Effects of dietary protein on composition and turnover of apoproteins in plasma lipoproteins of rabbits

1981 ◽  
Vol 59 (8) ◽  
pp. 642-647 ◽  
Author(s):  
D. C. K. Roberts ◽  
M. E. Stalmach ◽  
M. W. Khalil ◽  
J. C. Hutchinson ◽  
K. K. Carroll

The hypercholesterolemia and atherosclerosis produced in rabbits by feeding cholesterol-free, semipurified diets are due to the use of casein as the protein component of such diets and can be prevented by replacing the casein with isolated soy protein. To investigate the reasons for the differing effects of these dietary proteins on plasma cholesterol levels, plasma lipoproteins were isolated from rabbits fed semipurified diets containing either casein or isolated soy protein, labeled with 125I, and reinjected into rabbits fed one or other of these two diets. 125I-labeled apoproteins of intermediate density lipoprotein, isolated from rabbits on either diet, turned over more rapidly in rabbits fed soy protein compared with those fed casein. 125I-labeled apoproteins of very low density lipoprotein from rabbits fed soy protein were transferred to high density lipoprotein more rapidly than those from rabbits fed casein. In this case, the results were determined primarily by the diet fed to the donor rabbits, but the diet fed to the recipients also appeared to have some influence. The apoproteins of plasma lipoproteins from rabbits fed casein or soy protein were separated by isoelectric focussing and tentatively identified by comparison of their isoelectric points with those of apoproteins from human plasma lipoproteins. The concentration of apoprotein E was markedly increased in the very low density and intermediate density lipoproteins of casein-fed rabbits, and apoprotein C was also increased in the very low density lipoprotein of rabbits fed casein, compared with those fed soy protein. Effects of dietary proteins on plasma cholesterol may be secondary to their effects on the composition and metabolism of the protein components of plasma lipoproteins.

1977 ◽  
Vol 53 (3) ◽  
pp. 221-226
Author(s):  
D. Reichl ◽  
N. B. Myant ◽  
J. J. Pflug ◽  
D. N. Rudra

1. The transport of apoprotein B from the lipoproteins of plasma into the lipoproteins of lymph draining the foot has been studied in four men with type III hyperlipoproteinaemia. 2. Three subjects were given autologous 125I-labelled very-low-density lipoprotein (VLDL) and 131I-labelled low-density lipoprotein (LDL) by intravenous injection; the fourth was given autologous 125I-labelled VLDL and 131I-labelled intermediate-density lipoprotein (IDL) plus LDL. 3. The 125I/131I ratios in serum and lymph apoprotein B, and the 125I and 131I specific radioactivities of apoprotein B in VLDL, IDL and LDL from serum and lymph, indicate that apoprotein B in the circulating VLDL can reach peripheral lymph without the intermediacy of circulating LDL.


Author(s):  
D. A. Helen Sheeba ◽  
R. Gandhimathi

Introduction: Hyperlipidemia is a medical condition indicated by an increase in one or more plasma lipids, such as triglycerides, cholesterol, cholesterol esters, phospholipids, and/or plasma lipoproteins, such as very low-density lipoprotein and low-density lipoprotein, as well as decreased levels of high-density lipoprotein. This increase in plasma lipids is one of the most important risk factors for cardiovascular disease. In the meanwhile, statins and fibrates remain the most common anti-hyperlipidemic drugs for treating high plasma cholesterol and triglycerides. Conclusion: Hence this review focused to study of hyperlipidemia. This review is useful to research work in hyperlididemia.


1976 ◽  
Vol 35 (01) ◽  
pp. 178-185 ◽  
Author(s):  
Helena Sandberg ◽  
Lars-Olov Andersson

SummaryHuman plasma lipoprotein fractions were prepared by flotation in the ultracentrifuge. Addition of these fractions to platelet-rich, platelet-poor and platelet-free plasma affected the partial thromboplastin and Stypven clotting times to various degrees. Addition of high density lipoprotein (HDL) to platelet-poor and platelet-free plasma shortened both the partial thromboplastin and the Stypven time, whereas addition of low density lipoprotein and very low density lipoprotein (LDL + VLDL) fractions only shortened the Stypven time. The additions had little or no effect in platelet-rich plasma.Experiments involving the addition of anti-HDL antibodies to plasmas with different platelet contents and measuring of clotting times produced results that were in good agreement with those noted when lipoprotein was added. The relation between structure and the clot-promoting activity of various phospholipid components is discussed.


2020 ◽  
Vol 9 (24) ◽  
Author(s):  
Ozan Dikilitas ◽  
Benjamin A. Satterfield ◽  
Iftikhar J. Kullo

Background Atherosclerosis in >1 vascular bed (ie, polyvascular disease), often a feature of peripheral artery disease (PAD), is associated with high morbidity and mortality. We sought to identify risk factors for polyvascular involvement in patients with PAD. Methods and Results We performed 2‐sample Mendelian randomization using an inverse‐variance‐weighted approach, to assess 60 exposures including size and lipid content of atherogenic lipoproteins, blood pressure, glycated hemoglobin, and smoking as causal mediators for polyvascular disease in patients with PAD. Genetic instruments for these exposures were obtained from prior genome‐wide association studies. Patients with PAD were from the Mayo Vascular Disease Biorepository, and polyvascular disease (ie, concomitant coronary heart disease, cerebrovascular disease, and/or abdominal aortic aneurysm) was ascertained by validated phenotyping algorithms. Of 3279 patients with PAD, 61% had polyvascular disease. Genetically predicted levels of the lipid content and/or particle measures of very small and small size very low‐density lipoprotein, intermediate‐density lipoprotein, and large low‐density lipoprotein were associated with polyvascular disease: odds ratios (OR) of 1.80 (95% CI, 1.23–2.61), 1.70 (95% CI, 1.17–2.61), and 1.40 (95% CI, 1.09–1.80) per 1 SD increase in genetically determined levels, respectively. Both genetically predicted diastolic and systolic blood pressure were associated with polyvascular disease; OR per 10 mm Hg genetic increase in diastolic and systolic blood pressure were 1.66 (95% CI, 1.19–2.33) and 1.31 (95% CI, 1.07–1.60), respectively. Conclusions Lifetime exposure to increased lipid content and levels of very small and small very low‐density lipoprotein, intermediate‐density lipoprotein, and large low‐density lipoprotein particles as well as elevated blood pressure are associated with polyvascular involvement in patients with PAD. Reduction in levels of such exposures may limit progression of atherosclerosis in patients with PAD.


2007 ◽  
Vol 403 (2) ◽  
pp. 359-367 ◽  
Author(s):  
Kyriakos E. Kypreos ◽  
Vassilis I. Zannis

We have investigated the ability of apoE (apolipoprotein E) to participate in the biogenesis of HDL (high-density lipoprotein) particles in vivo using adenovirus-mediated gene transfer in apoA-I−/− (apolipoprotein A-I) or ABCA1−/− (ATP-binding cassette A1) mice. Infection of apoA-I−/− mice with 2×109 pfu (plaque-forming units) of an apoE4-expressing adenovirus increased both HDL and the triacylglycerol-rich VLDL (very-low-density lipoprotein)/IDL (intermediate-density lipoprotein)/LDL (low-density lipoprotein) fraction and generated discoidal HDL particles. ABCA1−/− mice treated similarly failed to form HDL particles, suggesting that ABCA1 is essential for the generation of apoE-containing HDL. Combined infection of apoA-I−/− mice with a mixture of adenoviruses expressing both apoE4 (2×109 pfu) and human LCAT (lecithin:cholesterol acyltransferase) (5×108 pfu) cleared the triacylglycerol-rich lipoproteins, increased HDL and converted the discoidal HDL into spherical HDL. Similarly, co-infection of apoE−/− mice with apoE4 and human LCAT corrected the hypercholesterolaemia and generated spherical particles, suggesting that LCAT is essential for the maturation of apoE-containing HDL. Overall, the findings indicate that apoE has a dual functionality. In addition to its documented functions in the clearance of triacylglycerol-rich lipoproteins, it participates in the biogenesis of HDL-sized apoE-containing particles. HDL particles generated by this pathway may account at least for some of the atheroprotective functions of apoE.


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