Sh. Quarfordt et al., PLASMA-LIPOPROTEINS AFTER TRIGLYCERIDE CLEARANCE IN CHOLESTEROL-FED RATS, The Journal of clinical investigation, 91(6), 1993, pp. 2532-2538
The clearance of particulate triglyceride from the plasma of cholester
ol-fed rats with appreciable stores of hepatic cholesterol ester produ
ces a substantial increment in plasma cholesterol. Most of this plasma
cholesterol increment arises from existing tissue sources. The increm
ent begins from 4 to 6 h after clearance and is due to the appearance
of larger cholesterol-rich, triglyceride-poor, beta migrating lipoprot
eins, which are isolated in the d < 1.063 fraction with an apoprotein
(Apo) content consisting primarily of Apo E and smaller amounts of Apo
B. A concurrent decrease in a lipoproteins occurs with the beta lipop
rotein increment. Within 1 d of clearance the beta lipoproteins fall a
nd alpha lipoproteins increase. The increase in total plasma Apo E and
Apo B initially parallels that of the cholesterol, but it persists ev
en when cholesterol falls. A modest decrease in plasma Apo A1 was obse
rved during the time alpha lipoproteins declined. A significant increa
se in plasma lecithin cholesterol acyl transferase preceded the increa
se in beta lipoprotein cholesterol. This enzyme increment was absent i
n rats with little lipoprotein response despite increased hepatic chol
esterol. In vivo inhibition of this enzyme with dithionitrobenzoic aci
d virtually eliminated the postclearance hypercholesterolemia. Plasma
particulate triglyceride clearance induces an increase in beta lipopro
teins. Coupling of this clearance and hepatic lipoprotein secretion oc
curs by an unknown mechanism modulated b lecithin cholesterol acyl tra
nsferase.