A Comparison of the Secretion of Two Components of Very Low Density Lipoproteins by Perfused Rat Liver

1973 ◽  
Vol 51 (4) ◽  
pp. 490-494 ◽  
Author(s):  
Abraham I. Kook ◽  
David Rubinstein

The synthesis and secretion by perfused rat liver of the lipid and protein moieties of the α- and β-lipoprotein-containing components of the very low density lipoproteins was studied, following additions of [3H]palmitate and [14C]leucine to the perfusate. The lipid moieties of both components became labelled early in the perfusion, and had a pattern of labelling similar to that of their protein moieties. The protein of the α-lipoprotein component became labelled at the same time as the lipid. The appearance of the isotope in the β-lipoprotein component was delayed, but it then surpassed that of the α-lipoprotein component in both total radioactivity and specific activity. From these data a working hypothesis has been developed which suggests that the protein but not the lipid of the β-lipoprotein component is incorporated into very low density lipoprotein in the sequence in which it is synthesized, while the α-lipoprotein component is drawn randomly from a large pool.

1981 ◽  
Vol 59 (8) ◽  
pp. 709-714 ◽  
Author(s):  
P. Julien ◽  
A. Angel

In the present study, very low density lipoprotein (VLDL, d < 1.006) in cardiac lymph was characterized to determine its role as a metabolic substrate in the interstitial compartment. A major efferent cardiac lymph trunk was cannulated in fasting (18 h) dogs (20–27 kg). Three to five millilitres of lymph were collected over 3–4 h at 4 °C. Cardiac lymph VLDL concentration was 1.7 ± 0.7 mg protein∙100 mL−1 compared with 1.8 ± 0.8 mg protein∙100 mL−1 in plasma. The VLDL triglyceride concentration in lymph was 1.0 ± 0.3 mg triglyceride∙100 mL−1 with triglyceride/protein ratio of 0.9 compared with plasma VLDL triglyceride of 5.0 ± 1.6 mg∙100 mL−1 with a triglyceride/protein ratio of 5.5. Electron microscopy of VLDL revealed globular particles with a mean diameter of 388 Å in lymph and 661 Å in plasma. Thus, cardiac lymph VLDL are smaller and contain less triglyceride per particle than plasma VLDL. Following i.v. administration of human 125I-labelled low density lipoprotein ([125I]LDL, d 1.025–1.045), cardiac lymph/plasma LDL specific activity ratio was 0.52 ± 0.15 (n = 3) and 0.55 ± 0.15 (n = 4) at 3 and 27 h, respectively. The fact that the specific activity ratio did not reach 1 at plateau suggests continuous addition of unlabelled LDL in the cardiac interstitium, presumably from VLDL precursors. These findings demonstrate that on a protein basis the concentration of VLDL in cardiac lymph equals that of plasma, and also suggests that VLDL degradation and LDL production occur in the cardiac interstitial space.


1975 ◽  
Vol 150 (3) ◽  
pp. 315-321 ◽  
Author(s):  
S J Petersburg ◽  
A Madeley ◽  
D S Robinson

High and low rates of very-low-density-lipoprotein triacylglycerol release from the perfused rat liver were achieved by using livers taken respectively from animals that had been given fructose for 48h or from animals that had been starved for 18h. 2. The higher rates of very-low-density-lipoprotein triacylglycerol release by the livers of the fructose-fed rats were associated with higher rates of very-low-density-lipoprotein protein release. 3. When the livers were perfused in the presence of [3H]leucine, radioactivity was incorporated into the very-low-density-lipoprotein apoproteins. The higher rates of very-low-density-lipoprotein triacylgycerol and protein release by the livers of fructose-fed rats were associated with a greater total incorporation of radioactivity into those apoproteins that entered the running gel during polyacrylamide-gel electrophoresis. However, the distribution of radioactivity among the various apoproteins was not significantly changed by the dietary treatments used.


1981 ◽  
Vol 59 (6) ◽  
pp. 447-453 ◽  
Author(s):  
Simon-Pierre Noël ◽  
David Rubinstein

[3H]Cholesterol labelled very low density lipoproteins ([3H]chol-VLDL) were prepared to study the hepatic uptake of cholesterol associated with VLDL and its remnants in the perfused liver system. [3H]Chol-VLDL was incubated with rat postheparin plasma to produce labelled remnants in vitro. The degree of lipolysis of [3H]chol-VLDL depended on the ratio of triacylglycerols to lipase in the incubation medium. Therefore, the produced remnant of d < 1.019 g∙mL−1 had a variable lipid composition depending on the degree of lipolysis. [3H]Chol-VLDL or its remnants were added to liver perfusate and the radioactivity remaining in the perfusate was measured. The kinetic disappearance of [3H]chol-VLDL and its remnants in the perfused liver system indicated that remnant of d < 1.019 g∙mL−1 was taken up by the liver faster than the original VLDL preparation (t1/2 of 8 min vs. 51 min). Appearance of the label in bile during the perfusion was significantly faster when livers were perfused with [3H]chol-VLDL remnants as opposed to uncatabolized [3H]chol-VLDL.The results indicate that first of all, VLDL remnants produced in vitro and reisolated at density less than 1.019 g∙mL−1 do not have a fixed lipid composition but a rather variable one depending on the degree of lipolysis. Secondly, the rat liver may preferentially recognize this VLDL remnant of d < 1.019 g∙mL−1 and take it up more readily than uncatabolized VLDL. Finally when equimolar amount of cholesterol from VLDL or VLDL remnants are circulated in the liver perfusion, the VLDL remnants convey a significantly greater mass of cholesterol to the bile.


Lipids ◽  
1993 ◽  
Vol 28 (5) ◽  
pp. 419-425 ◽  
Author(s):  
Zu Jun Zhang ◽  
Henry G. Wilcox ◽  
Lawrence Castellani ◽  
Thomas V. Fungwe ◽  
Marshall B. Elam ◽  
...  

1989 ◽  
Vol 260 (1) ◽  
pp. 207-214 ◽  
Author(s):  
B S Robinson ◽  
Z Yao ◽  
D J Baisted ◽  
D E Vance

The metabolism of lysophosphatidylcholine was studied in cultured rat hepatocytes deficient in choline and methionine. Even though the cells were defective in phosphatidylcholine biosynthesis, the albumin-stimulated release of lysophosphatidylcholine (1.9 nmol/h per mg of cellular protein) was similar to that in hepatocytes supplemented with choline. Albumin also stimulated (1.4-fold) the release of phosphatidylcholine from the deficient cells. The extra phosphatidylcholine and lysophosphatidylcholine in the medium were largely recovered in the albumin fraction (density greater than 1.18 g/ml), suggesting that albumin released these lipids from hepatocytes because of binding to this protein. The secretion of glycerophosphocholine was decreased by about 40% by the addition of albumin. When choline-deficient hepatocytes were supplemented with lysophosphatidylcholine, it was transported into the cells and mainly acylated to form phosphatidylcholine, which increased in mass by 30-35% in the first 4 h of incubation. Lysophosphatidylcholine was shown to be as effective as choline in restoring the secretion of very-low-density lipoproteins to normal amounts, as judged by the secretion of triacylglycerol, phosphatidylcholine and the apolipoproteins associated with very-low-density lipoproteins. Thus phosphatidylcholine synthesis via reacylation of lysophosphatidylcholine, via the CDP-choline pathway or via methylation of phosphatidylethanolamine, will satisfy the requirements for secretion of very-low-density lipoprotein from hepatocytes.


1978 ◽  
Vol 176 (1) ◽  
pp. 169-174 ◽  
Author(s):  
P Thomopoulos ◽  
M Berthelier ◽  
D Lagrange ◽  
M J Chapman ◽  
M H Laudat

The effect of human plasma lipoproteins on lipogenesis from glucose has been studied in isolated rat adipocytes. The very-low-density lipoproteins increased lipogenesis specifically, whereas low-density lipoproteins and high-density lipoproteins were without effect. Such stimulation could be reproduced with partially delipidated very-low-density lipoproteins. Nod-esterified fatty acids and glycerol were also without effect. Pretreatment of the adipocytes with trypsin did not alter the effect of very-low-density lipoprotein. The presence of Ca2+ was required for the full activation of lipogenesis. The synthesis of acylglycerol fatty acids and of acylglycerol glycerol were equally increased. The effect of very-low-density lipoprotein was not additive to that of insulin. It is suggested that very-low-density lipoprotein may directly stimulate lipogenesis in fat-cells, particularly in states when the lipoproteins are present at high concentration in the circulation.


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