Very Low Density Lipoprotein Apolipoprotein Research Articles

Lipoprotein (a) is not a metabolic product of other lipoproteins containing apolipoprotein B

125I-Labeled autologous very low density lipoprotein (VLDL) was injected intravenously into three lipoprotein (a) positive individuals. One other lipoprotein (a) positive subject received 125I-labeled VLDL from a lipoprotein (a) negative donor. Specific activity of apolipoprotein B in VLDL, low density lipoprotein (LDL) and lipoprotein (a) was measured for 5 days. In the lipoprotein (a) fraction only traces of radioactivity could be detected, which were caused by contamination with labeled LDL. No precursor-product relationship existed between apolipoprotein B in VLDL or LDL and apolipoprotein B in lipoprotein (a). One lipoprotein (a)-positive individual was kept on a fat-free diet for 4 days to prevent chylomicron formation; no change in the serum level of lipoprotein (a) could be detected under these conditions. The data of this study indicate that lipoprotein (a) is not a metabolic product of VLDL or LDL. Also chylomicrons are not likely to play a role as a precursor for lipoprotein (a). It is concluded that lipoprotein (a) is synthesized as a separate lipoprotein.

The effect of a low-cholesterol, high-polyunsaturate diet on serum lipid levels, apolipoprotein B levels and triglyceride fatty acid composition

1. (1) Seven healthy normolipaemic men aged 28–46 years (mean 33 years) were studied for four weeks on their usual diet, the mean polyunsaturated to saturated fat (P : S) ratio of which was approximately 0.23 and the cholesterol content 667 mg/day, and for four weeks on an isocaloric diet, containing similar proportions of protein, carbohydrate and fat, but with a mean P : S ratio of approximately 2.82 and a cholesterol content of 112 mg/day. 2. (2) Total serum cholesterol levels decreased by 18.7 ± 5.2% (mean ± SEM) on the polyunsaturated fat (PUF) diet. This was attributable to a similar reduction in serum low density lipoprotein (LDL) cholesterol. Serum very low density lipoprotein (VLDL) cholesterol showed no clear change. Total serum triglyceride levels decreased by 19.7 ± 7.1% due to a reduction in both serum VLDL and LDL triglyceride concentration. 3. (3) Total serum apolipoprotein B concentration fell by 23 ± 2.6% during the PUF diet. There was a decrease of similar magnitude in serum LDL apolipoprotein B, but no sustained effect on serum VLDL apolipoprotein B. 4. (4) Serum VLDL and LDL lipid to apolipoprotein B ratios did not change significantly during the study. 5. (5) Serum triglyceride fatty acid composition significantly altered during the PUF diet. The percentage of linoleic acid rose from 16 ± 0.90% to 36 ± 0.89%, whilst the percentage of combined saturated and monounsaturated acids fell correspondingly. These changes took place within 2 days of starting the PUF diet.

Metabolism of 125I-labeled lipoproteins by the isolated rat lung.

The capacity of the isolated perfused rat lung to metabolize the protein moieties of serum lipoproteins was assessed using homologous (rat) and heterologous (human) plasma lipoproteins. The protein and lipid moieties of the plasma lipoproteins were labeled in vivo with Na[125I]. In selected cases the lipoprotein peptides were labeled in vivo with 14C- or 3H-labeled amino acids. Uptake of lipoprotein label during perfusion was monitored by measure of losses in perfusate label and by rises in pulmonary tissue labeling as shown by radioassay and by light and electron microscope radioautography. Lipoprotein degradation was assessed by fractionation of perfusate and lung tissue radioactive material into trichloroacetic acid (TCA)-isoluble, TCA-soluble, and ether-ethanol-soluble fractions. When heparin was included in the perfusion medium, there was selective degradation of the protein portion of very low density lipoprotein (VLDL) in the perfusate and concomitant uptake of radioactive label by the lungs. Low density lipoprotein (LDL)) was neither taken up nor catabolized by the isolated rat lung in the absence or presence of heparin. By light and electron microscopy, the label was localized over the interalveolar septa, predominantly the capillary endothelium. Disappearance of TCA-insoluble radioactivity from the perfusate was associated with the generation of both TCA-soluble iodide and noniodide radioactivity. Greater than 50% of the radioactive label taken up by the lungs was found in the delipidated TCA-insoluble fraction. This study provides in vitro evidence for pulmonary catabolism of VLDL apolipoproteins and uptake of peptide catabolic products of VLDL by the lung.