Abstract
Effects of LCAT on hyperlipidemia are very interesting. To study LCAT reaction on lipoprotein metabolism in the normal state, the followings were studied: location of LCAT in the blood, esterification of cholesterol in lipoproteins by LCAT, relationship between LCAT activity and serum lipoprotein concentration, lipid concentration and the degree of obesity in 130 of healthy controls.
LCAT activity was assayed by Glomset and Akanuma's method and lipoprotein concentration was measured by the ultracentrifugation method.
LCAT was the most active in Density>1.210g/ml protein and the degree of LCAT activity was gradually in Density>1.210g/ml protein fraction>in high density lipoprotein3 (HDL3)>in high density lipoprotein2 (HDL2)>in low density lipoprotein (LDL), in very low density lipoprotein (VLDL).
Furthermore, LCAT in the protein had activity sufficiently in the substrate-lipoprotein.
It seemed that LCAT is not necessarily combined with lipoproteins in the blood.
On the other hand, concerning to the substrate of LCAT reaction, HDL (especially HDL3) was supposed to be the most effective substrate.
Significant positive correlations were observed between LCAT activity and VLDL, LDL, total cholesterol, esterified cholesterol, unesterified cholesterol, triglyceride, phospholipid levels and the degree of obesity.
Because of this observation in the normal state, it is suspected that LCAT activity may not affect lipoprotein and lipid concentrations but rather lipoprotein and lipid concentrations may affect LCAT activity.
