Effects of Intralipid on Cholesterol Esterification in Human Plasma

Effects of Intralipid on cholesterol esterification in human plasma were investigated. LCAT activities were estimated by a slightly modified method of Stokke and Norum. Intralipid significantly stimulated cholesterol esterification rates in the fresh human plasma. However, Intralipid significantly inhibited cholesterol erterification rated in the post-heparin plasma (PHP).In order to study on the mechanism of the stimulation of LCAT activities by Intralipid, the changes in the radioactivities of esterified cholesterol (EC) and of free cholesterol. (FC) in chylomicron (Chyl), very low density lipoprotein (VLDL), intermediate density lipoprotein (IDL), low density lipoprotein (LDL) and high density lipoprotein (HDL) during 4 hours' incubation of H3-free cholesterol with the fresh fasting plasma with or without Intralipid were estimated. The radioactivities of EC in Chyl were significantly higher in the incubation with Intralipid. The radioactivities of EC in VLDL and IDL tended to be higher in the incubation with Intralipid than without Intralipid but were not significantly different.The radioactivities of FC in Chyl were significantly higher in the incubation with Intralipid than without Intralipid but no time related changes were observed. The radioactivities of EC in LDL and HDL equally increased during the incubation with or without Intralipid. The radioactivities of FC in LDL and HDL decreased equally during the incubation with or without Intralipid.The affinities of FC and of CE to lipoprotein fractions were also investigated. H3-FC or C14-CE labeled albumin was incubated with the fresh plasma at 4°C for 2 hours and then, was incubated with Intralipid for 30 minutes. The radioactivities distributions were measured. C14-CE had high affinity to Chyl and VLDL fraction. However, H3-FC had high affinity to LDL and HDL.We concluded that EC formed in the plasma, mainly in HDL was trasfered to Intralipid and cholesterol esterification continued without the inhibition by the product of LCAT reaction.