Abstract
High-density lipoprotein (HDL) remodeling within the plasma compartment and the association between lecithin-cholesterol acyltransferase (LCAT) and cholesterol ester transfer protein (CETP) activity, and lipid, lipoprotein concentrations and composition were investigated. The aim was to examine the high sensitivity of C-reactive protein (hsCRP), lipid, apolipoprotein B (apoB), apoAI, total apoAII, apoAIInonB, apoB-containing apoAII (apoB:AII), total apoCIII, apoCIIInonB, apoB-containing apoCIII (apoB:CIII) concentration and LCAT and CETP activity to gain an insight into the association between them and LCAT and CETP, 57 post-renal transplant (Tx) patients with and without statin therapy and in 15 healthy subjects. Tx patients had moderate hypertriglyceridemia, hypercholesterolemia, and dyslipoproteinemia, disturbed triglyceride-rich lipoproteins (TRLs) and HDL composition, decreased LCAT, and slightly increased hsCRP but no CETP activity. Spearman’s correlation test showed the association between lipids and lipoproteins and LCAT or CETP, and multiple ridge stepwise forward regression showed that immunosuppressive therapy in Tx patients can disturb HDL and TRLs composition. The results suggest that inhibition or activation of LCAT is due, in part, to HDL-associated lipoprotein. Lipoprotein composition of apoAI, apoAIInonB, and apoCIIInonB in HDL particle and apoB:AII TRLs can contribute to decrease LCAT mass in Tx patients. Tx patients without statin and with lower triglycerides but higher HDL cholesterol concentration and disturbed lipoprotein composition of ApoAI and apoAII in HDL particle can decrease LCAT, increase LDL cholesterol, aggravate renal graft, and accelerate atherosclerosis and chronic heart diseases.
Highlights
Lecithin-cholesterol acyltransferase (LCAT) is a plasma enzyme that esterifies cholesterol and raises high-density lipoprotein cholesterol (HDL-C)
The aim was to examine the high sensitivity of C-reactive protein, lipid, apolipoprotein B, apoAI, total apoAII, apoAIInonB, apoB-containing apoAII, total apoCIII, apoCIIInonB, apoB-containing apoCIII concentration and lecithin-cholesterol acyltransferase (LCAT) and cholesterol ester transfer protein (CETP) activity to gain an insight into the association between them and LCAT and CETP, 57 post-renal transplant (Tx) patients with and without statin therapy and in 15 healthy subjects
The results suggest that inhibition or activation of LCAT is due, in part, to High-density lipoprotein (HDL)-associated lipoprotein
Summary
Lecithin-cholesterol acyltransferase (LCAT) is a plasma enzyme that esterifies cholesterol and raises high-density lipoprotein cholesterol (HDL-C). Cholesteryl esters (CE) are significantly more hydrophobic than free cholesterol and are formed by LCAT partition from the surface of lipoprotein to the hydrophobic core. This transforms the small pre-b HDL into larger, spherical-shaped a-migrating forms of high-density lipoprotein (HDL). After cholesterol esterification by LCAT, the cholesteryl esters on the HDL are transferred to apoB-containing lipoproteins by cholesteryl ester transfer protein (CETP), approximately 25 % of cholesteryl esters are directly formed on apoB-containing lipoproteins.
Sign-in/Register to view highlights & summary 
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call