Lecithin: Cholesterol acyl transfer rate and high density lipoprotein level in coronary artery disease

Wallentin, Lars; Moberg, Birgitta

doi:10.1016/0021-9150(82)90181-2

Cited by 17 publications

(1 citation statement)

References 32 publications

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“…In a recently described kindred, heterozygous L C A T deficiency was the underlying cause of the qualitative and quantitative differences observed in plasma lipoproteins, with heterozygotes having higher fasting plasma triglicerides and ApoB, and lower H D L and ApoA1 levels, than unaffected family members (Frohlich et al 1988). On the other hand, a reduced fractional L C A T rate and a decreased H D L cholesterol/total cholesterol ratio were consistently found in a group of patients with angina pectoris and significant lesions at coronary angiography compared with controls (Wallentin and Moberg 1982). This paper reports, to our knowledge, the first mutation in a L C A T deficient gene; further definition of other mutations causing LCAT deficiency should lead not only to a better understanding of the genetics and biochemistry of the disease but to the generation of a battery of DNA diagnostic probes that could be employed in subjects at risk for atherosclerosis with low HDL and plasma cholesterol ester levels.…”

Section: Discussionmentioning

confidence: 99%

Lecithin cholesterol acyl transferase deficiency: molecular analysis of a mutated allele

Taramelli¹,

Pontoglio

Candiani³

et al. 1990

Hum Genet

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The enzyme, lecithin cholesterol acyltransferase (LCAT), is responsible for the esterification of plasma cholesterol mediating the transfer of an acyl group from lecithin to the 3-hydroxy group of cholesterol. Deficiency of the enzyme is a well-known syndrome with a widespread geographic occurrence. We have cloned an allele from a patient homozygous for the LCAT deficiency. The only change that we could detect is a C to T transition in the fourth exon of the gene; this causes a substitution of Arg for Trp at position 147 of the mature protein. The functional significance of such a substitution with respect to the enzyme defect was demonstrated by transfecting the mutated LCAT gene in the cell line COS-1.

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Section: Discussionmentioning

confidence: 99%

Lecithin cholesterol acyl transferase deficiency: molecular analysis of a mutated allele

Taramelli¹,

Pontoglio

Candiani³

et al. 1990

Hum Genet

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Lecithin: Cholesterol Acyltransferase Activity in Familial Hypercholesterolemia Treated with Simvastatin and Simvastatin Plus Low‐Dose Colestipol

Desager

Horsmans

Harvengt

1991

The Journal of Clinical Pharma

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In 19 patients with heterozygous familial hypercholesterolemia (FH), the effects of simvastatin (S) 20 mg/d, 40 mg/d, and 40 mg/d plus low-dose colestipol (10 g/d) on plasma lipids, plasma lipoproteins, and plasma lecithin: cholesterol acyltransferase (LCAT) activity were investigated after an original dose-range escalation/descalation design. The drug regimen was changed every 8 weeks. A significant reduction in total cholesterol and LDL-cholesterol was observed, reaching 39% and 54% for the drug combination (week 28), and total apoprotein B and LDL-apoprotein B were reduced by 39% and 50%, respectively. Triglycerides were significantly lowered by S alone (up to 29% with 40 mg/d). HDL-cholesterol increased during therapy but the cholesterol content in HDL2-HDL3 fractions (isolated by ultracentrifugation) did not change significantly during the different steps. The ratio LDL-C/HDL-C fell by 57% at week 28. Plasma LCAT activity expressed as FER was significantly enhanced by S alone (+33%), and a further increase on drug combination regimen (+58%) was observed. This effect could be considered as a consequence of the increased fractional clearance of LDL-C. It tended to be sustained during the descalation part of the study. Biochemical adverse effects were scarce and transient. In conclusion, the combination therapy increased the plasma LCAT/FER activity without a preferential enhancement in HDL2-C concentration. This original design allowed to define the most appropriate individual cholesterol-lowering drug dosage in FH patients.

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Lecithin: Cholesterol Acyltransferase (LCAT) Deficiency Syndromes

Fröhlich

McLeod

1986

Lipoprotein Deficiency Syndromes

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Lecithin: Cholesterol acyl transfer rate and high density lipoprotein level in coronary artery disease

Cited by 17 publications

References 32 publications

Lecithin cholesterol acyl transferase deficiency: molecular analysis of a mutated allele

Lecithin cholesterol acyl transferase deficiency: molecular analysis of a mutated allele

Lecithin: Cholesterol Acyltransferase Activity in Familial Hypercholesterolemia Treated with Simvastatin and Simvastatin Plus Low‐Dose Colestipol

Lecithin: Cholesterol Acyltransferase (LCAT) Deficiency Syndromes

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