Abstract
The rat liver secretes very low density lipoproteins (VLDL) containing either apoB-100 or apoB-48. After oral fat intake, chylomicrons containing apoB-48 and endogenously synthesized VLDL are mixed in the blood and the triglyceride clearance from these triglyceride-rich lipoprotein species compete for the same lipolytic pathway, i.e., lipoprotein lipase. A situation mimicking alimentary lipemia was induced by a short-term intravenous primed infusion of a chylomicron-like triglyceride emulsion to fed and fasted rats. The plasma concentration of apoB-100 and apoB-48 was monitored in triglyceride-rich lipoprotein subfractions after separation with density gradient ultracentrifugation by analytical SDS-PAGE. The net liver secretory output of VLDL was quantified by lipolytic blockade induced by Triton WR 1339. The chylomicron-like triglyceride emulsion induced a linear increase of large VLDL (Sf 60-400 subfraction containing both apoB-100 and apoB-48), almost to the same extent as that induced by Triton. The clearance of postprandial triglyceride-rich lipoproteins and both lipolysis and clearance of intravenously injected labeled rat chylomicrons was efficiently inhibited by the emulsion but not so complete as for fasting VLDL. The linearity of the VLDL increase and the very early response in the Intralipid-treated rats suggest that enhanced synthesis of VLDL is not a major cause for the accumulation. Rather, the present data indicate that a high plasma concentration of a chylomicron-like triglyceride emulsion competes efficiently with liver-derived VLDL for the same lipolytic pathway, which leads to accumulation in plasma of endogenous VLDL in the postprandial state.
Highlights
The rat liver secretes very low density lipoproteins (VLDL)containing either apoB-100or apoB-48
In this study we address the issue of accumulation of triglyceride-rich lipoproteins after an oral fat load by using specific methods for identification of endogenous triglyceride-richlipoprotein particles during experimental postprandial hypertriglyceridemia in the rat and comparing the results with complete inhibition of lipolysis in vivo
The chyle was layered under 9 mg/l NaC1,50 pg/ml gentamycin and 5 mM EDTA and Influence of Intralipid on apoB48 and B-100 measurements centrifuged in a Beckman SW 50 rotor at 30,000 rpm for 30 min at +4"C(14).The top layer was recovered and the chylomicrons were resuspended in the same buffer
Summary
Ejby, Denmark) weighting 190-210 g were used in the experiments. The rats had been acclimatized in the animal house for at least 1week before start of the experiment. They were kept on a 12-h light cycle (7 AM to 7 PM) and were allowed free access to standard pellet diet. When fasted rats were studied, the pellets were removed at 7 PM the day before the experiment. There were six rats in each group (Co, control; IL, Intralipid; Tri, Triton WR 1339).Experiments were performed on groups of fasted and fed rats separately. Rats were anesthetized by an intramuscular injection of Hypnorm (0.5 ml/kg bwt) and Stesolid Novum (2.5 mg diazepam/kg bwt) (Dumex, Copenhagen, Denmark). All experimental procedures were approved by the local ethics committee (UmeA University)
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