lecithin cholesterol acyltransferase deficiency/debelost

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

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Prijava / prijava

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

Lecithin cholesterol acyltransferase null mice are protected from diet-induced obesity and insulin resistance in a gender-specific manner through multiple pathways.

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Prijava / prijava

Complete lecithin cholesterol acyltransferase (LCAT) deficiency uniformly results in a profound HDL deficiency. We recently reported unexpected enhanced insulin sensitivity in LCAT knock-out mice in the LDL receptor knock-out background (Ldlr(-/-)×Lcat(-/-); double knock-out (DKO)), when compared

Lecithin:Cholesterol Acyltransferase (LCAT) Deficiency Promotes Differentiation of Satellite Cells to Brown Adipocytes in a Cholesterol-dependent Manner.

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Prijava / prijava

Our laboratory previously reported that lecithin:cholesterol acyltransferase (LCAT) and LDL receptor double knock-out mice (Ldlr(-/-)xLcat(-/-) or DKO) spontaneously develop functioning ectopic brown adipose tissue (BAT) in skeletal muscle, putatively contributing to protection from the diet-induced

The role of lecithin:cholesterol acyltransferase in the modulation of cardiometabolic risks - a clinical update and emerging insights from animal models.

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Prijava / prijava

Lecithin cholesterol acyltransferase (LCAT) is the key enzyme in mediating the esterification of cholesterol on circulating lipoproteins. It has long been suggested that LCAT plays a crucial role in reverse cholesterol transport, a process depicting the removal of cellular cholesterol through efflux

Primary and secondary hypertriglyceridaemia.

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Prijava / prijava

Familial hypertriglyceridaemia is inherited in an autosomal dominant manner. The responsible genetic abnormality is unknown but recently, a novel gene encoding apolipoprotein AV has been linked to familial hypertriglyceridaemia. All patients develop the same phenotype with elevated levels of very

Novel metabolic phenotypes in lecithin cholesterol acyltyransferase-deficient mice.

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Prijava / prijava

OBJECTIVE Lecithin cholesterol acyltyransferase (LCAT) deficiency is a rare monogenic disorder causing lipoprotein dysregulation and multiple organ dysfunctions, including renal impairment. LCAT knockout mice have been shown informative in elucidating mechanisms of many major clinical morbid

[Familial hypoalphalipoproteinemia. Vergani's disease].

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Prijava / prijava

Deficiencies of lipoproteins occur as genetic disorders or may be presenting features of underlying disease. Familial high density lipoprotein (HDL), or alpha-lipoprotein, deficiency so far described includes Tangier disease, Lecithin: cholesterol acyltransferase (LCAT) deficiency, A-I Variants

Impact of apolipoprotein A1- or lecithin:cholesterol acyltransferase-deficiency on white adipose tissue metabolic activity and glucose homeostasis in mice.

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Prijava / prijava

High density lipoprotein (HDL) has attracted the attention of biomedical community due to its well-documented role in atheroprotection. HDL has also been recently implicated in the regulation of islets of Langerhans secretory function and in the etiology of peripheral insulin sensitivity. Indeed,

Diagnosis and treatment of high density lipoprotein deficiency.

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Prijava / prijava

Low serum high density lipoprotein cholesterol level (HDL-C) <40 mg/dL in men and <50 mg/dL in women is a significant independent risk factor for cardiovascular disease (CVD), and is often observed in patients with hypertriglyceridemia, obesity, insulin resistance, and diabetes. Patients with marked

Lecithin:Cholesterol Acyltransferase: Symposium on 50-years of biomedical research from its discovery to latest findings

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Prijava / prijava

Lecithin:cholesterol acyltransferase (LCAT) converts free cholesterol to cholesteryl esters in the process of reverse cholesterol transport. Familial LCAT deficiency (FLD) is a genetic disease that was first described by Kaare R. Norum and Egil Gjone in 1967. This report is a summary from a 2017

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