Abstract

Lecithin:cholesterol acyltransferase (LCAT) is the enzyme responsible for cholesterol esterification in plasma. LCAT is a major factor in HDL remodeling and metabolism, and it has long been believed to play a critical role in macrophage reverse cholesterol transport (RCT). The effect of LCAT on human atherogenesis is still controversial. In the present study, the plasma LCAT concentration was measured in all subjects (n = 540) not on drug treatment at the time of enrollment in the multicenter, longitudinal, observational IMPROVE study. Mean and maximum intima-media thickness (IMT) of the whole carotid tree was measured by B-mode ultrasonography in all subjects. In the entire cohort, LCAT quartiles were not associated with carotid mean and maximum IMT (P for trend 0.95 and 0.18, respectively), also after adjustment for age, gender, HDL-cholesterol (HDL-C), and triglycerides. No association between carotid IMT and LCAT quartiles was observed in men (P=0.30 and P=0.99 for mean and maximum IMT, respectively), whereas carotid IMT increased with LCAT quartiles in women (P for trend 0.14 and 0.019 for mean and maximum IMT, respectively). The present findings support the concept that LCAT is not required for an efficient reverse cholesterol transport and that a low plasma LCAT concentration and activity is not associated with increased atherosclerosis.

Highlights

  • Lecithin:cholesterol acyltransferase (LCAT) is the enzyme responsible for cholesterol esterification in plasma

  • The present findings support the concept that lecithin:cholesterol acyltransferase (LCAT) is not required for an efficient reverse cholesterol transport and that a low plasma LCAT concentration and activity is not associated with increased atherosclerosis.—Calabresi, L., D

  • The present study shows that low plasma levels of LCAT are not associated with increased carotid intima-media thickness (IMT) in individuals at high cardiovascular risk

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Summary

Introduction

Lecithin:cholesterol acyltransferase (LCAT) is the enzyme responsible for cholesterol esterification in plasma. Mean and maximum intimamedia thickness (IMT) of the whole carotid tree was measured by B-mode ultrasonography in all subjects. LCAT quartiles were not associated with carotid mean and maximum IMT (P for trend 0.95 and 0.18, respectively), after adjustment for age, gender, HDLcholesterol (HDL-C), and triglycerides. The lecithin:cholesterol acyltransferase (LCAT) enzyme catalyzes the transacylation of the sn-2 fatty acid of lecithin to the free 3-OH group of cholesterol, generating cholesteryl ester (CE) and lysolecithin [1]. LCAT preferentially binds to high density lipoproteins (HDL), where it is activated by apolipoprotein A-I; a minority of plasma LCAT circulates bound to apoB-containing lipoproteins [1]

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