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Taken together, these results suggest that apoE-containing discoidal HDLs do not require LCAT-dependent maturation to mediate efficient Abeta clearance
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increased cholesterol esterification by LCAT is atheroprotective
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Gene transfer of WT LCAT in LCAT(-/-) mice increased 11.8-fold the plasma cholesterol, whereas the LCAT[T147I] and LCAT[P274S] mutants caused a 5.2- and 2.9-fold increase, respectively.
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DYRK1A overexpression decreases plasma lecithin:cholesterol acyltransferase activity and apolipoprotein A-I levels.
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adrenal glucocorticoid function in LCAT knockout (KO) mice
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a novel function of apoA-IV in the biogenesis of discrete HDL-A-IV particles with the participation of ABCA1 and LCAT
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Studies suggest that absence of lecithin cholesterol acyltransferase (LCAT) may protect against insulin resistance, diabetes and obesity.
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Data show that LCAT activity was significantly higher in long chain base biosynthesis protein 2 (Sptlc2)+/- and sphingomyelin synthase 2 (Sms2)-/- mice, but markedly lower in ApoE-/- and Ldlr-/- mice.
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Lecithin:cholesterol acyltransferase deficiency protects against cholesterol-induced hepatic endoplasmic reticulum stress in mice.
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LCAT deficiency confers gender-specific protection against diet-induced obesity and insulin resistance at least in part through regulation in UPR, white adipose tissue adipogenesis, and brown adipocyte partitioning
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Oxidative stress is markedly elevated in lecithin:cholesterol acyltransferase-deficient mice and is paradoxically reversed in the apolipoprotein E knockout background in association with a reduction in atherosclerosis
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LCAT contributes significantly to the cholesteryl ester (CE) fatty acid pool of apoB lipoprotein and is the only source of plasma long chain polyunsaturated CE in LDL receptor and apoE knockout mice.
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hypertriglyceridemia and the improved fasting glucose phenotype seen in the lecithin-cholesterol acyltransferase and ldl receptor double knockout mice are in part attributable to up-regulation of hepatic sterol regulatory element binding factor-1c gene
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LCAT has a role in regulating plasma HDL cholesterol levels and biliary cholesterol excretion
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apoE is a more significant activator of LCAT than apoA-I on mouse apoB lipoproteins
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ACAT2 provides core CE of newly secreted VLDL, whereas LCAT adds CE during LDL particle formation
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In LCAT deficient mice, alterations in hepatic expression of the gene for fads2, soat2, and dgat2, results in changes in total hepatic and cholesterol ester-associated polyunsaturated fatty acids.
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LCAT deficiency induces complex alterations in hepatic signal transduction cascades.
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These data show that brain LCAT esterifies cholesterol on glial-derived apoE-lipoproteins, and influences CSF apoE and apoA-I levels.
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LCAT overexpression does not promote an increased rate of macrophage reverse cholesterol transport.
