lecithin cholesterol acyltransferase deficiency/triglyceride

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Lecithin-cholesterol acyltransferase deficiency presenting with acute pancreatitis: effect of infusion of normal plasma on triglyceride-rich lipoproteins.

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A 38-year-old Asian man presented with acute pancreatitis, marked hypertriglyceridaemia and macroproteinuria, 20 years after the diagnosis of lecithin-cholesterol acyltransferase (LCAT) deficiency. After recovery, he exhibited macroproteinuria and chylomicronaemia despite treatment with a

Impaired intermediate-density lipoprotein triglyceride hydrolysis in familial lecithin:cholesterol acyltransferase (LCAT) deficiency.

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A new lecithin:cholesterol acyltransferase (LCAT)-deficient family was found in Japan. In the proband, both LCAT activity and LCAT mass were deficient. The patient's parents, child, and sister, diagnosed as heterozygotes, had half-normal LCAT activity and LCAT mass. In the patient, an increase of

[Impaired intermediate-density lipoprotein triglyceride hydrolysis in familial lecithin: cholesterol acyltransferase (LCAT) deficiency].

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Lecithin/cholesterol acyltransferase modulates diet-induced hepatic deposition of triglycerides in mice.

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Lecithin/cholesterol acyltransferase (LCAT) is responsible for the esterification of the free cholesterol of plasma lipoproteins. Here, we investigated the involvement of LCAT in mechanisms associated with diet-induced hepatic triglyceride accumulation in mice. LCAT-deficient (LCAT(-/-)) and control

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

Plasma lipoproteins in familial lecithin: cholesterol acyltransferase deficiency: lipid composition and reactivity in vitro.

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Plasma lipoproteins from patients with familial lecithin:cholesterol acyltransferase (LCAT) deficiency have been fractioned by preparative ultra-centrifugation and gel filtration and their lipid content and reactivity studied. All of the lipoproteins are abnormal with respect to lipid concentration

Abnormal plasma lipoproteins and lecithin-cholesterol acyltransferase deficiency in alcoholic liver disease.

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Serial studies of plasma lipids and lipoproteins were performed in 4 patients with acute alcoholic liver disease characterized by a massive fatty liver and laboratory evidence of intrahepatic cholestasis. There were striking alterations in the plasma lipoprotein electrophoretic patterns

Lipid and apolipoprotein concentrations in prenodal leg lymph of fasted humans. Associations with plasma concentrations in normal subjects, lipoprotein lipase deficiency, and LCAT deficiency.

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The extent to which lipid and apolipoprotein (apo) concentrations in tissue fluids are determined by those in plasma in normal humans is not known, as all studies to date have been performed on small numbers of subjects, often with dyslipidemia or lymphedema. Therefore, we quantified lipids,

Splenomegaly with sea-blue histiocytosis, dyslipidemia, and nephropathy in a patient with lecithin-cholesterol acyltransferase deficiency: a clinicopathologic correlation.

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A 31-year-old man with no significant medical history presented with a 5-day history of progressive left upper quadrant abdominal pain. Physical examination revealed a tender guarded abdomen, no icterus, and bilateral corneal "arcus senilis"-like changes. Laboratory workup showed a mild normocytic,

Bile acids and plasma high density lipoproteins: biliary lipid metabolism in fish eye disease.

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Cholesterol in plasma high density lipoproteins (HDL) has been proposed to serve as preferential precursor for bile acid biosynthesis in the liver. Furthermore, a negative relationship between plasma levels of HDL cholesterol and biliary saturation with cholesterol has been reported in healthy

Lecithin cholesterol acyltransferase deficiency protects from diet-induced insulin resistance and obesity--novel insights from mouse models.

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Reduced plasma level of high-density lipoprotein cholesterol is an independent risk factor for atherosclerotic heart disease and is also a major diagnostic feature for the metabolic syndrome. Lecithin cholesterol acyltransferase (LCAT), an enzyme mediating the esterification of cholesterol in

Normalization of high density lipoprotein in fish eye disease plasma by purified normal human lecithin: cholesterol acyltransferase.

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Plasma from a patient with fish eye disease has been enriched with autologous high density lipoproteins (HDL) and supplemented with highly purified normal human plasma lecithin:cholesterol acyltransferase (LCAT). Incubation of such plasma at 37 C in vitro resulted in normalization of its low HDL

Hypertriglyceridemia in lecithin-cholesterol acyltransferase-deficient mice is associated with hepatic overproduction of triglycerides, increased lipogenesis, and improved glucose tolerance.

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Lecithin-cholesterol acyltransferase deficiency is frequently associated with hypertriglyceridemia (HTG) in animal models and humans. We investigated the mechanism of HTG in the ldlr-/- x lcat-/- (double knockout (dko)) mice using the ldlr-/- x lcat+/+ (knock-out (ko)) littermates as control. Mean

Plasma lipid transfer in fish-eye disease.

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Fish-eye disease is a familial condition characterized by corneal opacities and dyslipoproteinaemia with, i.a., pronounced enrichment of plasma low density lipoprotein (LDL) with triglycerides. Cholesterol ester and triglyceride transferase activities in lipoprotein-free plasma have been measured in

Fish eye disease: a new familial condition with massive corneal opacities and dyslipoproteinaemia.

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Fish eye disease (FED) is characterized by severe corneal opacities, causing impaired vision, and dyslipoproteinaemia: hypertriglyceridaemia, raised levels of very low density lipoproteins (VLDL), triglyceride enrichment of low density lipoproteins (LDL) and reduction of high density lipoproteins

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