Lcat Activity
Mostrando 1-12 de 27 artigos, teses e dissertações.
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1. Perfil lipÃdico e correlaÃÃo entre concentraÃÃo e atividade de Lecitina: colesterol aciltransferase (LCAT) em plasma de pacientes com esquistossomose mansÃnica hepatointestinal e hepatoesplÃnica
Schistosomiasis, a disease caused by helminth Schistosoma mansoni affects about 200 million people worldwide. Due to deposition of eggs of the parasite in the liver, the disease may progress to a more mild, hepatointestinal (HI), for the most severe, hepatosplenic (HS). Previous studies show a relationship between lipid metabolism and the hepatosplenic form
Publicado em: 2009
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2. Plasma kinetics and biodistribution of free cholesterol and cholesterol ester of a nanoemulsion that binds to LDL receptors in animals without and with atherosclerosis / Cinética plasmática e biodistribuição de colesterol livre e colesterol esterificado de uma nanoemulsão (LDE) que se liga aos receptores de LDL em animais controle e com indução de aterosclerose
I n previously studies, it was shown that free cholesterol (FC) and cholesterol ester (CE) of a cholesterol-rich nanoemulsion (LDE) behaves differently in patients with coronary artery disease (CAD). The FC plasma clearance and arterial deposition is greater than CE. In the present study we evaluate the plasma kinetics, estimated by the fractional clearance
Publicado em: 2007
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3. Metabolismo de lipoproteinas plasmaticas em tabagistas : proteinas reguladoras e modificações quimicas das lipoproteinas de baixa densidade
A aterosclerose é uma doença imuno-inflamatória e de caráter multifatorial. O tabagismo é um de seus principais fatores de risco, existindo grande controvérsia na literatura quanto aos mecanismos fisiopatológicos de sua aterogenicidade. Avaliamos os efeitos metabólicos e oxidantes do fumo em urna população sadia adulta, composta de fumantes crônic
Publicado em: 2002
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4. Fish eye syndrome: a molecular defect in the lecithin-cholesterol acyltransferase (LCAT) gene associated with normal alpha-LCAT-specific activity. Implications for classification and prognosis.
We have identified the molecular defect in two siblings presenting with classical clinical and biochemical features of Fish Eye disease (FED), including corneal opacities, HDL cholesterol < 10 mg/dl, normal plasma cholesteryl esters, and elevated triglycerides. In contrast to previously reported patients with FED who are unable to esterify HDL-associated cho
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5. Expression of human lecithin-cholesterol acyltransferase in transgenic mice. Effect of human apolipoprotein AI and human apolipoprotein all on plasma lipoprotein cholesterol metabolism.
Human (Hu) lecithin-cholesterol acyltransferase (LCAT) is a key enzyme in the plasma metabolism of cholesterol. To assess the effects of increased plasma levels of LCAT, four lines of transgenic mice were created expressing a Hu LCAT gene driven by either its natural or the mouse albumin enhancer promoter. Plasma LCAT activity increased from 1.2- to 1.6-fold
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6. Genetic and phenotypic heterogeneity in familial lecithin: cholesterol acyltransferase (LCAT) deficiency. Six newly identified defective alleles further contribute to the structural heterogeneity in this disease.
The presence of lecithin:cholesterol acyltransferase (LCAT) deficiency in six probands from five families originating from four different countries was confirmed by the absence or near absence of LCAT activity. Also, other invariate symptoms of LCAT deficiency, a significant increase of unesterified cholesterol in plasma lipoproteins and the reduction of pla
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7. Effects of site-directed mutagenesis at residues cysteine-31 and cysteine-184 on lecithin-cholesterol acyltransferase activity.
Native lecithin-cholesterol acyltransferase (LCAT; phosphatidylcholine-sterol acyltransferase; phosphatidylcholine:sterol O-acyltransferase, EC 2.3.1.43) protein, and LCAT in which either or both of the enzyme free cysteines had been replaced with glycine residues by site-directed mutagenesis, has been expressed in cultured Chinese hamster ovary cells stably
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8. A unique genetic and biochemical presentation of fish-eye disease.
This paper describes a novel genetic defect which causes fish-eye disease in four homozygous probands and its biochemical presentation in 34 heterozygous siblings. The male index patient presented with premature coronary artery disease, corneal opacification, HDL deficiency, and a near total loss of plasma lecithin:cholesterol acyltransferase (LCAT) activity
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9. A cholesteryl ester transfer complex in human plasma.
Immunoadsorption affinity chromatography has been used to define the structure of lipoproteins in human plasma containing lecithin:cholesterol acyltransferase (EC 2.3.1.43) (LCAT) and transfer protein (apo D). The whole of LCAT was absorbed by antibodies specific for apo D and for apo A-1, indicating that the enzyme is present in plasma exclusively as a comp
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10. The role of lecithin: cholesterol acyltransferase for lipoprotein (a) assembly. Structural integrity of low density lipoproteins is a prerequisite for Lp(a) formation in human plasma.
The composition of lipoproteins in the plasma of patients with LCAT deficiency (LCAT-D) is grossly altered due to the lack of cholesteryl esters which form the core of normal lipoproteins. When plasma from LCAT-D patients and their relatives was examined we found that nine heterozygotes had plasma Lp(a) levels of 2-13 mg/dl whereas none of 11 affected homozy
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11. Altered epitope expression of human interstitial fluid apolipoprotein A-I reduces its ability to activate lecithin cholesterol acyl transferase.
In human peripheral interstitial fluid, esterification of cholesterol by lecithin cholesterol acyltransferase (LCAT) was found to occur at a rate of only 10% of that in plasma (5.6 +/- 1.8 compared with 55.6 +/- 7.8 nmol/ml per h). Measurement of cholesterol esterification in the presence of excess reconstituted apoA-I HDL (rA-I HDL) revealed an LCAT activit
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12. Overexpression of lecithin:cholesterol acyltransferase in transgenic rabbits prevents diet-induced atherosclerosis.
Lecithin:cholesterol acyltransferase (LCAT) is a key plasma enzyme in cholesterol and high density lipoprotein (HDL) metabolism. Transgenic rabbits overexpressing human LCAT had 15-fold greater plasma LCAT activity that nontransgenic control rabbits. This degree of overexpression was associated with a 6.7-fold increase in the plasma HDL cholesterol concentra