester transfer protein (CETP).This protein exchanges triglycerides of VLDL against cholesteryl ... "National Reference System for Cholesterol - Cholesterol Reference Method Laboratory Network - HDL Cholesterol Certification ... converts the free cholesterol into cholesteryl ester (a more hydrophobic form of cholesterol), which is then sequestered into ... "The target of regulating the ATP-binding cassette A1 protein (ABCA1): promoting ABCA1-mediated cholesterol efflux in different ...
It also inhibits HDL-C hepatic uptake by suppressing production of the cholesterol ester transfer protein (CETP) gene. It ... Niacin reduces synthesis of low-density lipoprotein cholesterol (LDL-C), very low-density lipoprotein cholesterol (VLDL-C), ... participating in many hydrogen transfer processes. NAD is important in catabolism of fat, carbohydrate, protein, and alcohol, ... and raise blood high density lipoprotein cholesterol (HDL-C, often referred to as "good" cholesterol). There are two forms: ...
Huang Z; Inazu A; Nohara A; Higashikata T; Mabuchi H (December 2002). "Cholesteryl ester transfer protein inhibitor (JTT-705) ... The drug was aimed at raising the blood levels of HDL cholesterol. Prevailing observations indicate that high HDL levels ... Changes in inflammation and cholesterol efflux capacity may in part explain the benefits associated with the protective ... "Roche Drops After Halting Cholesterol Drug Development". Bloomberg. Michelle Fay Cortez (November 5, 2012), "Roche's Good ...
An Introduction to Biological Membranes (Second ed.). Abbey M, Nestel PJ (1994). "Plasma cholesteryl ester transfer protein ... Elaidic acid increases plasma cholesterylester transfer protein (CETP) activity which lowers HDL cholesterol. Oleic acid Tardy ... Its salts and esters are called elaidates. Elaidic acid is an unsaturated trans fatty acid, with code C18:1 trans-9. This ...
The protein, as a component of HDL particles, enables efflux of fat molecules by accepting fats from within cells (including ... Paradoxically, carriers of this mutation have very low HDL-C (HDL-Cholesterol) levels, but no increase in the risk of heart ... Chylomicrons secreted from the intestinal enterocyte also contain apo-AI, but it is quickly transferred to HDL in the ... which is responsible for the formation of most plasma cholesteryl esters. Apolipoprotein AI has also been isolated as a ...
... is an intracellular protein located in the endoplasmic reticulum that forms cholesteryl esters from cholesterol. Sterol O- ... The role of this enzyme is to transfer fatty acyl groups from one molecule to another. ACAT is an important enzyme in bile acid ... cholesterol acyltransferase. It gives the cholesterol ester cholesterol oleate. from Sigrid Hahn; Hans-Ulrich Klör (2001). ... cholesterol ester Thus, the two substrates of this enzyme are acyl-CoA and cholesterol, whereas its two products are CoA and ...
... transfers cholesteryl esters to the VLDL in exchange for phospholipids and triglycerides via cholesterylester transfer protein ... Very-low-density lipoproteins transport endogenous triglycerides, phospholipids, cholesterol, and cholesteryl esters. It ... cholesterol, cholesteryl esters, and triglycerides. As it circulates in blood, it picks up apolipoprotein C-II (apoC-II) and ... VLDL now meets back up with HDL where apoC-II is transferred back to HDL (but keeps apoE). HDL also ...
Fielding PE, Fielding CJ (June 1980). "A cholesteryl ester transfer complex in human plasma". Proceedings of the National ... "Site-specific detection and structural characterization of the glycosylation of human plasma proteins lecithin:cholesterol ... It has a high degree of homology to plasma retinol-binding protein and other members of the alpha 2 microglobulin protein ... Protein Engineering. 10 (6): 621-5. doi:10.1093/protein/10.6.621. PMID 9278274. Zeng C, Spielman AI, Vowels BR, Leyden JJ, ...
... which catalyzes fatty acid transfer between phosphatidylcholine and cholesterol. Pancreatic lipase, also known as pancreatic ... Protein Pept. Sci. 1 (1): 91-103. doi:10.2174/1389203003381487. PMID 12369922. Ranaldi S, Belle V, Woudstra M, Rodriguez J, ... Triglyceride lipases (EC 3.1.1.3) are a family of lipolytic enzymes that hydrolyse ester linkages of triglycerides. Lipases are ... Such a region is also present in lipases of prokaryotic origin and in lecithin-cholesterol acyltransferase (EC 2.3.1.43) (LCAT ...
The triglycerides are rebuilt in the enterocytes from their fragments and packaged together with cholesterol and proteins to ... cis and trans-fat-rich meals showed that cholesteryl ester transfer (CET) was 28% higher after the trans meal than after the ... cholesterol) or low levels of high-density lipoprotein (HDL, "good" cholesterol). These parameters in turn are believed to be ... "bad cholesterol"), lowering levels of high-density lipoprotein (HDL, often termed "good cholesterol"), increasing triglycerides ...
Proteins are made from amino acids that have been activated by attachment to a transfer RNA molecule through an ester bond. ... M. tuberculosis can also grow on the lipid cholesterol as a sole source of carbon, and genes involved in the cholesterol-use ... Proteins are made of amino acids arranged in a linear chain joined by peptide bonds. Many proteins are enzymes that catalyze ... The polysaccharides produced can have structural or metabolic functions themselves, or be transferred to lipids and proteins by ...
Their 2002 Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids ... and cholesteryl ester transfer". The American Journal of Clinical Nutrition. 77 (5): 1119-24. doi:10.1093/ajcn/77.5.1119. PMID ... cis and trans fat rich meals showed that cholesteryl ester transfer (CET) was 28% higher after the trans meal than after the ... Cholesterol, Protein, and Amino Acids (Macronutrients). National Academies Press. pp. i. Archived from the original on 18 ...
... s containing a sulfuric ester (sulfate) group, known as sulfatides, also occur in the myelin sheath of nerves. These ... The biosynthesis of monoglycosylceramides requires a direct transfer of the carbohydrate moiety from a sugar-nucleotide, such ... Monoglycosylceramides in conjunction with cholesterol are prevalent in the lipid-raft micro domain, which are important sites ... in the binding of proteins, and enzyme-receptor interactions. Degradation of glycosphingolipids occurs in the lysosome, which ...
... complexes for signal transduction or signaling Managing protein and lipid interactions Functioning as a substrate Transferring ... of cholesterol. At approximately 8 mol% of cholesterol the start of the liquid-disordered phase begins. This same relationship ... Phospholipids consist of two non-polar hydrocarbon chains with ester or ether bonds to the phosphate group which is also linked ... Initially all the model membranes were organized in a liquid order phase but as the addition of cholesterol increase a liquid- ...
His group identified Tangier disease (HDL deficiency) and cholesteryl ester storage disease, two inborn errors of cholesterol ... He played a prime role in the identification of several apolipoproteins (proteins that characterise the nature of a blood lipid ... but completed his studies at the University of Michigan after being transferred there by the army. During a cycling trip in the ... Subsequently he spent a year in the laboratory of Ivan Frantz, a cholesterol biochemist, at Massachusetts General Hospital. In ...
2007). "Regulation of secretory transport by protein kinase D-mediated phosphorylation of the ceramide transfer protein". J. ... Palmitic acid esters of hydroxy-stearic acids (PAHSAs) are among the most bioactive members able to activate G-protein coupled ... receptors This large and diverse class of steroids are biosynthesized from isoprenoids and structurally resemble cholesterol. ... Sph is also known to interact with protein targets such as the protein kinase H homologue (PKH) and the yeast protein kinase ( ...
... and zinc transporter protein, with an IC50 of 66.3 nM (relative to Kd = 17.9 nM for testosterone). This protein appears to be ... CYP27A1 converts cholesterol into 27-hydroxycholesterol, an oxysterol that has multiple biological functions including direct, ... Antigonadotropic agents like high-dose CPA, high-dose androgens (e.g., testosterone esters), and GnRH antagonists (though ... due to transfer through the hepatic portal system prior to reaching circulation). In men receiving 150 mg/day bicalutamide, ...
Allosteric inhibition and activation by Protein-protein interactions (PPI). Indeed, some proteins interact with and regulate ... which is the rate limiting step controlling the synthesis of cholesterol. Cholesterol can be used as is, as a structural ... The oxaloacetate is returned to mitochondrion as malate (and then back into oxaloacetate to transfer more acetyl-CoA out of the ... Harden and Young deduced that this process produced organic phosphate esters, and further experiments allowed them to extract ...
New research has found that protein CoAlation plays an important role in regulation of the oxidative stress response. Protein ... Acetyl-CoA fatty acyl-CoA (activated form of all fatty acids; only the CoA esters are substrates for important reactions such ... Lipmann initially intended to study acetyl transfer in animals, and from these experiments he noticed a unique factor that was ... as mono-, di-, and triacylglycerol synthesis, carnitine palmitoyl transferase, and cholesterol esterification) Propionyl-CoA ...
... fewer fat molecules with same protein transport shell), containing a higher proportion of cholesterol esters.[citation needed] ... Lipoproteins transfer lipids (fats) around the body in the extracellular fluid, making fats available to body cells for ... where H is HDL cholesterol, L is LDL cholesterol, C is total cholesterol, T are triglycerides, and k is 0.20 if the quantities ... LDL is then shipped to the lysosome, where cholesterol esters in the LDL are hydrolysed. LDL receptors are typically returned ...
... a Gi/o-coupled G protein-coupled receptor. Butyric acid is present as its octyl ester in parsnip (Pastinaca sativa) and in the ... Tsuji A (2005). "Small molecular drug transfer across the blood-brain barrier via carrier-mediated transport systems". NeuroRx ... McGee DJ, George AE, Trainor EA, Horton KE, Hildebrandt E, Testerman TL (2011). "Cholesterol enhances Helicobacter pylori ... Salts and esters of butyric acid are known as butyrates or butanoates. The acid does not occur widely in nature, but its esters ...
"Assessing Cholesterol Storage in Live Cells and C. elegans by Stimulated Raman Scattering Imaging of Phenyl-Diyne Cholesterol ... In CRH, CRS images are obtained at lipid and protein images and after some image processing, an image similar to H&E staining ... In SRS, the intensity of the energy transfer from the pump wavelength to the Stokes laser wavelength is measured as a signal. ... Ester; Suzuki-Uematsu, Satomi; Suzuki, Naoki (2016). "Monitoring peripheral nerve degeneration in ALS by label-free stimulated ...
DesK-P will transfer its phosphoryl group to DesR. Two DesR-P proteins will dimerize and bind to the DNA promoters of the des ... The glycolytic pathway also provides the glycerol with which three fatty acids can combine (by means of ester bonds) to form ... Thus NADPH is also required for the synthesis of cholesterol from acetyl-CoA; while NADH is generated during glycolysis.) The ... Another pathway uses two proteins, DesC and DesB, together to act as a Δ9-desaturase, which inserts a double bond into a ...
"Evaluation of phospholipid transfer protein and cholesteryl ester transfer protein as contributors to the generation of pre ... this protein may be involved in cholesterol metabolism. At least two transcript variants encoding different isoforms have been ... "Concerted actions of cholesteryl ester transfer protein and phospholipid transfer protein in type 2 diabetes: effects of ... Phospholipid transfer protein is a protein that in humans is encoded by the PLTP gene. The protein encoded by this gene is one ...
Tangier disease is characterized by very low blood plasma levels of HDL cholesterol, accumulation of cholesteryl esters in ... The enzyme cytochrome c oxidase, also known as Complex IV, is a large transmembrane protein complex found in mitochondria and ... diphosphatidylglycerol synthase catalyses a transfer of the phosphatidyl moiety of one phosphatidylglycerol to the free 3'- ... Cholesterol translocation from outer to the inner mitochondrial membrane Activates mitochondrial cholesterol side-chain ...
... cholesterol and animal protein, and higher levels of carbohydrates, fibre, magnesium, potassium, folate, vitamins C and E, and ... Choline is a nutrient that helps transfer signals between nerve cells and is involved in liver function. It is highest in dairy ... retinyl esters, tocopherols and selected carotenoids in twelve captive wild felid species at four zoos". The Journal of ... "Vitamin D is Synthesized From Cholesterol and Found in Cholesterol-Rich Foods". Cholesterol and Health. Archived from the ...
Also, J-protein (J20) and heat shock protein 70 (Hsp70) chaperones are thought to be involved in post-transcriptional ... Carotenoids can transfer excitation energy in one of two ways: 1) singlet-singlet energy transfer from carotenoid to ... al Acids and acid esters Torularhodin 3',4'-Didehydro-β,γ-caroten-16'-oic acid Torularhodin methyl ester Methyl 3',4'-didehydro ... the production of cholesterol starts by creating IPP and DMAPP using the MVA. For carotenoid production plants use MEP to ...
SCD-1 knockout mice did not increase de novo lipogenesis but created an abundance of cholesterol esters. SCD1 function has also ... Oshino N, Imai Y, Sato R (1966). "Electron-transfer mechanism associated with fatty acid desaturation catalyzed by liver ... Protein Science. 14 (3): 812-822. doi:10.1110/ps.04951405. ISSN 0961-8368. PMC 2279270. PMID 15722453. Hulver MW, Berggren JR, ... Oleate and palmitoleate are major components of membrane phospholipids, cholesterol esters and alkyl-diacylglycerol. In humans ...
Lipid anchored protein Remnant cholesterol Reverse cholesterol transport Vertical Auto Profile Gofman JW, Jones HB, Lindgren FT ... They transfer it over into the blood stream. In the hepatocytes, triacylglycerols and cholesteryl esters are assembled with ... The external shell also contains phospholipids and cholesterol. All cells use and rely on fats and cholesterol as building ... These are subdivided by density or by the protein contents/ proteins they carry. While the research is currently ongoing, ...
Protein Atlas, Protein Atlas. "Tissue expression of LPL - Summary - The Human Protein Atlas". www.proteinatlas.org. The Human ... "Angptl4 upregulates cholesterol synthesis in liver via inhibition of LPL- and HL-dependent hepatic cholesterol uptake". ... "Identification of a lipoprotein lipase cofactor-binding site by chemical cross-linking and transfer of apolipoprotein C-II- ... "Lipoprotein lipase mediates an increase in the selective uptake of high density lipoprotein-associated cholesteryl esters by ...
They can be attached to protein to specific functional groups, such as - amino groups (active ester, carboxylate, ... The absorbed wavelengths, energy transfer efficiency, and time before emission depend on both the fluorophore structure and its ... "Hydroxy-terminated conjugated polymer nanoparticles have near-unity bright fraction and reveal cholesterol-dependence of IGF1R ... Fluorescent proteins GFP (green), YFP (yellow) and RFP (red) can be attached to other specific proteins to form a fusion ...
A methyl ALA ester (Metvix) is now available for basal cell carcinoma and other skin lesions. Benzyl (Benvix) and hexyl ester ( ... Such interactions may allow electron-transfer reactions to take place via the short-lived excited singlet state and lead to the ... ROS initiate reactions with many biomolecules, including amino acid residues in proteins, such as tryptophan; unsaturated ... lipids like cholesterol and nucleic acid bases, particularly guanosine and guanine derivatives, with the latter base more ...
... play important roles in reverse cholesterol transport in humans. CETP transfers cholesteryl ester (CE) from high-density ... Cholesteryl ester transfer protein (CETP) and apolipoprotein E (apo E) ... Plasma concentrations of cholesteryl ester transfer protein in hyperlipoproteinemia. Relation to cholesteryl ester transfer ... Role of cholesteryl ester transfer protein in reverse cholesterol transport R McPherson et al. Clin Cardiol. 1991 Feb. ...
Interaction of the cholesterol ester transfer protein I405V polymorphism with alcohol consumption in smoking and non-smoking ... healthy men, and the effect on plasma HDL cholesterol and apoAI concentration... 20. maí 2020 Gudnason V, Thormar K, Humphries ...
LCAT, lecithin:cholesterol acyltransferase; CETP, cholesteryl ester transfer protein; PONI, paraoxonase 1; S1P, sphingosine-1- ... The Great Complexity of HDL: High-density lipoprotein (HDL) particles carry a large number of proteins and lipids, which ... HDLs transport cholesterol and other lipids between different cells like a reusable ferry, but serve many other functions ... functions are exerted by entire HDL particles or distinct proteins or lipids carried by HDL rather than by its cholesterol ...
Cholesterol ester transfer protein. A major player in cholesterol metabolism].. Hansen PR. Ugeskr Laeger; 1999 Sep; 161(38): ... 8. Cholesteryl ester transfer protein (CETP) inhibition beyond raising high-density lipoprotein cholesterol levels: pathways by ... An interaction between the TaqIB polymorphism of cholesterol ester transfer protein and smoking is associated with changes in ... 1. Streptozotocin-induced increase in cholesterol ester transfer protein (CETP) and its reversal by insulin in transgenic mice ...
ABC, ATP Binding Cassette; CE, cholesteryl ester; CETP, CE transfer protein; FC, free cholesterol, HDL, high density ... Myeloid differentiation primary response protein 88 couples reverse cholesterol transport to inflammation. Smoak KA, Aloor JJ, ... Cholesterol is metabolized by CYP7A1 into bile acids in the liver; free cholesterol, bile acids, and LPS are then transported ... Adenovirus Modulates Toll-Like Receptor 4 Signaling by Reprogramming ORP1L-VAP Protein Contacts for Cholesterol Transport from ...
Cholesterol Ester Transfer Proteins/metabolism; Cholesterol/metabolism*; Cricetinae; Cross-Sectional Studies; Diabetes Mellitus ... Title: Enhanced cholesterol efflux to HDL through the ABCA1 transporter in hypertriglyceridemia of type 2 diabetes. ... HDL mediated cholesterol efflux through the ABCA-1 transporter was measured using BHK cell lines in samples of 71 participants ... Our objective was to examine the role of hypertriglyceridemia on the capacity of HDL to facilitate ABCA-1 mediated cholesterol ...
... with high-density lipoprotein cholesterol and discuss the implications of the trial data for cholesteryl ester transfer protein ... A recent therapeutic class is the cholesteryl ester transfer protein inhibitor. These drugs can increase circulating high- ... density lipoprotein cholesterol levels by inhibiting the exchange of cholesteryl ester from high-density lipoprotein for ... Impaired gas transfer, due to micro- angiopathy in type 2 diabetes, suggests that individuals will be vulnerable to the pro- ...
... show that lowering cholesterol levels will reduce risk. Cholesterol in the circulation is embedded in lipoproteins. The major ... Currently available cholesterol-lowering drugs are statins, ezetimibe, bempedoic acid, bile acid sequestrants, proprotein ... This hypothesis is based on epidemiological evidence that both within and between populations higher cholesterol levels raise ... Highest priority for cholesterol-lowering therapy goes to patients with established ASCVD (secondary prevention). RCTs in such ...
... cholesterol ester transfer protein (CETP). LCAT-mediated conversion of free cholesterol to cholesteryl esters facilitates the ... Subsequently, the cholesteryl esters can be exchanged between the plasma lipoproteins, which is mediated by a transfer protein ... The esters accumulated in the liver cells can be hydrolyzed by cholesterol esterase to release free cholesterol, which is ... The cholesteryl esters can be directly transported to the liver by HDL, or indirectly by LDL after the ester is transferred ...
Nephrotic-range proteinuria in adults is characterized by protein excretion of 3. ... and cholesterol ester transfer protein. [32, 33] ... A urine protein/creatinine value of more than 2-3 mg/mg ... with resultant increases in total cholesterol and LDL-cholesterol. The level of high-density lipoprotein (HDL) cholesterol is ... as well as another protein, C-mip. CD80 and C-mip, in turn, may interfere with the proteins Nck and Fyn, leading to ...
Increased high density lipoprotein cholesterol concentration in alcoholics is related to low cholesteryl ester transfer protein ... Some studies hypothesized that this effect is due to an alcohol-induced defect in cholesteryl ester transfer protein (CETP) ( ... Reduction in the concentration and activity of plasma cholesteryl ester transfer protein by alcohol. J Lipid Res, 33:737-744, ... While some studies have shown that chronic alcohol consumption increases HDL cholesterol (Hartung et al., 1990; Langer et al., ...
NOVEL BENZYLAMINE DERIVATIVES AND THEIR UTILITY AS CHOLESTEROL ESTER-TRANSFER PROTEIN INHIBITORS ... and the use of substituted benzylamino quinolines as cholesterol ester-transfer protein inhibitors. ... Furthermore, the present invention relates to the use of said disubstituted triazine derivatives as inhibitors for a protein ... which is operably linked to a nucleic acid molecule encoding a reporter protein, with a test agent and determining whether the ...
Two of the genes are involved in the cholesterol pathway-a formerly unknown biological pathway for development of the disease. ... and cholesterol ester transfer protein (CETP). Two more genes in the cholesterol pathway-lipoprotein lipase (LPL) and ATP ... Cholesterol Genes Tied to Age-Related Macular Degeneration. In AMD, small yellowish deposits made partly of cholesterol form ... One hallmark of AMD is the appearance of drusen-deposits of protein, cholesterol and other lipids-under the retinal pigment ...
Cholesterol Ester Transfer Protein Cholesterol Ester Transport Protein, CETP Cholesteryl Ester Exchange Protein Cholesteryl ... Ester Transfer Protein Registry Number. 0. Public MeSH Note. 2007; CHOLESTEROL ESTER TRANSFER PROTEINS was indexed under ... Cholesterol Ester Transfer Proteins Preferred Concept UI. M0067633. Registry Number. 0. Scope Note. Proteins that bind to and ... Cholesterol Ester Transfer Proteins Preferred Term Term UI T097636. LexicalTag NON. ThesaurusID NLM (2007). ...
Still think eating eggs raises cholesterol? Still think high cholesterol causes heart disease? If you answered yes to any of ... eg, variants of the gene coding for cholesteryl-ester transfer. protein, or CETP).. This means that sacharids, also unsaturated ... variants of the gene coding for cholesteryl-ester transfer protein, or CETP). ... Given the cholesterol numbers to look out for…. HDL ,, 40. TG ,, 150. TG / HDL , 3.8 (i.e. Pattern A ). LPA Lipo Protein , 75 ...
transfer protein [20], the key enzyme for the transfer of cholesterol. esters from HDL to LDL and very low-density lipoprotein ... The potential benefit of cholesterol ester transfer protein inhibition is still under investigation. The combination therapy of ... cholesteryl-ester transfer protein and increased levels of inflam-. matory marker [27], positive correlation with ... LDL) referred as "bad cholesterol"and decreases the level of high-. density lipoprotein (HDL) referred as "good cholesterol"and ...
... has identified three new genes associated with this blinding eye disease-two involved in the cholesterol pathway. ... cholesterol pathway: human hepatic lipase (LIPC) and cholesterol ester transfer protein (CETP). Scientists identified two ... It is believed that early stages of AMD are affected by accumulation of oxidation products of cholesterol and other lipids in ... "We suspect that these genetic variations found in the cholesterol pathway impact the retina differently from the circulatory ...
Deviations in many genes were associated with HDL cholesterol levels, including cholesterol ester transfer protein (which moves ... we investigated deviations in genes that code for proteins involved in physiologic pathways related to HDL cholesterol. Blood ... Interpretive Summary: The amount of cholesterol carried in blood in high density lipoprotein (HDL) particles is an indicator of ... Selected genes corresponded to folate metabolism, vitamins B-12, A, and E, and cholesterol pathways or lipid metabolism. ...
... includes patients with deficiency of cholesteryl ester transfer protein, lecithin cholesterol acyltransferase, phospholipid ... Apolipoproteins (plasma proteins involved in metabolism of cholesterol, triglycerides, phospholipids, and proteins in the blood ... transfer protein, lipoprotein lipase, hepatic lipase, or apo-CII, ANGPTL3, and Tangier disease. - Plasma triglyceride levels , ... Plasma cholesterol levels ,200 mg/dl or ,120 mg/dl includes patients with diagnoses such as familial hypercholesterolemia, ...
Cholesterol Ester Transfer Protein Cholesterol Ester Transport Protein, CETP Cholesteryl Ester Exchange Protein Cholesteryl ... Ester Transfer Protein Registry Number. 0. Public MeSH Note. 2007; CHOLESTEROL ESTER TRANSFER PROTEINS was indexed under ... Cholesterol Ester Transfer Proteins Preferred Concept UI. M0067633. Registry Number. 0. Scope Note. Proteins that bind to and ... Cholesterol Ester Transfer Proteins Preferred Term Term UI T097636. LexicalTag NON. ThesaurusID NLM (2007). ...
Decrease in plasma low-density lipoprotein cholesterol, apolipoprotein B, cholesteryl ester transfer protein, and oxidized low- ... Soy sterol esters and B-sitostanol ester as inhibitors of cholesterol absorption in human small bowel. Am J Clin Nutr 2000;71: ... Comparison of the effects of plant sterol ester and plant stanol ester-enriched margarines in lowering serum cholesterol ... Reducing cholesterol levels in people with an inherited tendency toward high cholesterol (familial hypercholesterolemia). ...
... exchange of triglycerides for LDL and HDL cholesteryl esters, mediated by cholesteryl ester transfer protein (CETP), results in ... but significant increase in LDL cholesterol; no effect on HDL cholesterol in the whole group, while in male type 2 diabetic ... When muscle protein synthesis was determined dietary n-3 fatty acids were found to alter net protein synthesis. The results ... EFFECTS OF w3 FATTY ACIDS ON LDL-CHOLESTEROL IN DIABETIC PATIENTS. ...
These changes were not mediated by cholesteryl-ester-transfer protein. Treatment of humans for 1 week with oral RVX-208 ... Results showed that hepatic SR-BI mRNA, protein, and uptake of cholesterol from HDL were halved following 48 h of exposure to ... BET proteins are epigenetic "readers," which play a primary role in transcription. Here, we briefly describe the BET family of ... In AGMs, RVX-208 raises serum pre-beta(1)-LpA-I and alpha-LpA-I levels and enhances cholesterol efflux. Data in humans point to ...
About a dozen genetic markers have been found, including the Cholesterol Ester Transfer Protein gene, which indicates lower ...
Microsomal Triglyceride Transfer Protein Deficiency. Microsomal Triglyceride Transfer Protein Deficiency Disease. Tree number(s ... CHOLESTEROL ESTERS; PHOSPHOLIPIDS) and is required in the secretion of BETA-LIPOPROTEINS (low density lipoproteins or LDL). ... It is caused by mutation of the microsomal triglyceride transfer protein that catalyzes the transport of lipids (TRIGLYCERIDES ... It is caused by mutation of the microsomal triglyceride transfer protein that catalyzes the transport of lipids (TRIGLYCERIDES ...
... action of cholesteryl ester, transfer proteins and hepatic and peripheral actions of insulin [1]. Even more, it has been ... Hyperglycaemia progressively increases the transfer of cholesterol esters from HDL-C to VLDL-C particles [1]. The denser LDL ... Plasma HDL cholesterol, triglyceride and total cholesterol levels in non-insulin treated Nigerian diabetics. Tropical and ... the size and density of LDL-cholesterol (LDL-C) and the total cholesterol/HDL-C ratio (TC/HDL-C) [1]. The term diabetic ...
For instance, the usual mouse model for atherosclerosis lacks cholesteryl ester transfer protein (hCETP), which in humans is ... As a fat-soluble antioxidant, it protects proteins (like LDL-cholesterol), enzymes, fats (all cell walls/ membranes) and ... 73 Clinical research shows that DHA supplementation helps increase HDL cholesterol levels (the "good cholesterol").74,75 ... cholesterol (7 to 27 percent), and total cholesterol (12 to 26 percent). ...
In contrast, the CETP agonist probucol leads to HDL-C lowering followed by an increment of tissue cholesterol removal ( ... The cholesteryl ester transfer protein (CETP) system moves cholesteryl esters (CE) from high density lipoproteins (HDL) to ... The cholesteryl ester transfer protein (CETP) system moves cholesteryl esters (CE) from high density lipoproteins (HDL) to ... Cholesteryl ester transfer protein: An enigmatic pharmacology - Antagonists and agonists. Shizuya Yamashita;M. Ruscica. Co- ...
A meta-analysis of drug interventions for raising HDL, which included niacin, fibrates, and cholesteryl ester transfer protein ... Medications to Raise High-Density Lipoprotein Cholesterol Level Do Not Improve Cardiovascular Outcomes: There is some evidence ...
Cholesterol Ester Transfer Proteins 100% * HDL Cholesterol 63% * Genotype 50% * European Continental Ancestry Group 43% ... CETP genotypes and HDL-cholesterol phenotypes in the HERITAGE Family Study. Spielmann, N., Leon, A. S., Rao, D. C., Rice, T., ... The TNF-α G-308A polymorphism is associated with C-reactive protein levels: The HERITAGE Family Study. Lakka, H. M., Lakka, T. ... Quantitative trait locus on chromosome 20q13 for plasma levels of C-reactive protein in healthy whites: The HERITAGE Family ...
  • Finally, we illustrate our approach by analyzing the relationship between coding variants and levels of high-density lipoprotein (HDL) cholesterol in 11,556 individuals from the HUNT and SardiNIA studies, demonstrating association for coding variants in the APOC3, CETP, LIPC, LIPG, and LPL genes and illustrating the value of family samples, meta-analysis, and gene-level tests. (nih.gov)
  • However, several large randomized trials utilizing cholesteryl ester transfer protein (CETP) inhibitors did not show benefit for reducing cardiovascular events in spite of raising HDL levels. (medscape.com)
  • The study has also shed light on a new biological pathway for AMD disease development, by uncovering two genes associated with AMD risk in the high-density lipoprotein (HDL) cholesterol pathway: human hepatic lipase (LIPC) and cholesterol ester transfer protein (CETP). (nih.gov)
  • Cholesterol ester transfer protein (CETP) gene polymorphism and selected parameters of lipid metabolism in children from families with history of cardiovascular system diseases. (cdc.gov)
  • Association of cholesteryl ester transfer protein (CETP) gene polymorphism, high density lipoprotein cholesterol and risk of coronary artery disease: a meta-analysis using a Mendelian randomization approach. (cdc.gov)
  • A meta-analytic evaluation of cholesteryl ester transfer protein (CETP) C-629A polymorphism in association with coronary heart disease risk and lipid changes. (cdc.gov)
  • Background: We aimed to identify independent genetic determinants of circulating CETP (cholesteryl ester transfer protein) to assess causal effects of variation in CETP concentration on circulating lipid concentrations and cardiovascular disease risk. (tilburguniversity.edu)
  • Therefore, the results of our study are fully consistent with the notion that CETP concentration is causally associated with CAD through low-density lipoprotein cholesterol. (tilburguniversity.edu)
  • The patients had reduced postheparin hepatic triglyceride lipase (HTGL) activities, and one of them has recently been identified to be homozygous for a missense mutation in exon 15 (D442: G) in the cholesteryl ester transfer protein (CETP) gene. (qxmd.com)
  • LDL are formed from IDL with the involvement of hepatic lipase (HL) and are enriched with HDL cholesterol, with the involvement of the cholesterol ester transfer protein (CETP) [ 1 - 3 ]. (archivesofmedicalscience.com)
  • ABCA1 - ATP-binding cassette transporter A1, CETP - cholesterol ester transfer protein, EL - endothelial lipase, HL - hepatic lipase, LCAT - lecithin cholesterol acyltransferase, LPL - lipoprotein lipase, PLTP - phospholipid transfer protein, TG - triglycerides. (archivesofmedicalscience.com)
  • Fats, or lipids, such as cholesterol and triglycerides, are carried in the blood in particles called lipoproteins. (nih.gov)
  • Apolipoproteins (plasma proteins involved in metabolism of cholesterol, triglycerides, phospholipids, and proteins in the blood) and enzymes involved in lipid metabolism are measured. (nih.gov)
  • In the previously cited study by Khan et al 9 , type 2 diabetics who were given 1, 3 or 6 grams of cinnamon a day for 60 days experienced significant drops in triglycerides (23 to 30 percent), low-density lipoprotein (LDL) cholesterol (7 to 27 percent), and total cholesterol (12 to 26 percent). (totalhealthmagazine.com)
  • There are 2 major types of lipids in the blood: cholesterol and triglycerides. (who.int)
  • Hyperlipidemia is a set of metabolic disorders that can be genetic or acquired that are characterized by excess lipids in the blood which can include cholesterol and/or triglycerides. (igenomix.fr)
  • Objective - Niacin potently decreases plasma triglycerides and LDL-cholesterol. (tno.nl)
  • The acid cholesteryl ester hydrolase activity in the tissues appeared to be normal. (nih.gov)
  • Early steps in reverse cholesterol transport: cholesteryl ester hydrolase and other hydrolases. (jmir-inc.com)
  • Selected genes corresponded to folate metabolism, vitamins B-12, A, and E, and cholesterol pathways or lipid metabolism. (usda.gov)
  • Many oxazoles showed a higher CYP450 dependent microsomal metabolism than the corresponding ethyl esters. (bvsalud.org)
  • The maternal lipid metabolism during pregnancy is characterized by progressive increases in plasma cholesterol and triglyceride levels accompanied by increases in low density lipoprotein (LDL) and very low density lipoprotein (VLDL), leading to maternal hyperlipidemia during late pregnancy [ 4 ]. (biomedcentral.com)
  • Metabolism: Metabolized by ester hydrolysis to active metabolite which undergoes glucuronide conjugation in liver. (medicineindia.org)
  • 25 mg/dl includes patients with deficiency of cholesteryl ester transfer protein, lecithin cholesterol acyltransferase, phospholipid transfer protein, lipoprotein lipase, hepatic lipase, or apo-CII, ANGPTL3, and Tangier disease. (nih.gov)
  • Lecithin: cholesterol acyltransferase (LCAT) activity is associated with HDL containing apo A-I. Google Scholar. (jmir-inc.com)
  • Hepatic lipase and cholesteryl ester transfer protein mass and activity remained unchanged. (ox.ac.uk)
  • We used a mathematical technique called linear regression to determine which gene deviations were associated with higher or lower HDL cholesterol levels. (usda.gov)
  • About a dozen genetic markers have been found, including the Cholesterol Ester Transfer Protein gene, which indicates lower risk of heart disease and dementia, as well as the APOC3 gene that protects against cardiovascular disease and diabetes. (yoyenta.com)
  • The protein encoded by this gene is found in plasma, where it is involved in the transfer of cholesteryl ester from high density lipoprotein (HDL) to other lipoproteins. (nih.gov)
  • Description of the protein which includes the UniProt Function and the NCBI Gene Summary. (nih.gov)
  • Publication: Quantile-Dependent Expressivity and Gene-Lifestyle Interactions Involving High-Density Lipoprotein Cholesterol. (nih.gov)
  • Key Message: Quantile-dependent expressivity provides a potential explanation for some reported gene-lifestyle interactions for HDL-cholesterol. (nih.gov)
  • The lipid part is bound to specific proteins - apolipoproteins (apo), which determine the physical and biological properties of lipoproteins [ 3 ]. (archivesofmedicalscience.com)
  • Endogenous TG are synthesized in hepatocytes, where jointly with cholesterol and apolipoproteins (apoB 100, apoE, apoC) constitute building material for VLDL secreted into the blood, where their remnants (IDL) are formed by an action of endothelial lipase (EL). (archivesofmedicalscience.com)
  • A potential liability of these compounds was their generally high in vivo clearance due to ethyl ester hydrolysis. (bvsalud.org)
  • Within the circulation, THs are mainly bound to proteins (3) and appear only in minor free fractions (FT3, FT4), which are considered as the biologically active pool. (deepdyve.com)
  • HDLs are among a family of lipoproteins that transport essential fats, such as cholesterol, through the bloodstream. (nih.gov)
  • Complementing the AHA Presidential Advisory's focus on fats, this document found plant-based proteins to be significantly more heart healthy than animal-based proteins. (wordpress.com)
  • Serum retinol binding protein transports ingested retinol from the intestine to the liver and other tissues. (elifesciences.org)
  • Regulates the reverse cholesterol transport, by which excess cholesterol is removed from peripheral tissues and returned to the liver for elimination (PubMed:17237796). (nih.gov)
  • Supply of cholesterol to the peripheral tissues, where it is essential for the formation of cell membranes and biosynthesis of steroid hormones, and to the liver, where it is used for the synthesis of bile acids ( hepatic pathway ) ( Figure 2 ). (archivesofmedicalscience.com)
  • Reverse cholesterol transport is a mechanism by which the body removes excess cholesterol from peripheral tissues and delivers them to the liver, where it will be redistributed to other tissues or removed from the body by the gallbladder. (jmir-inc.com)
  • As cholesterol in HDL becomes esterified, it creates a concentration gradient and draws in cholesterol from tissues and from other lipoproteins (Figures 26-5 and 26-6), thus enabling HDL to function in reverse cholesterol transport (Figure 25-5). (jmir-inc.com)
  • 1] Cholesterol from non-hepatic peripheral tissues is transferred to HDL by the ABCA1 (ATP-binding cassette transporter). (jmir-inc.com)
  • Reverse cholesterol transport is a multi-step process resulting in the net movement of cholesterol from peripheral tissues back to the liver first via entering the lymphatic system, then the bloodstream. (jmir-inc.com)
  • Cholesterol -- A white crystalline substance found in animal tissues and various foods that is normally synthesized by the liver and is important as a constituent of cell membranes and a precursor to steroid hormones. (nih.gov)
  • It is believed to affect blood cholesterol levels by removing cholesterol from plasma and tissues and carrying it back to the liver for action by bile and eventual excretion. (nih.gov)
  • Enhanced cholesterol efflux to HDL through the ABCA1 transporter in hypertriglyceridemia of type 2 diabetes. (nih.gov)
  • Our objective was to examine the role of hypertriglyceridemia on the capacity of HDL to facilitate ABCA-1 mediated cholesterol efflux in type 2 diabetes (T2DM).HDL mediated cholesterol efflux through the ABCA-1 transporter was measured using BHK cell lines in samples of 71 participants with T2DM in the presence or absence of high triglyceride levels (TG). (nih.gov)
  • Scientists identified two additional genes, lipoprotein lipase (LPL) and ATP binding cassette transporter 1 (ABCA1), that may be involved in the cholesterol pathway as well, but more research is needed to confirm these findings. (nih.gov)
  • Lipoproteins are a family of large particles composed of an "envelope", which contains phospholipids and free cholesterol, and a core containing TG and cholesterol esters. (archivesofmedicalscience.com)
  • Serum amyloid A (SAA) proteins are strongly induced in the liver by systemic infection and in the intestine by bacterial colonization, but their exact functions remain unclear. (elifesciences.org)
  • It had been suggested that Serum Amyloid A (SAA) proteins, a family of proteins made by some liver and intestinal cells, could be involved in the response to infection, because these proteins' levels increase during infection. (elifesciences.org)
  • Plasma proteins -- Proteins present in blood serum, including serum albumin, blood coagulation factors, and many other types of proteins. (nih.gov)
  • Involved in the transfer of neutral lipids, including cholesteryl ester and triglyceride, among lipoprotein particles. (nih.gov)
  • BACKGROUND: The phenotypic expression of a high-density lipoprotein (HDL) genetic risk score has been shown to depend upon whether the phenotype (HDL-cholesterol) is high or low relative to its distribution in the population (quantile-dependent expressivity). (nih.gov)
  • Matrix metalloproteinases (MMPs) are largely responsible for the degradation of extracellular matrix proteins in the PDL. (tno.nl)
  • Efflux of cholesterol from peripheral cells to extracellular acceptors. (jmir-inc.com)
  • Proteins that specifically bind to IRON. (umassmed.edu)
  • Retinol must bind to specific proteins to be able to move through the bloodstream and be transported around the body. (elifesciences.org)
  • went on to solve the crystal structure of a mouse SAA protein, and showed that four SAA molecules bind together to form a 'pocket' that can hold a retinol molecule. (elifesciences.org)
  • found that mice fed a diet poor in vitamin A produced fewer SAA proteins in their liver and intestinal cells. (elifesciences.org)
  • We evaluated key steps of the reverse cholesterol transport, ie, cellular free cholesterol efflux, cholesteryl ester transfer protein-mediated cholesteryl ester (CE) transfer from HDL to apolipoprotein B-containing lipoproteins, and hepatic HDL-CE uptake, in patients displaying FH (n = 12) and in healthy normolipidemic control subjects (n = 12). (jmir-inc.com)
  • Reverse cholesterol transport designates the process by which cholesterol from lipid-loaded peripheral cells, such as macrophage foam cells, passages through the plasma high-density lipoprotein (HDL) compartment to the liver and is excreted via the feces [9]. (jmir-inc.com)
  • Instead a microsomal triglyceride transfer protein, which exists as a complex with protein disulphide isomerase in the endoplasmic reticulum, has been implicated. (ox.ac.uk)
  • We have cloned and sequenced the human cDNA encoding microsomal triglyceride transfer protein. (ox.ac.uk)
  • Microsomal triglyceride transfer protein is expressed in ovary, testis and kidney, in addition to liver and small intestine. (ox.ac.uk)
  • SR-BI is an 82-kDa integral membrane protein, belonging to the CD36 family, whose physiologicalrole isrelated totheselective uptake ofHDL cholesteryl ester, the process by which the core cholesteryl ester is taken into the cell without the endocytic uptake and degradation of the whole HDL. (jmir-inc.com)
  • It lowers circulating triglyceride levels by activating lipoprotein lipase which is a key enzyme in the degradation of VLDL (very low density lipoprotein) cholesterol. (medicineindia.org)
  • The amount of cholesterol carried in blood in high density lipoprotein (HDL) particles is an indicator of heart disease risk, with high levels being favorable. (usda.gov)
  • We report here that personal counseling resulted in significant (p=0.0001) reductions in plasma concentrations of total cholesterol, LDL, fasting glucose and 2h glucose. (nih.gov)
  • A tight regulation of both placental ApoD transcription and protein content is most probably at the basis of the low circulating ApoD concentrations in women with excessive GWG. (biomedcentral.com)
  • The selected examples showed larger genetic effect sizes for lifestyle conditions associated with higher vis-à-vis lower average HDL-cholesterol concentrations. (nih.gov)
  • Plasma levels of total cholesterol, HDL cholesterol, and triglyceride in all subjects were 6.28 +/- 1.78, 3.15 +/- 0.90, and 1.08 +/- 0.53 mmol/L, respectively. (qxmd.com)
  • A large genetic study of age-related macular degeneration (AMD) has identified three new genes associated with this blinding eye disease-two involved in the cholesterol pathway. (nih.gov)
  • We suspect that these genetic variations found in the cholesterol pathway impact the retina differently from the circulatory system, so cholesterol levels in the blood may not provide meaningful information about AMD risk," Swaroop explained. (nih.gov)
  • Start studying Unit 9 reverse cholesterol transport pathway. (jmir-inc.com)
  • Reverse cholesterol transport (RCT) is a pathway by which accumulated cholesterol is transported from the vessel wall to the liver for excretion, thus preventing atherosclerosis. (jmir-inc.com)
  • Exacerbated postprandial hypertriglyceridemia (PP-HTG) and metabolic context both modulate the overall efficacy of the reverse cholesterol transport (RCT) pathway, but the specific contribution of exaggerated PP-HTG on RCT efficacy remains indeterminate. (jmir-inc.com)
  • Therefore, we investigated deviations in genes that code for proteins involved in physiologic pathways related to HDL cholesterol. (usda.gov)
  • Blood samples were drawn from 759 individuals, and HDL cholesterol levels were measured, and deviations in 23 genes were determined. (usda.gov)
  • Deviations in many genes were associated with HDL cholesterol levels, including cholesterol ester transfer protein (which moves cholesterol among lipoproteins), beta-carotene mono-oxygenase 1 (which converts beta-carotene to vitamin A), and transporters that move the vitamin folate into cells. (usda.gov)
  • Additionally, HDL mediated efflux was measured in 13 diabetic and non-diabetic participants fasting and four hours after a high-fat test challenge.HDL mediated cholesterol efflux function was increased in participants with T2DM with hypertriglyceridemia when compared to participants with T2DM without hypertriglyceridemia (efflux ratio mean±standard deviation (SD), T2DM+TG: 1.17±0.25 vs. T2DM - TG: 1.03±0.19, p=0.0098). (nih.gov)
  • Iron-Binding Proteins" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (umassmed.edu)
  • Allows the net movement of cholesteryl ester from high density lipoproteins/HDL to triglyceride-rich very low density lipoproteins/VLDL, and the equimolar transport of triglyceride from VLDL to HDL (PubMed:3600759, PubMed:24293641). (nih.gov)
  • Genetic analysis of long-lived families reveals novel variants influencing high density-lipoprotein cholesterol. (cdc.gov)
  • This suggests these reported interactions could be the result of selecting subjects for conditions that differentiate high from low HDL-cholesterol (e.g., lean vs. overweight, active vs. sedentary, high-fat vs. high-carbohydrate diets, alcohol drinkers vs. abstainers, nonsmokers vs. smokers) producing larger versus smaller genetic effect sizes. (nih.gov)
  • Molecular biology -- The branch of biology dealing with the formation, structure, and function of macromolecules essential to life, such as DNA, RNA, and proteins, especially their role in cell replication and the transmission of genetic information. (nih.gov)
  • This review aims to summarize recent studies demonstrating … San Francisco, U.S.A. Reverse cholesterol transport in insulin resistance and type 2 diabetes mellitus. (jmir-inc.com)
  • macrophage- reverse cholesterol transport (m-RCT), is an important anti-atherogenic mechanism. (jmir-inc.com)
  • Increasing reverse cholesterol transport may someday be a way to reduce atherosclerosis and heart disease. (jmir-inc.com)
  • Initial steps in reverse cholesterol transport: the role of short-lived cholesterol acceptors O. L. Francone Search for other works by this author on: Oxford Academic. (jmir-inc.com)
  • The reverse cholesterol transport (RCT) is the process that may counteract the pathogenic events leading to the formation of atheroma. (jmir-inc.com)
  • Factors affecting high-density lipoprotein cholesterol in HIV-infected patients on nevirapine-based antiretroviral therapy. (cdc.gov)
  • Although high-density lipoprotein cholesterol is not a causal risk factor for CAD, it has been unequivocally demonstrated that low-density lipoprotein cholesterol lowering is proportionally associated with a lower CAD risk. (tilburguniversity.edu)
  • 0.05), and high-density lipoprotein subfraction 2 cholesterol remained unchanged. (ox.ac.uk)
  • It is prodrug which has greater LDL (low density lipoprotein) cholesterol lowering potential. (medicineindia.org)
  • It also reduces VLDL levels and increases HDL (high density lipoprotein) cholesterol. (medicineindia.org)
  • High-density lipoprotein cholesterol (HDLC) -- The portion of plasma lipoprotein cholesterol with most density. (nih.gov)
  • Low-density lipoprotein cholesterol (LDLC) -- The protein-lipid combination that transports the major amount of the cholesterol in the blood. (nih.gov)
  • The cells are grown in the laboratory and the amount of cholesterol that enters or leaves the cells is measured, providing information on abnormalities in cholesterol transport. (nih.gov)
  • The increase in HDL cholesterol is partly due to transfer of surface lipid components from catabolised VLDL to HDL and also due to increased production of HDL apoproteins by liver. (medicineindia.org)
  • Still think high cholesterol causes heart disease? (thehealthyskeptic.org)
  • However, the similar ApoD levels in low cholesterol (LC) and high cholesterol (HC) women suggest that the plasma ApoD variation is not cholesterol dependant. (biomedcentral.com)
  • But there is a correlation between certain types of cholesterol in the blood and heart disease, like high levels of the small, dense LDL are connected to an increased risk of heart attacks. (thehealthyskeptic.org)
  • The cholesterol in your diet doesn't necessarily effect the levels of these different types of cholesterol in your blood right? (thehealthyskeptic.org)
  • But is it right to say that cholesterol in the diet doesn't effect heart disease but certain levels of certain types of cholesterol in the blood can lead to heart disease? (thehealthyskeptic.org)
  • However, the relationship between HDL cholesterol levels in the blood and AMD is still unclear. (nih.gov)
  • The most common risk factors are cigarette smoking, diabetes, high blood pressure and elevated cholesterol. (wordpress.com)
  • While LDLC helps in synthesis of bile acid and steroid hormones, elevated blood levels of LDLC--or 'bad cholesterol'--have been linked to heart disease because it carries the cholesterol through the blood to the cells. (nih.gov)
  • The structure of lipoproteins is maintained primarily by hydrophobic interactions between nonpolar components of lipids and proteins. (archivesofmedicalscience.com)
  • explain why LDL and total cholesterol are not useful markers for heart disease. (thehealthyskeptic.org)
  • In daily practice, non-HDL cholesterol level (ie, LDL + very LDL cholesterol [total cholesterol - HDL cholesterol]) is the most readily available measure of the total pool of these atherogenic lipoproteins. (medscape.com)
  • This graph shows the total number of publications written about "Iron-Binding Proteins" by people in this website by year, and whether "Iron-Binding Proteins" was a major or minor topic of these publications. (umassmed.edu)
  • Atherosclerosis accounts for up to 80% of cholesterol (LDL-C) and the total choles- deaths in diabetic patients due to coronary terol/HDL-C ratio (TC/HDL-C) [ 1 ]. (who.int)
  • Synthesis of cholesterol in the abnormal tonsil was brisk, but not obviously greater than in similar unaffected tissue (7). (nih.gov)
  • Protein chemistry -- A branch of chemistry which encompasses a range of techniques and approaches that can aid the investigation of protein structure and function. (nih.gov)
  • Dyslipidaemia obesity and insulin changes highly acceler- encompasses changes in HDL-cholesterol ate the progression to atherosclerosis [ 2 ]. (who.int)
  • It is believed that early stages of AMD are affected by accumulation of oxidation products of cholesterol and other lipids in the retinal pigment epithelium, a layer of cells in the back of the eye. (nih.gov)
  • Patients with established coronary disease and low HDL cholesterol levels are at high risk for recurrent events and should be targeted for aggressive nonpharmacological (ie, dietary modification, weight loss, physical exercise) and pharmacological treatment. (medscape.com)