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lecithin cholesterol acyltransferase deficiency/albumine
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Changes in lipoprotein profile and urinary albumin excretion in familial LCAT deficiency with lipid lowering therapy.
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Familial lecithin:cholesterol acyltransferase deficiency (FLD) is a monogenic autosomal recessive condition, affecting cholesterol esterification and leads to progressive renal impairment and end-stage renal failure, probably due to the abnormal lipoprotein (X) (Lp(X)). We report a case of FLD, whom
Plasma beta-2-microglobulin and urinary albumin: creatinine ratio in lecithin: cholesterol acyltransferase deficiency.
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LCAT Enzyme Replacement Therapy Reduces LpX and Improves Kidney Function in a Mouse Model of Familial LCAT Deficiency.
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Familial LCAT deficiency (FLD) is due to mutations in lecithin:cholesterol acyltransferase (LCAT), a plasma enzyme that esterifies cholesterol on lipoproteins. FLD is associated with markedly reduced levels of plasma high-density lipoprotein and cholesteryl ester and the formation of a nephrotoxic
Studies on the pre-alpha-lipoprotein in patients with familial lecithin: cholesterol acyltransferase deficiency.
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The present study shows that regular alpha1- and pre-alpha-lipoproteins cannot be detected in serum of patients with familial lecithin: cholesterol acyltransferase (LCAT) deficiency. After electrophoresis on agarose gel only one single band of albumin mobility was observed in the
Lipid-free apolipoprotein (apo) A-I is converted into alpha-migrating high density lipoproteins by lipoprotein-depleted plasma of normolipidemic donors and apo A-I-deficient patients but not of Tangier disease patients.
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Plasma of patients with Tangier disease (TD) is devoid of alpha-LpA-I (apolipoprotein A-I-containing lipoprotein), which in normolipidemic plasma constitutes the majority of high density lipoprotein (HDL). The residual amounts of apolipoprotein A-I (apo A-I) in TD plasma have electrophoretic
Lipoprotein-X.
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Lipoprotein-X is an abnormal lipoprotein that appears in the sera of patients with obstructive jaundice, and thus is a sensitive indicator of cholestasis. In patients with familial plasma lecithin, Cholesterol acyltransferase (LCAT) deficiency, there is an inverse relationship between plasma Lp-X
Characterization and potential uses of rabbit polyclonal antibodies against human plasma lecithin-cholesterol acyltransferase.
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Familial and secondary deficiency of plasma lecithin-cholesterol acyltransferase (LCAT) produce circulating lipoprotein particles with gross structural and compositional abnormalities; these have adverse effects on a variety of cellular functions. Factors affecting hepatic synthesis and secretion of
Enzymic esterification of cholesterol in rat intestinal mucosa catalyzed by acyl-CoA: cholesterol acyltransferase.
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Previous work has shown CoA-dependent esterification of cholesterol in rat intestinal mucosa. Using (1-(14)C)oleoyl-CoA as the labeled substrate, we have proved that the esterification is catalyzed by acyl-CoA: cholesterol acyltransferase (ACAT) existing in the 'microsomal fraction' of the mucosal
Apolipoprotein and lipid distribution between vesicles and HDL-like particles formed during lipolysis of human very low density lipoproteins by perfused rat heart.
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A study was undertaken to determine the relative association of lipid and apolipoproteins among lipoproteins produced during lipolysis of very low density lipoproteins (VLDL) in perfused rat heart. Human VLDL was perfused through beating rat hearts along with various combinations of albumin (0.5%),
Influence of bile acids and free fatty acids on physicochemical properties of LP-X.
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In this study it is demonstrated, that incubation of both, bile acids and free fatty acids with LP-X, the abnormal plasmalipoprotein found in patients suffering from cholestasis or LCAT-deficiency, results in striking alterations of the physico-chemical and immunological properties of LP-X: 1. The
High density lipoprotein subpopulations from galactosamine-treated rats and their transformation by lecithin:cholesterol acyltransferase.
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It is known that an acute hepatotoxicity is produced in rats by intraperitoneal administration of galactosamine; a consequence of this treatment is a marked deficiency of lecithin:cholesterol acyltransferase (LCAT) activity in the plasma compartment. In this study high density lipoprotein (HDL) from
Endocrine Dysfunctions in Patients with Inherited Metabolic Diseases.
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OBJECTIVE
Inherited metabolic diseases (IMDs) can affect many organ systems, including the endocrine system. There are limited data regarding endocrine dysfunctions related to IMDs in adults, however, no data exist in pediatric patients with IMDs. The aim of this study was to investigate endocrine
Role of lecithin:cholesterol acyltransferase and apolipoprotein A-I in cholesterol esterification in lipoprotein-X in vitro.
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Lipoprotein-X (Lp-X) is an abnormal particle present in the plasma of patients with familial lecithin:cholesterol acyltransferase (LCAT) deficiency syndromes or cholestatic liver disease. Compared to other lipoproteins, Lp-X contains a high content of unesterified cholesterol (30%, w/w) to
Biochemistry and clinical relevance of lipoprotein X.
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Lipoprotein X (LP-X) is an abnormal lipoprotein that appears in the sera of patients with obstructive jaundice and is thus a marker for cholestasis. The presence of LP-X in serum does not allow discrimination between intra- and extra-hepatic cholestasis. In addition LP-X is present in the plasma of
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